NIEUW: Blog reclamevrij maken?
Op zoek naar een bepaalde info ? Geef dan hieronder een trefwoord in...
Zoeken in blog

Foto
Welkom ! Welkom ! Welkom ! Welkom ! Welkom ! Welkom ! Welkom ! Welkom ! Welkom ! Welkom ! Welkom ! Welkom !
Foto
Gastenboek
  • buy furosemide australia is there an over the counter furosemide
  • cialis with dapoxetine Si
  • celexa cost cvs order celexa online no prescription
  • viagra with dapoxetine Si
  • naproxen dosage over the counter can you buy naproxen 250 mg over the counter

    Druk oponderstaande knop om een berichtje achter te laten in mijn gastenboek

    Foto
    Raadpleeg steeds je arts !
    Foto
    Laatste commentaren
  • oknyeqgyrx (Evgidell)
        op Fibromyalgie - Chronische slaapstoornissen
  • bwysukkjhdficj (Grdmorgo)
        op Fibromyalgie - Chronische slaapstoornissen
  • how much cost viagra samples (GenaHoF)
        op Even geduld...
  • agadckfkpnmxdq (TbsRuirl)
        op Fibromyalgie - Chronische slaapstoornissen
  • Frerajod adjurnerxc (BrcSteamb)
        op Fibromyalgie - Chronische slaapstoornissen
  • ymjubvdizuyinq (Gbrteems)
        op Fibromyalgie - Chronische slaapstoornissen
  • mlfqbwrqeoihbw (Ltvstync)
        op Fibromyalgie - Chronische slaapstoornissen
  • sgqdrubnlynuqd (RnlFrork)
        op Fibromyalgie - Chronische slaapstoornissen
  • wfvdwszughkmrq (Fvrtwelt)
        op Fibromyalgie - Chronische slaapstoornissen
  • bseajpbfcpahms (FvlTrity)
        op Fibromyalgie - Chronische slaapstoornissen
  • Foto
    Blog als favoriet !
    Foto
    Willekeurig SeniorenNet Blogs
    ikke1
    blog.seniorennet.be/ikke1
    Willekeurig SeniorenNet Blogs
    ludovikus
    blog.seniorennet.be/ludovik
    Willekeurig SeniorenNet Blogs
    vaktermenkeuken
    blog.seniorennet.be/vakterm
    Willekeurig SeniorenNet Blogs
    lady488
    blog.seniorennet.be/lady488
    Willekeurig SeniorenNet Blogs
    wetters
    blog.seniorennet.be/wetters
    Foto
    Mijn favorieten
  • Kennis=macht=gezondheid - Pillie Willie
  • Vlaamse Liga voor Fibromyalgie PatiŽnten
  • Lotgenoten Fibromyalgie Nederland
  • APS-Therapie
  • Alles over fibromyalgie
  • Fibromyalgie-Online
  • Leven met CVS / Leven met Fibromyalgie
  • Gezondheidspein.nl
  • TopSiteGuide.BelgischeTop100
  • Fibromyalgie PR-site
    Foto
    Fibromyalgie
    Strijd om erkenning
    20-12-2007
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Is chronic fatigue syndrome a physical or a psychological affliction ?
    Klik op de afbeelding om de link te volgen

     







    Is chronic fatigue syndrome
    a physical
    or
    a psychological affliction ?

    University of Calgary,
    2007, December 19

    ScienceDaily ó One of the most difficult things for people suffering from Chronic Fatigue Syndrome (CFS) is that many believe the condition to be a psychological, not physical affliction.
    New research by the Faculty of Kinesiology hopes to measure one of the syndrome's most obvious symptoms -- information that could help doctors in the diagnosis CFS.

    "Diagnosis of the syndrome, generally follows eliminating every other possible cause, which leads some to speculate that the condition isn't real," says Dr. Brian MacIntosh : "One thing we know is that CFS sufferers feel profound fatigue and worsening of other symptoms following even moderate physical activity. Using our expertise in the field of exercise physiology we believe we can measure this post exertion malaise and say with certainty if an individual has recovered from exercise or if that activity is making them even more fatigued."

    MacIntosh, who is the Faculty of Kinesiology's Associate Dean of Graduate Studies, is an expert in the area of muscle fatigue.
    Much of his research has centered on high-performance athletes in peak physical condition, however he says that this research fits in well with his overall area of interest.

    "The tools we have developed in high performance sport are perfectly suited to track muscle fatigue in this application so without question we will be able to get some concrete answers," he says.

    The research trial will put CFS patients on a stationary bike to perform a VO2 Max test -- similar to trials used to evaluate the fitness level of professional athletes.
    The individual will pedal to the point of fatigue, at which point researchers will take several measurements including a blood sample in which lactate will be quantified.
    The next day the patient will return and follow the same workout protocol.

    "Most healthy individuals should be able to easily match their performance from the previous day," MacIntosh explains : "Since CFS patients by definition report profound fatigue from even moderate physical exertion and take greater than 24 hours to recover, we would expect to see a decrease in their physical performance and we should be able to measure that in several ways."

    This work may shed some light on whether the fatigue experienced by people with CFS is primarily in the muscles or in the nervous system.
    MacIntosh believes that the results of this work could lead to a definitive diagnosis of CFS, giving another tool in the otherwise limited toolbox of diagnostic tests and perhaps, more importantly, shed some light on the broader issue of human muscle fatigue.

    "We've all experienced fatigue in our lives," says MacIntosh : "For example when we have the flu or any similar illness, we feel that fatigue makes our arms and legs feel like they're made of lead... I'm hoping that this research may lead to a greater understanding of human muscle fatigue in general."


    Cfr. :
    http://www.sciencedaily.com/releases/2007/12/071218115629.htm

    20-12-2007 om 20:01 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 0/5 - (0 Stemmen)
    >> Reageer (0)
    18-12-2007
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Met positief denken red je het niet - Invloed van psyche op ziekte schromelijk overschat
    Klik op de afbeelding om de link te volgen

     










    Met positief denken
    red je het niet
    Invloed van psyche
    op ziekte
    schromelijk overschat

    Elke van Riel
    (illustraties L. Masselink) Intermediair.nl, 1
    4-11-07

    Gemoedstoestand en gezondheid beÔnvloeden elkaar, maar anders dan velen denken.
    Zo heeft iemands psychische gesteldheid nauwelijks invloed op het ontstaan en verloop van kanker.
    En auto-immuunziekten en hart- en vaatziekten beÔnvloeden juist de hersenen en daarmee de stemming.

    Hebben onze gedachten invloed op onze gezondheid ?
    Volgens de grote schare aanhangers van de bestseller 'The Secret' wel.
    Sterker : onze gedachten zouden de werkelijkheid en daarmee ook onze gezondheid bepalen.
    Kanker zou zelfs een gevolg zijn van negatieve gedachten - een nogal belastend idee voor mensen met deze ziekte en bovendien aantoonbaar onjuist.

    Het overschatten van de rol die onze geest speelt bij ziekte is hardnekkig.
    Al zeker twintig jaar verschijnt een gestage stroom boeken met titels als 'De zin van ziek zijn', 'Genees jezelf !' en 'Heel je lichaam'.
    Uitgangspunt is steevast dat ziekte het product is van een bepaalde verstoring van de psyche.
    ĎPositief denken' zou daarom de sleutel zijn tot genezing.

    Nu zijn er inderdaad verbanden tussen gemoedstoestand en gezondheid.
    Zo bleek jaren geleden al uit een Amerikaans onderzoek dat de griepprik minder goed aansloeg bij verdrietige en sombere mensen; hun immuunsysteem draaide kennelijk op een lager pitje.
    Niemand zal griep echter een psychosomatische ziekte noemen.

    Medisch onbegrepen klachten worden door artsen nogal eens afgedaan als iets dat Ďtussen de oren' zit.
    ĎDat is de ergste kreet die ik ken', zegt Cobi Heijnen, hoogleraar psychoneuro-immunologie aan de Universiteit Utrecht en gespecialiseerd in stress : ĎDaarmee laat je patiŽnten met reŽle klachten verschrikkelijk in de steek'.

    In het stressonderzoek is de laatste vijftien jaar duidelijk geworden hoe zeer lichaam en geest samenhangen : hersenen, hormonen en afweersysteem vormen ťťn groot netwerk, waarvan de delen elkaar op allerlei manieren beÔnvloeden.
    Zo leidt langdurige blootstelling aan stresshormonen tot duidelijk waarneembare veranderingen in de hersenen en het immuunsysteem.
    Bij ratten bleek toediening van stresshormonen vlak na de geboorte op langere termijn te leiden tot hoge bloeddruk, nierproblemen, hormonale veranderingen, afwijkingen aan hart- en bloedvaten en veranderingen in het immuunsysteem.
    Dat verkorte het leven van de ratten met een kwart.

    Stress kan dus ziek maken.
    Het verergert daarnaast ook veel kwalen, zonder er direct de oorzaak van te zijn.
    Dat geldt bijvoorbeeld voor auto-immuunziekten, zoals multiple sclerose en reuma.
    Heijnen : ĎJe krijgt geen immunologische afwijkingen door stress. Maar er is wel een verband andersom : van lichaam op hersenen.'
    Zo komen bij reuma ontstekingsfactoren in het bloed.
    Deze Ďboodschapperstofjes', cytokinen, dringen door tot de hersenen en beÔnvloeden daar rechtstreeks hormonale systemen, gevoelens en gedrag.
    Ze veroorzaken niet alleen hoofdpijn en spierpijn, algehele malaise, een lagere pijndrempel en extreme vermoeidheid, maar ook depressie.
    Dit mechanisme is bij dieren overtuigend aangetoond, aldus Heijnen : ĎDe depressieve klachten bij auto-immuniteit werden lang afgedaan als een psychisch gevolg van de pijn. Maar vooral door de komst van een nieuwe generatie reumamedicijnen - de zogeheten cytokine-antagonisten (TNF-Alpha remmers) - dringt het inzicht do
    or dat dit niet klopt. Ze remmen lokale ontstekingen, maar hebben ook een positief effect op vermoeidheid, pijnbeleving ťn stemming.'

    Bij alle chronische ontstekingsziekten: hart- en vaatziekten en Ė opmerkelijk - ook bij depressie, beÔnvloeden cytokinen de hersenen.
    Ze veroorzaken daar de productie van nog meer cytokinen en - via een nog onbekend mechanisme - een (ernstiger) depressie.
    ĎDaarvoor kun je antidepressiva geven, maar je kunt ook die cytokinen beÔnvloeden.'

    Heijnens hypothese is dat bij medisch onverklaarbare klachten als het chronische vermoeidheidssyndroom (cvs) een ontregeling van het immuunsysteem een ontregeling in de hersenen veroorzaakt.
    Daarom gaat ze nu bij mensen met cvs-klachten proberen de cytokineproductie in de hersenen te remmen.
    Ze doet dit samen met haar collega Lorenz van Doornen, hoogleraar gezondheidspsychologie aan de Universiteit Utrecht.
    ĎDit is echt een nieuwe stap', zegt Van Doornen : ĎLange tijd was het uitgangspunt dat de hersenen het lichaam sturen, maar nu komen we tot het inzicht dat het wel eens omgekeerd kan zijn : de hersenen monitoren voortdurend of er ergens iets mis is in het lichaam en hoe ze zich daaraan moeten aanpassen.'
    Iedereen kent dit terugkoppelingsmechanisme van het lichaam richting hersenen zelf van een griepje.
    Bij koorts ben je katterig en moe : je lichaam probeert energie die het nodig heeft voor herstel te sparen.

    De hersenen maken soms echter fouten bij het monitoren.
    Het idee wint terrein dat onverklaarbare chronische pijn, zoals posttraumatische spierdystrofie (blijvende pijn na herstel van letstel), verklaard kan worden door een schakelfout in het brein.
    Het pijngeheugen in de hersenen blijft dan actief, terwijl het lichamelijke probleem al voorbij is.
    Dat biedt aanknopingspunten voor nieuwe, op de hersenen gerichte, behandelwijzen.

    De omkering van het perspectief - door van het lichaam naar de hersenen te kijken in plaats van andersom - leidt ook tot een nieuwe interpretatie van onderzoeksuitkomsten.
    Zo is in recent onderzoek van de Tilburgse hoogleraar medische psychologie Johan Denollet een relatie aangetoond tussen depressie en hartinfarcten.
    HartpatiŽnten die zich vaak zorgen maken, geÔrriteerd zijn of een slecht zelfbeeld hebben - Ďtype D'-personen - hebben vier keer zoveel kans om binnen zes tot negen maanden een hartaanval te krijgen of zelfs te overlijden, dan zorgelozer patiŽnten.
    Er bleek ook een negatief effect op het immuunsysteem, de bloedstolling en het hartritme.

    Van Doornen : ĎDe eerste verklaring is dat zorgelijke en zwartkijkende mensen meer kans hebben op een infarct. Maar wij denken nu dat het deels andersom is. Aderverkalking zorgt ervoor dat het immuunsysteem actief wordt, de hersenen detecteren de signaalstofjes van de ziekte en mŠken vervolgens somber.'
    Dit idee wordt ondersteund door onderzoek waaruit blijkt dat de kans op hart- en vaatproblemen niet afneemt wanneer patiŽnten voor hun depressie worden behandeld.
    De depressie is dus niet de oorzaak van de ziekte, maar het gevolg.

    Horen bij bepaalde ziektes bepaalde persoonlijkheden? is de titel van een lezing die Van Doornen dit najaar zal houden.

    Bepaalde persoonlijkheid - Bepaalde ziektes ?
    "Over ratten, muizen, katten en mensen"
    Prof. dr. Lorenz J.P. van Doornen
    De vraag of bepaalde persoonlijkheidstypes het risico op bepaalde ziektes verhogen houdt de wetenschap al langdurig bezig.
    Dat er een ďkankerpersoonlijkheidĒ zou bestaan lijkt inmiddels weerlegd maar voor het idee dat bepaalde persoonlijkheidstrekken het risico op hart-en vaatziekten verhogen en dat ze zelfs levensduur enigszins voorspellen is wel vrij stevige evidentie.
    De interessante vraag dient zich dan aan welke mechanismen een dergelijk verband zouden kunnen verklaren.
    Het kan zijn dat persoonlijkheid gerelateerd is aan een al of niet verantwoorde levenswijze : alcohol, roken, sporten voeding etc.
    Het is ook mogelijk dat een bepaalde persoonlijkheid gekoppeld is aan het meer ervaren van stress en/of het sterker lichamelijk reageren op stress, wat op zijn beurt dan de lichamelijke schade zou aanrichten.
    Het kan ook zijn dat de relatie is tussen persoonlijkheid en ziekterisico niet oorzakelijk is : persoonlijkheid, ziekterisico en life style zouden een overlappende genetische basis kunnen hebben.
    Voor al deze mogelijkheden is wat evidentie maar het vreemde is dat ze slechts een deel verklaren van de relatie tussen persoonlijkheid en ziekterisico en dat nog onbekende mechanismes een rol spelen.
    Dieronderzoek biedt het voordeel dat men veel factoren constant kan houden en daardoor scherpere antwoorden kan krijgen.
    Bij muizen en ratten blijkt ook een relatie te bestaan tussen persoonlijkheid en vatbaarheid voor bepaalde ziekten.
    De exploratieve en aggressieve dieren blijken resistenter tegen kanker, maar juist weer gevoeliger voor hart-en vaatziekten dan hun timidere tegenhangers.
    Onderzoek bij dieren naar de rol van stresshormonen, immuunsysteem en genetica kan bijdragen aan hypotheses ten aanzien van de oorzaak van de relatie tussen persoonlijkheid en ziekte bij mensen.
    Professor Lorenz van Doornen studeerde psychofysiologie aan de Vrije Universiteit (VU) in Amsterdam. Tot 1997 bleef hij als UD en UHD verbonden aan de VU.
    Zijn onderzoek betrof de psychofysiologie van stress en hart- en vaatziekten.
    In 1997 werd hij benoemd tot hoogleraar Gezondheidspsychologie aan de Universiteit van Utrecht.
    Zijn onderzoek richt zich op de fysiologische effecten van stress en de gevolgen daarvan voor de gezondheid.
    Deze benadering is specifiek gericht op burnout, chronische vermoeidheid en medisch onverklaarde klachten.
    Het hoofdthema van het onderzoek betreft de stressfysiologische benadering van gezondheidspsychologische onderwerpen.
    Dit is geÔmplementeerd in het project psychofysiologie van burnout en het project vermoeidheid bij adolescenten.

    Cfr. :
    http://www.uu.nl/uupublish/content-cln/lezingLvanDoornen.pdf

    ĎJa', is zijn antwoord, maar Ďpersoonlijkheid' is vooral een fysiologisch begrip.
    ĎIk ben een materialist. Ik zie psyche en hersenen als ťťn ding. De genen bepalen voor vijftig procent persoonlijkheidskenmerken als stressbestendigheid en neuroticisme. Opvoeding, ervaringen en de hoeveelheid stresshormonen in de baarmoeder bepalen de andere helft.'

    Naar mogelijke verbanden tussen persoonlijkheid en ziekte wordt al langer onderzoek gedaan.
    Van mensen met cvs is bijvoorbeeld bekend dat ze vaak zeer precies, gedreven en ambitieus zijn.
    Heijnen : ĎHet boeiende is echter dat veel gestresste, ambitieuze en neurotische mensen zo'n ziekte niet krijgen. Naar ons idee spelen dus ook immunologische afwijkingen een rol. Immuunactiviteit en stress versterken elkaar, want ze hebben eenzelfde effect op veel hersendelen.'

    Ook tussen kanker en persoonlijkheid werden jarenlang verbanden verondersteld.
    Mensen van het Ďtype C'- passief, meegaand, geremd in het uiten van negatieve gevoelens - zouden meer kans hebben om kanker te ontwikkelen.
    Maar alle onderzoeken naar mogelijke verbanden tussen kanker en psyche ten spijt : er is niet of nauwelijks een verband.
    Vechtlust, wanhoop, optimisme of acceptatie hebben geen invloed op het ontstaan van kanker of het ziekteverloop, aldus psychofysioloog Bert Garssen.
    Hij is hoofd wetenschappelijk onderzoek bij het Helen Dowling Instituut in Utrecht, dat in 1988 zelfs werd opgericht om de relatie tussen psyche en het ontstaan en verloop van kanker te ontrafelen.
    Het Instituut richt zich inmiddels op het zo goed mogelijk omgaan met de ziekte.

    ĎAls de relatie tussen immuunsysteem en kanker perfect was, bestond er geen kanker', aldus Garssen.
    Het immuunsysteem moet afwijkende cellen opsporen, maar de meest voorkomende tumoren wekken weinig of geen immuunreacties op doordat ze mutaties ondergaan.
    Daarnaast groeien sommige kankercellen zo snel, dat het immuunsysteem het niet kan bijhouden.
    En soms zijn tumoren ingekapseld en daardoor ongrijpbaar voor het immuunsysteem.

    Garssen heeft tot nu toe ongeveer tachtig langlopende internationale studies vergeleken en vond geen verband tussen psyche, gedrag en kanker.
    Ook niet bij kankersoorten die door een virus veroorzaakt worden, zoals baarmoederhalskanker.

    Wat Garssen wel vond, was een mogelijke invloed op het verloop van kanker van hopeloosheid en repressie.
    Hoe hopelozer of hoe meer patiŽnten geneigd zijn negatieve emoties niet te uiten, hoe slechter het gaat.
    Terwijl mensen die hun ziekte volledig negeren, een wat beter perspectief lijken te hebben.

    PatiŽnten reageren wel eens geÔrriteerd op de uitkomsten van zijn literatuuronderzoek, merkt hij : ĎMensen willen graag een verklaring hebben voor het leed dat ze overkomt. Bovendien is het natuurlijk prettig om te denken dat je invloed kunt uitoefenen op je ziekte. Anderzijds is het ook belastend, als dat niet lukt. Maar helaas : je voorstellen dat het immuunsysteem een legertje is dat oprukt richting tumor haalt niets uit.'

    De invloed van het immuunsysteem op kanker is dus niet groot.
    Toch is het idee dat gedachten invloed kunnen hebben op andere ziekten niet zo vreemd.
    Het hormonale systeem en immuunsysteem worden namelijk wel degelijk beÔnvloed door psychologische factoren.
    Het gaat daarbij echter niet om gedachten, maar om gedrag.
    ĎMensen kunnen ander gedrag aanleren. Daarmee verander je mogelijk ook hun hele fysiologische patroon', zegt Heijnen.
    Cognitieve gedragstherapie blijkt effectief bij ongeveer zeventig procent van de cvs-patiŽnten, zo hebben wetenschappers van het Nijmeegse Kenniscentrum Chronische Vermoeidheid ontdekt.
    Stressmanagement door middel van bijvoorbeeld yoga en meditatie, blijkt eveneens heilzaam bij stressgerelateerde kwalen.
    Een methode als mindfulness (aandachttraining) heeft een positief effect op depressie, chronische pijn, hartklachten en maagdarmproblemen.

    ĎPositief denken' kan ook zo'n ontspannende werking hebben.
    Maar menen dat we onszelf kunnen Ďherprogrammeren' tot gezondheid - en mensen daarmee ook verantwoordelijk maken voor hun ziekte - is een brug te ver.
    Heijnen : ĎEr zijn zoveel van die believers... Die hardnekkige onzin heeft mijn vakgebied zo geschaad. Het is mensen beduvelen met een illusie van maakbaarheid.'


    Cfr. : http://www.intermediair.nl/artikel.jsp?id=1071554&rubriek=245 
     

    18-12-2007 om 20:07 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 5/5 - (6 Stemmen)
    >> Reageer (0)
    17-12-2007
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Vitamine B12 en de relatie met CVS/FM - Deel I
    Klik op de afbeelding om de link te volgen

     







    Vitamine B12
    en de relatie met
    het Chronisch Vermoeidheids Syndroom

    Stichting B12 Tekort : info@stichtingb12tekort.nl

    Voordat de diagnose CVS gesteld wordt, moet een tekort aan vitamine B12 worden uitgesloten.
    Veel (zo niet alle) van de klachten die bij CVS voorkomen, kunnen ook door een tekort aan vitamine B12 worden veroorzaakt.
    Als uit bloedonderzoek (serum B12) blijkt dat er inderdaad sprake is van een vitamine B12 tekort, zal eerst de behandeling met injecties gestart moeten worden.
    Pas als na langere tijd toediening van injecties de klachten blijven bestaan, kan eventueel de diagnose CVS gesteld worden.
    Uiteraard kunnen ook beide naast elkaar bestaan.

    Uit een onderzoek onder 12 patiŽnten met zowel CVS als fibromyalgie, bleek dat zij allen een verhoogde waarde van homocysteÔne hadden in het ruggenmergvloeistof.
    Er was een duidelijke relatie van deze verhoogde homocysteÔne waarden met vermoeidheid.
    Ook bleek er een duidelijke relatie van lage waarden vitamine B12 in het ruggenmergvloeistof met vermoeidheid en neurasthenie.
    Een vitamine B12 tekort veroorzaakt een deficiŽnte remythelisatie van homocysteÔne en is daardoor (mede) de oorzaak van het verhoogde homocysteÔne niveau.

    Indien door injecties met vitamine B12 de remythelisatie weer op gang komt, verlaagt het gehalte homocysteÔne.
    De conclusie is dat verhoogde homocysteÔne waarden in het centrale zenuwstelsel patiŽnten met zowel CVS als fibromyalgie kunnen karakteriseren.

    Uit een onderzoek onder 100 patiŽnten met CVS bleek dat 30% een verhoogde MMA waarde had. MMA (methylmalonzuur) is bij mensen met een tekort aan vitamine B12 vaak verhoogd.
    Dit doet vermoeden dat bij een grote groep CVS-patiŽnten er een vitamine B12 tekort bestaat, wat zeer waarschijnlijk de oorzaak is van veel, zo niet alle klachten van deze patiŽnten.

    Ook is uit onderzoek gebleken dat CVS-patiŽnten zonder tekort aan vitamine B12 baat kunnen hebben bij injecties.
    Lapp en Cheney hebben meer dan 2000 patiŽnten met CVS behandeld.
    In eerste instantie met relatief kleine hoeveelheden vitamine B12, maar later met 2000 tot 5000 mcg cyanocobalamine elke 2 Š 3 dagen.
    Bij 50 tot 80% verbeterde het energieniveau, het uithoudingsvermogen, het welbevinden en vaak al binnen 2 tot 3 weken na aanvang van de behandeling.
    Simpson gaf 1000 mcg cyanocobalamine aan een groep patiŽnten met CVS, die ook een verhoogd percentage afwijkende rode bloedcellen hadden.
    De rode bloedcellen van veel CVS-patiŽnten hebben een afwijkende vorm, waardoor het zuurstoftransport door het bloed vermindert.
    De helft van de patiŽnten die behandeld werden met vitamine B12 injecties voelde zich binnen 24 uur beter en dat ging gelijk op met de afname van de hoeveelheid afwijkende rode bloedcellen.
    PatiŽnten die geen verbetering bemerkten, hadden ook geen verbetering in de cellen.
    Simpson doet de suggestie dat de toediening van vitamine B12 CVS klachten kan doen afnemen, doordat de erythrocyte afwijkingen verminderen, wat kan leiden tot een verbetering van de zuurstofverzadiging in de weefsels.

    Bij een vermoeden van CVS moet eerst een vitamine B12 tekort worden uitgesloten, alvorens de diagnose gesteld kan worden.




    Vitamine B12 en de relatie met
    fibromyalgie

    Stichting B12 Tekort : info@stichtingb12tekort.nl


    Voordat de diagnose fibromyalgie gesteld wordt, moet een tekort aan vitamine B12 worden uitgesloten.
    Veel van de klachten die bij fibromyalgie voorkomen, kunnen ook door een tekort aan vitamine B12 worden veroorzaakt.
    Als uit bloedonderzoek (serum B12) blijkt dat er inderdaad sprake is van een vitamine B12 tekort, zal eerst de behandeling met injecties gestart moeten worden.
    Pas als na langere tijd toediening van injecties de klachten blijven bestaan, kan de diagnose fibromyalgie gesteld worden.
    Uiteraard kunnen beide ook naast elkaar bestaan.

    Ook is uit onderzoek gebleken dat fibromyalgiepatiŽnten zonder tekort aan vitamine B12 baat kunnen hebben bij injecties.
    Uit een onderzoek onder 12 patiŽnten met zowel CVS als fibromyalgie, bleek dat zij allen een verhoogde waarde van homocysteÔne hadden in het ruggenmergvloeistof.
    Er was een duidelijke relatie van deze verhoogde homocysteÔnewaarden met vermoeidheid.
    Ook bleek er een duidelijke relatie van lage waarden van vitamine B12 in het ruggenmergvloeistof met vermoeidheid en neurasthenie.
    Een vitamine B12 tekort veroorzaakt een deficiŽnte remythelisatie van homocysteÔne en is daardoor (mede) de oorzaak van het verhoogde homocysteÔneniveau.
    Indien door injecties met vitamine B12 de remythelisatie weer op gang komt, verlaagt het gehalte homocysteÔne.
    De conclusie is dat verhoogde homocysteÔnewaarden in het centrale zenuwstelsel patiŽnten met zowel CVS als fibromyalgie kunnen karakteriseren.

    Ook is gebleken dat patiŽnten met fibromyalgie nog wel eens afwijkende rode bloedcellen hebben, waardoor het zuurstoftransport vermindert.
    Ook dit is met vitamine B12 injecties vaak te verbeteren.

    Bij een vermoeden van fibromyalgie moet eerst een vitamine B12 tekort worden uitgesloten, alvorens de diagnose gesteld kan worden.

    Bronnen

    1. Myalgic encephalomyelitis (Letter)
      Simpson LO - J R Soc Med 1991;84:633
      Cfr. :
      http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1295578&blobtype=pdf

    2. The rationale for using high-dose cobalamine
      Lapp CW, Cheney PR - The CFIDS Chronicle Physicians' Forum Fall 1993;19-20
      Cfr. :
      http://www.afme.org.uk/res/img/resources/To%20B12%20or%20not%20to%20B12.txt

    3. Increased concentrations of homocysteine in the cerebrospinal fluid in patients with fibromyalgia and chronic fatigue syndrome
      Regland B, Andersson M, Abrahamsson L, Bagby J, Dyrehag LE, Gottfries CG. Scand J Rheumatol. 1997;26(4):301-7
      Cfr. :
      http://lib.bioinfo.pl/pmid:9310111

    Cfr. : http://www.stichtingb12tekort.nl/index.html



    Cfr. ook :


    Nederlandstalig

    1. De diagnostiek van vitamine B12 deficiŽntie herzien
      W.J.Wiersinga, S.E.J.A.de Rooij, J.G.M.Huijmans, J.C.Fischer en J.B.L.Hoekstra - Nederlands Tijdschrift Geneeskunde, 2005;149:2789-94
      Cfr. : http://home.hetnet.nl/~hindrikdejong/NTvG-nr49-2005.pdf

    2. Gecombineerde strengziekte door vitamine B12-deficiŽntie, eenvoudige diagnose, effectieve therapie
      Mw. J.C.F. Jongen, assistent; dr. P.J. Koehler en dr. C.L. Franke, neurologen. (Atrium Medisch Centrum, Heerlen) - Ned. Tijdschr. v. Geneeskunde 2001, nr. 26 (rubriek : 'Klinische lessen')
      "Dames en Heren,
      Een tekort aan vitamine B12 kan de oorzaak zijn van de gecombineerde strengziekte, een aandoening van de achter- en zijstrengen van het ruggenmerg, waarin soms ook de perifere zenuwen, de oogzenuw en de hersenen betrokken zijn.
      Herkenning van het klinische beeld is van vitaal belang voor de patiŽnt.
      De diagnose is met enkele eenvoudige tests te stellen; maandelijke injecties met vitamine B12 verlossen de patiŽnt van de klachten of geven aanzienlijke verbetering.
      " (hierna worden de 4 patiŽnten en hun klachten besproken en hoe de diagnose werd gesteld en worden de effecten van lachgas bij narcose vermeld wanneer de B12-spiegel al laag is; hierdoor kan een gecombineerde strengziekte worden "uitgelokt").
      "De prognose van de gecombineerde strengziekte is gunstig, hoewel ongeveer de helft van de patiŽnten restverschijnselen houdt, veelal bestaand uit tintelingen; 6% houdt er matig tot ernstig invaliderende verschijnselen aan over.
      Dames en Heren, gecombineerde strengziekte is een voorbeeld van een ernstige invaliderende neurologische aandoening, waarvoor bij vroege, veelal eenvoudige diagnostiek een adequate behandeling voorhanden is. Bij het beeld van een spastisch-atactisch syndroom moeten wij deze diagnose daarom altijd overwegen. Ook als er bij MRI van de cervicale wervelkolom afwijkingen gevonden worden, mag de diagnose niet verworpen worden. Bij een typisch klinische beeld en bijbehorende afwijkende laboratoriumbevindingen is MRI van de cervicale wervelkolom niet noodzakelijk. Zo snel mogelijk beginnen met de behandeling is van het grootste belang.
      "
      Cfr. :
      http://home.hetnet.nl/~hindrikdejong/moeilijk.htm

    3. Interpretatie van Medisch Laboratoriumonderzoek
      Dr. J.A. Raymakers, Dr. H.J.H. Kreutzer, Dr. P.M. Schneeberger - Bohn Stafleu van Loghum, Houten, 24-02-2005 - ISBN-13: 9789031330997 (p. 16-20)
      Verscheen in 1982 voor het eerst en beleeft met deze herziening alweer zijn vijfde druk.
      Cfr. :
      http://home.bsl.nl/boek/9789031330997/Interpretatie_van_medisch_laboratoriumonder
      zoek;jsessionid=3B8A58643A75CE0112E147448ABB530D

    4. Klinische Probleemstellingen - Onderzoek en diagnostiek van 236 aandoeningen
      Prelum Uitgevers, november 2007 Ė Reeks : Klinische Diagnostiek, deel 1 Ė ISBN : 9789085620426
      Cfr. :
      http://www.geneeskundeboek.nl/leesverder.pl?isbn=9789085620426

    5. Klinische-diagnostiek.nl
      College voor zorgverzekeringen (CVZ), 2003 Ė p. 22-24
      Cfr. :
      http://www.klinische-diagnostiek.nl/

    6. Vitamine B12 (Memoboek)
      Samenwerkende Artsen Laboratoria Nederland (SAN)
      Cfr. :
      http://memoboek.dynapaper.nl/84/vitamineb12.Html


    Anderstalig

    1. Accelerator Mass Spectrometry (AMS)
      21-12-2006
      Is Accelerator Mass Spectrometry (AMS) belangrijk voor het bepalen van de B12-opname als vervanger van de Schillingtest ? - Cfr. p. 4 and 5 on :
      http://www.llnl.gov/pao/employee/articles/2006/08-25-06-newsline.pdf

    2. Alcohol abuse - An important cause of severe hyperhomocysteinemia
      Carmel R, James SJ, Department of Medicine, New York Methodist Hospital, Brooklyn, NY 11215, USA - Nutr Rev. 2002 Jul;60(7 Pt 1):215-21 - PMID: 12144201
      Alcohol has complex direct effects on homocysteine metabolism, which are incompletely understood and indirect effects mediated by interactions with vitamin metabolism and other factors.
      Both transmethylation and transsulfuration pathways are affected.
      Alcohol abuse is a common cause of hyperhomocysteinemia that often fluctuates and is sometimes severe. The causative role of alcohol in hyperhomocysteinemia is often overlooked by clinicians when evaluating patients and by investigators when conducting surveys.
      A married couple with severe hyperhomocysteinemia owing to surreptitious alcohol abuse, a case study illustrating many of these issues, is presented.
      A steep rise in S-adenosylhomocysteine as well as homocysteine levels was demonstrated with increased alcohol ingestion, with a decreased S-adenosylmethionine:S-adenosylhomocysteine ratio.
      Both patients had severe neurologic symptoms as well as macrocytic red blood cells, which, along with the high homocysteine levels, were misattributed to cobalamin deficiency, in one case despite serum cobalamin levels that were normal.
      Cfr. :
      http://www.ingentaconnect.com/content/ilsi/nure/2002/00000060/00000007/art00005

    3. Approaches to vitamin B12 deficiency - Early treatment may prevent devastating complications
      T. S. Dharmarajan, MD; Edward P. Norkus, PhD Ė Vol 110 / nr. 1 / july 2001 / Postgraduate medicine
      Cfr. :
      http://www.postgradmed.com/issues/2001/07_01/dharmarajan.htm

    4. CDC growth charts
      US National Center for Health Statistics, January 9, 2006
      Cfr. :
      http://www.cdc.gov/nchs/about/major/nhanes/growthcharts/charts.htm

    5. Chronic Renal Failure Promotes Severe Variant of Vitamin B 12 Deficiency 
      Thomas Duning, Darius GŁnter Nabavi, Rainer Dziewas, Harald Kugel, Wolf-RŁdiger Schšbitz Eur Neurol 2006;56:62-65
      Cfr. :
      -
      http://content.karger.com/ProdukteDB/produkte.asp?Doi=95148
      -
      http://www.ncbi.nlm.nih.gov/sites/entrez

    6. Clinical Medicine - 6th Ed
      Parveen Kumar, Michael Clark - Elsevier/Saunders, London, 2005, p. 1263
      Cfr. :
      -
      http://www.ebookee.com/Kumar-Clinical-Medicine-6th-ed_40538.html
      -
      http://www.studentconsult.com/bookshop/title.cfm?shopISBN=0702027634

    7. Clinical significance of low cobalamin levels in older hospital patients
      van Asselt DZ, Blom HJ, Zuiderent R, Wevers RA, Jakobs C, van den Broek WJ, Lamers CB, Corstens FH, Hoefnagels WH, Department of Geriatric Medicine, University Hospital Nijmegen, The Netherlands - Neth J Med. 2000 Aug;57(2):41-9 - PMID: 10924940
      Background - It is still a commonly held belief that many of the frequently found low cobalamin (Cbl, vitamin B12) levels in older people do not represent deficiency and are therefore without clinical significance and should not be treated.
      In this study this notion will be challenged.
      Methods - In this prospective observational cohort design we studied 28 patients aged 65 years and older with low plasma Cbl (< or =150 pmol/l).
      A number of haematological (Hb, MCV, five- and six-lobed granulocytes), metabolic (plasma levels of methylmalonic acid and homocysteine) and gastrointestinal (plasma pepsinogen A and C and protein-bound and free Cbl absorption) parameters and the response to Cbl treatment, were measured.
      Cbl deficiency was considered to be present when at least one of the following three criteria was fulfilled :
      - haematological or metabolic abnormalities compatible with Cbl deficiency
      - Cbl malabsorption or atrophic gastritis
      - a response to Cbl supplementation.
      Results - Haematological or metabolic abnormalities were identified in 27 patients.
      Atrophic gastritis and Cbl malabsorption were identified in, respectively, 15 and 23 patients.
      Each treated patient showed a haematological or metabolic response to Cbl supplementation.
      All patients were considered Cbl deficient :
      - 8 patients (64%) fulfilled three criteria of Cbl deficiency
      - eight (29%) fulfilled two criteria and
      - two (7%) fulfilled one criterion.
      Conclusions - According to the generally accepted and a wide variety of criteria, we found that older patients with low Cbl levels were cobalamin deficient.
      Therefore, these patients should receive Cbl supplementation.
      Cfr. :
      -
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=10924940&ordinalpos=1&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
      - http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=10924940&dopt=AbstractPlus

    8. Clinical spectrum and diagnosis of cobalamin deficiency
      Stabler SP, Allen RH, Savage DG, Lindenbaum J, Department of Medicine, University of Colorado Health Sciences Center, Denver 80262 - Blood. 1990 Sep 1;76(5):871-81 - PMID: 2393714
      To better estimate how frequently patients with low serum cobalamin (Cbl) levels in current clinical practice are truly deficient in Cbl and to determine the incidence of atypical or nonclassic presentations of Cbl deficiency, we prospectively studied 300 unselected consecutive patients with serum Cbl concentrations less than 200 pg/mL seen at two medical centers over a 2-year period.
      Baseline hematologic, neuropsychiatric and biochemical measurements were obtained, followed by a course of parenteral Cbl therapy and reassessment.
      A response to Cbl therapy was defined as one or more of the following : (1) an increase in hematocrit of 0.05 or more; (2) a decrease in mean cell volume of 5 fL or more; (3) a clearing of hypersegmented neutrophilis and macroovalocytes from the peripheral blood smear; and (4) an unequivocal and prompt improvement of neuropsychiatric abnormalities.
      Of the 300 patients with serum Cbl levels less than 200 pg/mL, 86 had one or more responses to Cbl therapy and 59 had no response.
      In 155, insufficient data was available.
      In the Cbl-responsive patients, normal values were found for the following tests: hematocrit, 44%; mean cell volume less than or equal to 100 fL, 36%; white blood cell count, 84%; platelet count, 79%; serum lactic dehydrogenase, 43%; and serum bilirubin, 83%.
      Peripheral blood smears were nondiagnostic in 6% when reviewed by the investigators, but 33% as reported by routine laboratories.
      Serum Cbl levels in the 100 to 199 pg/mL range were present in 38%.
      Neuropsychiatric abnormalities were noted in 28%, often in the absence of anemia, macrocytosis or both.
      Serum levels of methylmalonic acid and/or total homocysteine were elevated greater than 3 SDs above the mean for normal subjects in 94% of the Cbl-responsive patients.
      We conclude that Cbl deficiency should be considered and investigated in patients with unexplained hematologic or neuropsychiatric abnormalities of the kind seen in Cbl deficiency, even if anemia, an elevated mean cell volume, a marked depression of the serum Cbl or other classic hematologic or biochemical abnormalities are lacking.
      Levels of serum methylmalonic acid and total homocysteine are useful as ancillary diagnostic tests in the diagnostis of Cbl deficiency.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=2393714&ordinalpos=7&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    9. Clinical utility of serum holotranscobalamin as a marker of cobalamin status in elderly patients with neuropsychiatric symptoms
      Nilsson K, Isaksson A, Gustafson L, Hultberg B - Clin Chem Lab Med 2004;42:637-43
      Cfr. :
      http://www.atypon-link.com/WDG/doi/abs/10.1515/CCLM.2004.109?cookieSet=1&journalCode=cclm

    10. Cobalamin and folate evaluation - Measurement of methylmalonic acid and homocysteine vs vitamin B12 and folate
      Klee GG - Clin Chem. 2000; 46: 1277-1283
      Vitamin B12 and folate are two vitamins that have interdependent roles in nucleic acid synthesis.
      Deficiencies of either vitamin can cause megaloblastic anemia; however, inappropriate treatment of B12 deficiency with folate can cause irreversible nerve degeneration.
      Inadequate folate nutrition during early pregnancy can cause neural tube defects in the developing fetus.
      In addition, folate and vitamin B12 deficiency and the compensatory increase in homocysteine are a significant risk factor for cardiovascular disease.
      Laboratory support for the diagnosis and management of these multiple clinical entities is controversial and somewhat problematic.
      Automated ligand binding measurements of vitamin B12 and folate are easiest to perform and widely used.
      Unfortunately, these tests are not the most sensitive indicators of disease.
      Measurement of red cell folate is less dependent on dietary fluctuations, but these measurements may not be reliable.
      Homocysteine and methylmalonic acid are better metabolic indicators of deficiencies at the tissue level.
      There are no "gold standards" for the diagnosis of these disorders, and controversy exists regarding the best diagnostic approach.
      Healthcare strategies that consider the impact of laboratory tests on the overall costs and quality of care should consider the advantages of including methylmalonic acid and homocysteine in the early evaluation of patients with suspected deficiencies of vitamin B12 and folate.
      Cfr. :
      http://www.clinchem.org/cgi/content/full/46/8/1277

    11. Cobalamin Status and Its Biochemical Markers Methylmalonic Acid and Homocysteine in different Age Groups from 4 Days to 19 Years 
      Anne-Lise BjÝrke Monsen, Helga Refsum, Trond Markestad, and Per Magne Ueland Clinical Chemistry 49:12 2067-2075 (2003)
      Cfr. :
      http://www.cababstractsplus.org/google/abstract.asp?AcNo=20043175914

    12. Cobalamin status during normal pregnancy and postpartum - A longitudinal study comprising 406 Danish women 
      Milman N, Byg K-E, Bergholt T, Eriksen L, Hvas A-M, Eur J Haematol 2006: 76: 521-525
      Cfr. :
      http://lib.bioinfo.pl/pmid:16548919

    13. Cobalamin-responsive disorders and unreliability of cobalamin, methylmalonic acid and homocysteine testing
      A. Majid Shojania :
      shojana@cc.umanitoba.ca
      Solomon1 claims that many patients with clinical features suggestive of cobalamin (Cbl) deficiency who have normal serum Cbl, methylmalonic acid (MMA) and homocysteine (HCys) levels may respond to Cbl therapy, while many patients with low serum Cbl, high serum MMA or high serum HCys levels may fail to respond to Cbl therapy.
      He concludes that these tests are unreliable for the diagnosis of Cbl deficiency.
      I do not think that there is much support for his conclusion.
      First of all, Solomon writes that resolution of signs and symptoms consistent with Cbl deficiency in 12 patients occurred prior to any Cbl therapy.
      How can he then attribute to Cbl therapy the resolution of signs and symptoms of those who received Cbl ?
      Second, the response to pharmacologic doses of Cbl does not support the diagnosis of Cbl deficiency.
      The dose of Cbl for a therapeutic trial of Cbl deficiency is 1 Ķg Cbl daily for 10 days.
      This dose would produce optimal reticulocyte response within 7 to 10 days and, if continued, would produce a complete hematologic response.2 Patients who do not respond to small doses of Cbl but respond to pharmacologic doses of Cbl are not Cbl deficient.
      Third, the criteria that Solomon has used for demonstrating a response to Cbl therapy (5 fL reduction of mean corpuscular volume [MCV] or an increase in hematocrit of 0.05 point within 3 months of Cbl therapy) are nonspecific.
      Such a response can be seen in a patient who has folate-deficiency anemia treated with high doses of Cbl.2 Similar hematologic changes may be seen in any patient with alcoholic liver disease or ethanol abuse who stops drinking ethanol; in patients recovering from acute hemolytic anemia, anemia associated with acute infection; or in patients with hypothyroidism treated with thyroid extract, irrespective of whether they are given Cbl.
      Fourth, of 8 patients who met Solomon's criteria for hematologic response, only 2 demonstrated an increase in hematocrit within 3 months of Cbl therapy.
      The other 6 patients showed only reduction of MCV. If the reduction of MCV were due to Cbl therapy, why did the hematocrit not increase ?
      Finally, Solomon reports that low or intermediate Cbl levels were present in 46% of the responders and 56% of the nonresponders, and increased MMA values were present in 73% of responders and 88% of nonresponders.
      Consequently, he claims that these tests are unreliable.
      In the presence of low serum Cbl or high serum MMA, failure of response to Cbl does not exclude Cbl deficiency, but indicates that the anemia or neurologic abnormalities were not due to Cbl deficiency.
      Serum Cbl, MMA, and HCys, like any other laboratory tests, may give false-positive or false-negative results in certain situations.
      One has to be familiar with these situations in order to interpret the laboratory results properly rather than claiming that these tests are unreliable
      Cfr. :
      http://bloodjournal.hematologylibrary.org/cgi/content/full/106/3/1136

    14. Cobalamin-responsive disorders in the ambulatory care setting - Unreliability of cobalamin, methylmalonic acid and homocysteine testing
      Solomon LR, Department of Medicine, Yale University Health Services, 17 Hillhouse Ave, PO Box 208237, New Haven, CT 06520-8237, USA :
      lawrence.solomon@yale.edu - Blood. 2005 Feb 1;105(3):978-85. Epub 2004 Oct 5 - PMID: 15466926
      Early recognition of cobalamin (Cbl)-responsive disorders in the ambulatory care setting is essential to prevent irreversible neurologic deficits.
      However, diagnostic algorithms using Cbl, methylmalonic acid (MMA) and homocysteine (HCys) measurements reflect studies in academic centers and their negative predictive values have not been established.
      Thus, records of 456 ambulatory patients evaluated for Cbl deficiency at a staff model HMO were reviewed.
      Pretherapy Cbl, MMA and HCys values in individual patients varied by 23%, 23% and 17%, respectively, over 2 to 6 weeks.
      Hematologic or neurologic responses to pharmacologic doses of Cbl occurred in 37 of the 95 evaluable patients.
      In these patients, pretherapy Cbl, MMA, and HCys values were normal in 54%, 23% and 50%, respectively.
      If therapy had been restricted to symptomatic patients with both low or intermediate Cbl levels and increased metabolite values, 63% of responders would not have been treated.
      Twenty-five patients did not respond to treatment, including 5 of 11 patients (45%) with low Cbl, 22 of 49 patients (45%) with high MMA and 13 of 30 patients (43%) with high HCys values.
      It is concluded that Cbl, MMA, and HCys levels fluctuate with time and neither predict nor preclude the presence of Cbl-responsive hematologic or neurologic disorders.

      Cfr. :
      -
      http://www.ncbi.nlm.nih.gov/sites/entrez
      -
      http://bloodjournal.hematologylibrary.org/cgi/content/abstract/2004-04-1641v1

    15. Cobento A/S
      Cobento strives to improve the quality of life for people suffering from vitamin B12 deficiency
      Cfr. :
      http://www.cobento.dk/

    16. Current concepts in cobalamin ceficiency
      Ralph Carmel, Department of Medicine, New York Methodist Hospital, Brooklyn, New York, 11215; Weill Medical College of Cornell University, New York, New York :
      rcarmel@pol.net - Annual Review of Medicine Vol. 51: 357-375, February 2000
      The application of sensitive metabolic tests, such as the deoxyuridine suppression test and measurement of homocysteine and methylmalonic acid, to cobalamin status has identified the entity of mild, preclinical cobalamin deficiency.
      This state, common in the elderly, responds to cobalamin therapy.
      Preclinical deficiency may exist within the nervous system as well, although this requires further study.
      Nevertheless, it is well to remember that not all low cobalamin levels and not all abnormal metabolite results reflect cobalamin deficiency.
      Interpretation of metabolic results still requires caution, as do proposals to raise the cut-off point for low cobalamin levels to capture some normal levels that are associated with metabolic abnormality.
      The recognition of mild, preclinical deficiency has opened up many important issues.
      These include identifying its causes, what should be done about it, and what the clinical impact of the hyperhomocysteinemia itself is.
      Although malabsorptive disorders, especially food-cobalamin malabsorption, underlie about half of all cases of preclinical deficiency, no cause can be found in the remainder of these cases; poor dietary intake appears to be uncommon. In addition, unusual states of neurologically symptomatic cobalamin deficiency are being recognized, such as nitrous oxide exposure in patients with unrecognized deficiency and severe deficiency in children of mildly deficient mothers.
      All of these have broadened and complicated the picture of cobalamin deficiency while providing greater opportunities for prevention.
      Cfr. :
      -
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=10774470&ordinalpos=1&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

      -
      http://arjournals.annualreviews.org/doi/abs/10.1146/annurev.med.51.1.357

    17. Current Diagnosis & Treatment in Neurology
      John C. M. Brust - McGraw-Hill Medical (1 edition), September 14, 2006 Ė ISBN-10 : 0071423664 Ė ISBN-13 : 978-0071423663
      Cfr. :
      -
      http://www.amazon.com/Current-Diagnosis-Treatment-Neurology/dp/0071423664
      - http://www.amazon.com/Current-Diagnosis-Treatment-Neurology-Brust/dp/0071423664

    18. Diagnosing vitamin B-12 deficiency on the basis of serum B-12 assay
      Vinod Devalia - BMJ 2006;333;385-386
      Cfr. :
      http://home.hetnet.nl/~hindrikdejong/BMJ-19aug2006.pdf


    Lees verder Deel II

     

    17-12-2007 om 23:03 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 0/5 - (0 Stemmen)
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Vitamine B12 en de relatie met CVS/FM - Deel II
    Klik op de afbeelding om de link te volgen

     




    Vitamine B12 en de relatie met CVS/FM

    Deel II


    1. Diagnosis of cobalamin deficiency Ė I - Usefulness of serum methylmalonic acid and total homocysteine concentrations
      Robert H. Allen, M.D. 1 *, Sally P. Stabler 1, David G. Savage 2, John Lindenbaum 2 - 1Department of Medicine and Department of Biochemistry, Biophysics and Genetics, University of Colorado Health Sciences Center, Denver - 2Department of Medicine, College of Physicians and Surgeons, Columbia University and Department of Medicine, Columbia-Presbyterian and Harlem Hospital Centers, New York - *Correspondence to : Robert H. Allen, Division of Hematology, Campus Box B170, University of Colorado Health Sciences Center, 4200 E. Ninth Avenue, Denver, CO 80262 - American Journal of Hematology, Volume 34, Issue 2 , Pages 90 Ė 98 - Published Online: 11 Jul 2006 - © 1990 Wiley-Liss, Inc., A Wiley Company
      The serum cobalamin assay is the primary diagnostic test for cobalamin deficiency.
      It appears to be an excellent screening test since most patients with clinically confirmed cobalamin deficiency have low levels.
      Recent studies indicate that the clinical picture of cobalamin deficiency is much more diverse than previously believed. It is also apparent that many patients with low serum cobalamin concentrations are not cobalamin deficient.
      Thus, there is a need for additional diagnostic tests to further distinguish patients with low serum cobalamin levels who are actually cobalamin deficient and will benefit from lifetime treatment from those who are not deficient and will not benefit.
      Serum levels of methylmalonic acid and total homocysteine have been shown to be markedly elevated in most patients with cobalamin deficiency and total homocysteine concentrations are markedly elevated in most patients with folate deficiency.
      The levels of these metabolites fall to normal if these patients are treated with the appropriate vitamin but remain essentially unchanged if the wrong vitamin is administered.
      These observations demonstrate that serum methylmalonic acid and total homocysteine levels are useful in diagnosing patients with cobalamin and folate deficiency and in distinguishing between these two vitamin deficiencies.
      Cfr. :
      -
      http://www3.interscience.wiley.com/cgi-bin/abstract/112699774/ABSTRACT
      -
      http://www3.interscience.wiley.com/cgi-bin/abstract/112699774/ABSTRACT?CRETRY=1&SRETRY=0

    2. Diagnosis of cobalamin deficiency : II. - Relative sensitivities of serum cobalamin, methylmalonic acid and total homocysteine concentrations
      Dr. John Lindenbaum 1 *, David G. Savage 1, Sally P. Stabler 2, Robert H. Allen 3 - 1Department of Medicine, Columbia-Presbyterian Medical Center, Department of Medicine, Harlem Hospital Center, and Department of Medicine, the College of Physicians and Surgeons, Columbia University, New York - 2Departments of Medicine and of Biochemistry, Biophysics, University of Colorado Health Sciences Center, Denver - 3Departments of Genetics, University of Colorado Health Sciences Center, Denver - *Correspondence to John Lindenbaum, Columbia-Presbyterian Medical Center, 630 West 168th Street, New York, NY 10032 - Department of Health and Human Services & National Institute of Diabetes and Digestive and Kidney Diseases; Grant Number: DK31765, DK21365 - American Journal of Hematology, Volume 34, Issue 2 , Pages 99 Ė 107 - Published Online : 11 Jul 2006 - © 1990 Wiley-Liss, Inc., A Wiley Company
      The serum cobalamin level has been generally considered to be essentially 100% sensitive in the detection of the clinical disorders caused by cobalamin deficiency.
      We tested this hypothesis in two groups of patients.
      In patients with pernicious anemia or previous gastrectomy who received less than monthly maintenance therapy, early hematologic relapse was associated with elevation of the serum methylmalonic acid, total homocysteine or both metabolites in 95% of instances, although the serum cobalamin was low in only 69%.
      In the absence of hematologic relapse, the methylmalonic acid was abnormal more than twice as frequently as the serum cobalamin.
      We also reviewed the records of 419 consecutive patients with recognized clinically significant cobalamin deficiency.
      Twelve patients were identified in whom deficiency was clearly present although the serum cobalamin was greater than 200 pg/ml.
      Anemia was usually absent or mild, but 5 had prominent neurological involvement that subsequently responded to cobalamin.
      Both the serum methylmalonic acid and total homocysteine were increased in each patient.
      The serum cobalamin was normal in 9 (5.2%) of 173 patients with recognized cobalamin deficiency seen in the last 5 years.
      Antibiotic treatment lowered the serum methylmalonic acid but not the total homocysteine level in two cobalamin-deficient patients, suggesting that propionic acid generated by the anaerobic gut flora may be a precursor of methylmalonic acid in deficient patients.
      We conclude that the serum cobalamin is normal in a significant minority of patients with cobalamin deficiency and that the measurement of serum metabolite concentrations facilitates the identification of such patients.
      Cfr. :
      http://www3.interscience.wiley.com/cgi-bin/abstract/112699776/ABSTRACT

    3. Dietary habits and nutritional status in adolescents over Europe - An overview of current studies in the Nordic countries
      Samuelson G - Eur J Clin Nutr. 2000;54(suppl 1):S21-S28
      Objective
      : To give an overview of the dietary habits among adolescents in the Nordic countries and to present results from studies showing the relationship between dietary habits and other lifestyle factors, nutritional status and socio-economic conditions.
      Design : A number of nutritional studies among adolescents performed during recent decades using recalls, dietary records and food frequency questionnaire.
      Setting : Denmark, Finland, Norway and Sweden.
      Subjects : Adolescents aged 13-18 y.
      Results : Food habits are characterized by an irregular meal pattern; many adolescents skip breakfast and also the school lunch, whereas most of them have dinner.
      However, snacking and light meals are very common, contributing 25-35% of the daily energy intake.
      Smoking is linked to their dietary habits as well as socio-economic conditions.
      Dietary intakes of vitamins and minerals are adequate for normal health and growth.
      Dietary calcium intake is high, whereas the intake of fibre, vitamin D, zinc and selenium and, in girls, iron is below the Nordic recommendations.
      Relatively low prevalence figures of iron deficiency were found.
      Many studies show a decrease over time in physical activity.
      The time spent in sedentary activities, such as television and video watching and computer games has increased during recent decades.
      Conclusion : Overweight and obesity are becoming more prevalent in all the Nordic countries, even though the prevalence figures are far below those in the USA.
      On the other hand, dieting girls are common, which might be a factor behind their irregular meal pattern and food choice.
      In a perspective, overweight and diseases attributable to obesity will be an immense challenge in the coming decades for both the individuals and the society as well.
      Cfr. :
      http://www.nature.com/ejcn/journal/v54/n1s/abs/1600980a.html

    4. Disorders of cobalamin (vitamin B12) metabolism - Emerging concepts in pathophysiology, diagnosis and treatment
      Although cobalamin (vitamin B12) was isolated almost 60 years ago, its biochemical, physiologic and neurologic effects remain incompletely defined.
      New observations suggest renal regulation of cobalamin metabolism; actions of cobalamin on nucleic acid and protein function; and a role for cobalamin in cytokine and growth factor regulation.
      Clinically, no gold standard has emerged for the diagnosis of cobalamin deficiency.
      Moreover, cobalamin resistance may occur in diabetes, renal insufficiency and advanced age, leading to functional cobalamin deficiency despite adequate cobalamin nutriture.
      Finally, high-dose cobalamin therapy may have salutary pharmacologic effects on neurologic function in a variety of disorders.
      Many studies lacked appropriate control groups.
      However, at this time, therapeutic trials with pharmacologic doses of cobalamin are suggested when findings consistent with cobalamin deficiency are present regardless of the results of diagnostic tests.
      While oral cobalamin immediate-release is adequate for many patients, its effectiveness in reversing neurologic abnormalities has yet to be established.
      Cfr. :
      -
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16814909&ordinalpos=1&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

      -
      http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=16814909&cmd=showdetailview&indexed=google

    5. Dr claims Vitamin B12 'cure'
      Ali Martin - The Sun, 30 Oct 2006
      Cfr. :
      http://www.thesun.co.uk/sol/homepage/news/article68857.ece

    6. Effects of Oral Contraceptives and Hormone Replacement Therapy on Markers of Cobalamin Status
      Bettina Riedel1,a, Anne-Lise BjÝrke Monsen2, Per Magne Ueland3 and JÝrn Schneede3, 1 Laboratory of Clinical Biochemistry, Section of Clinical Pharmacology, and2 Department of Pediatrics, Haukeland University Hospital, Bergen, Norway;3 Locus for Homocysteine and Related Vitamins, University of Bergen, Bergen, Norway - Aaddress correspondence to this author at : Laboratory of Clinical Biochemistry, Section of Clinical Pharmacology, Haukeland University Hospital, 5021 Bergen, Norway; fax 47-55-97-4605, e-mail
      bettina.marie.riedel@helse-bergen.no - Clinical Chemistry. 2005;51:778-781 - © 2005 American Association for Clinical Chemistry, Inc.
      Cfr. :
      http://www.clinchem.org/cgi/content/full/51/4/778

    7. Elevated serum methylmalonic acid concentrations are common among elderly Americans
      Morris MS, Jacques PF, Rosenberg IH, Selhub J - J Nutr. 2002;132: 2799-2803
      To describe serum methylmalonic acid (MMA) concentrations of elderly Americans and examine relationships between serum MMA and other factors, we used surplus serum samples collected from elderly (
      n = 1145) and young-adult (n = 1026) participants in Phase 2 of the third National Health and Nutrition Examination Survey (1991Ė1994).
      In 20% of participants 65 y old, serum MMA was >370 nmol/L, the 90th percentile of the distribution of participants aged 30Ė39 y.
      Consistent with previous reports, we observed strong, independent positive associations between serum MMA concentration and serum concentrations of creatinine and homocysteine.
      After controlling for demographic factors and creatinine, geometric mean MMA concentration was lower in non-Hispanic blacks [223.6 nmol/L; 95% confidence interval (CI), 198.8Ė251.5] than non-Hispanic whites (265.1 nmol/L; 95% CI, 240.3Ė292.4).
      However, the prevalence of elevated levels did not vary with race/ethnicity.
      Serum MMA concentration bore a strong inverse relation to serum vitamin B-12 concentration.
      Nevertheless, elevated serum MMA concentrations affected 15% of those with both normal serum creatinine concentrations and serum B-12 concentrations >148 pmol/L.
      We conclude that many elderly Americans demonstrate metabolic evidence of low B-12 status, that elevations occur frequently in the absence of traditional deficiency indicators and that levels vary with race/ethnicity and renal function.
      Cfr. :
      http://jn.nutrition.org/cgi/content/full/132/9/2799

    8. Etiology and diagnostic evaluation of macrocytosis
      Savage DG, Ogundipe A, Allen RH, Stabler SP, Lindenbaum J, Department of Medicine, Columbia University, College of Physicians and Surgeons, New York, New York, USA :
      savage@cuccfa.ccc.columbia.edu - Am J Med Sci. 2000 Jun;319(6):343-52 - PMID: 10875288
      Background
      - Elevation of mean cell volume (MCV) is a common clinical problem, but the etiologic spectrum and optimal diagnostic evaluation of macrocytosis are not well defined.
      Methods - We studied 300 consecutive hospitalized adult patients with MCV values > or = 100 fL.
      Assessment included complete blood counts, morphologic review, liver function tests and levels of serum cobalamin (Cbl), methylmalonic acid and total homocysteine.
      Results - The most common cause of macrocytosis was drug therapy, followed by alcohol, liver disease and reticulocytosis.
      Megaloblastic hematopoiesis accounted for less than 10% of cases.
      MCV values > 120 fL were usually caused by Cbl deficiency.
      Anisocytosis, macro-ovalocytosis and teardrop erythrocytes were most prominent in megaloblastic hematopoiesis.
      Elevated levels of serum methylmalonic acid and total homocysteine were useful in the diagnosis of Cbl deficiency.
      Conclusions - Drugs and alcohol are the most common causes of macrocytosis in hospitalized patients in a New York City teaching hospital.
      We have formulated tentative guidelines for the evaluation of high MCV values in this setting.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=10875288&ordinalpos=6&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    9. Evaluation of indicators of cobalamin deficiency defined as cobalamin-induced reduction in increased serum methylmalonic acid
      Bolann BJ, Solli JD, Schneede J, GrÝttum KA, Loraas A, Stokkeland M, Stallemo A, SchjÝth A, Bie RB, Refsum H, Ueland PM, Laboratory of Clinical Biochemistry, Haukeland University Hospital, N-5021 Bergen, Norway.
      bjorn.bolann@ikb.uib.no - Clin Chem. 2000 Nov;46(11):1744-50 - PMID: 11067808
      Background - Early detection of cobalamin deficiency is clinically important, and there is evidence that such deficiency occurs more frequently than previously anticipated.
      However, serum cobalamin and other commonly used tests have limited ability to diagnose a deficiency state.
      Methods - We investigated the ability of hematological variables, serum cobalamin, plasma total homocysteine (tHcy), serum and erythrocyte folate, gastroscopy, age and gender to predict cobalamin deficiency. Patients (n = 196; age range, 17-87 years) who had been referred from general practice for determination of serum cobalamin were studied.
      Cobalamin deficiency was defined as serum methylmalonic acid (MMA) >0.26 micromol/L with at least 50% reduction after cobalamin supplementation.
      ROC and logistic regression analyses were used. RESULTS: Serum cobalamin and tHcy were the best predictors, with areas under the ROC curve (SE) of 0. 810 (0.034) and 0.768 (0.037), respectively, but age, intrinsic factor antibodies and gastroscopy gave additional information.
      Conclusions - When cobalamin deficiency is suspected in general practice, serum cobalamin should be the first diagnostic test and the result should be interpreted in relation to the age of the patient.
      When a definite diagnosis cannot be reached, MMA and tHcy determination will provide additional discriminative information, but MMA, being more specific, is preferable for assessment of cobalamin status.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    10. Failure of assay to identify low cobalamin concentrations
      Ralph Carmel1,a, Shabneet Brar1, Atul Agrawal1 and P. Daniel Penha2, Departments of 1 Medicine and 2 Pathology, New York Methodist Hospital, Brooklyn, NY 11215 - a Author for correspondence - Clinical Chemistry. 2000;46:2017-2018 - © 2000 American Association for Clinical Chemistry, Inc.
      Cfr. :
      -
      http://www.clinchem.org/cgi/content/full/46/12/2017
      -
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=11106343&ordinalpos=2&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    11. Folate and vitamin B12 status in the Americas
      Allen LH, Western Human Nutrition Research Center and Program in International Nutrition, University of California, Davis, CA 95616, USA - Nutr Rev. 2004 Jun;62(6 Pt 2):S29-33; discussion S34 - PMID: 15298445
      There is growing interest in the potential for folic acid fortification in the Americas and recognition of the high prevalence of low plasma vitamin B12 concentrations reported in various studies.
      This review summarized available data on plasma vitamin B12 and folate concentrations in the Americas.
      At least 40% of individuals had deficient or marginal plasma vitamin B12 concentrations in almost all locations and across age groups.
      Low plasma folate concentrations were less common.
      It is hypothesized that vitamin B12 deficiency may result from a low intake of animal source foods, while a higher intake of refined flour may result in low plasma folate.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15298445&ordinalpos=4&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    12. Food and nutrition guidelines for healthy adolescents
      New Zealand Ministry of Health, July 7, 2006 :
      http://www.moh.govt.nz
      Cfr. :
      http://www.moh.govt.nz/moh.nsf/0/0697F789B648D3304C25666F0039933A/$File/foodnutritionguidelines-adolescents.pdf

    13. Functional vitamin B12 deficiency and Alzheimer disease 
      A. McCaddon, MRCGP; B. Regland, MD, PhD; P. Hudson, MSc; and G. Davies, MSc Neurology 2002;58:1395-1399
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=12011287&cmd=showdetailview&indexed=google

    14. Functional vitamin B12 deficiency and determination of holotranscobalamin in populations at risk
      Herrmann W, Obeid R, Schorr H, Geisel J - Clin Chem Lab Med 2003;41:1478-88
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    15. Greater prevalence of iron deficiency in overweight and obese children and adolescents
      Pinhas-Hamiel O, Newfield RS, Koren I, Agmon A, Lilos P, Phillip M., Pediatrics Endocrinology and Metabolism, Schneider Children's Medical Center, Petah-Tikva, Israel :
      orithami@sheba.health.gov.il - Int J Obes Relat Metab Disord. 2003 Mar;27(3):416-8 - PMID: 12629572
      Objective - To assess whether overweight children and adolescents, who often have poor dietary habits, are at increased risk of iron deficiency (ID).
      Methods - The study sample included 321 children and adolescents followed in two endocrine centers in Israel between 1999 and 2001.
      The subjects were divided into three groups on the basis of body mass index (BMI) for age and gender as follows : group 1-BMI below 85th percentile (normal weight); group 2-BMI above 85th, but below 97th percentile (overweight); and group 3-BMI above 97th percentile (obese).
      ID was defined as iron levels <8 micromol/l (45 mcg/dl) and iron-deficiency anemia (IDA) was defined as ID and hemoglobin level below 2 standard deviation score (SDS) for the mean for age and gender.
      Results - Iron levels below 8 micromol/l (45 mcg/dl) were noted in 38.8% of the obese children and 12.1% of the overweight children, compared with 4.4% of the normal-weight group (P<0.001).
      There was a significant negative correlation of low iron levels with BMI SDS (r=-0.44, P<0.001), but not with age or gender.
      Among the children with ID, 26.6% also had IDA. Groups 1, 2 and 3 accounted for 6.7%, 35%, and 58.3% of the children with IDA, respectively.
      Conclusions - ID is common in overweight and obese children.
      A significantly greater proportion of obese than normal-weight children have IDA.
      Insufficient dietary intake of iron, whether absolute or relative to body mass and increased iron needs may be a result of unbalanced nutrition or repeated short-term restrictive diets.
      Because of potentially harmful effects of ID, obese children should be routinely screened and treated as necessary.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=12629572&dopt=AbstractPlus

    16. High prevalence of cobalamin deficiency in elderly outpatients
      Pennypacker LC, Allen RH, Kelly JP, Matthews LM, Grigsby J, Kaye K et al. - J Am Geriatr Soc 1992;40:1197-204
      Cfr. :
      http://grande.nal.usda.gov/ibids/index.php?mode2=detail&origin=ibids_references&therow=283143

    17. High-dose vitamin therapy stimulates variant enzymes with decreased coenzyme binding affinity (increased K(m)) - Relevance to genetic disease and polymorphisms
      Ames BN, Elson-Schwab I, Silver EA, Department of Molecular and Cellular Biology, University of California, Berkeley, USA :
      bames@chori.org - Am J Clin Nutr. 2002 Apr;75(4):616-58 - PMID: 11916749
      As many as one-third of mutations in a gene result in the corresponding enzyme having an increased Michaelis constant, or K(m), (decreased binding affinity) for a coenzyme, resulting in a lower rate of reaction.
      About 50 human genetic dis-eases due to defective enzymes can be remedied or ameliorated by the administration of high doses of the vitamin component of the corresponding coenzyme, which at least partially restores enzymatic activity.
      Several single-nucleotide polymorphisms, in which the variant amino acid reduces coenzyme binding and thus enzymatic activity, are likely to be remediable by raising cellular concentrations of the cofactor through high-dose vitamin therapy.
      Some examples include the alanine-to-valine substitution at codon 222 (Ala222-->Val) [DNA: C-to-T substitution at nucleo-tide 677 (677C-->T)] in methylenetetrahydrofolate reductase (NADPH) and the cofactor FAD (in relation to cardiovascular disease, migraines and rages), the Pro187-->Ser (DNA: 609C-->T) mutation in NAD(P) :quinone oxidoreductase 1 [NAD(P)H dehy-drogenase (quinone)] and FAD (in relation to cancer), the Ala44-->Gly (DNA: 131C-->G) mutation in glucose-6-phosphate 1-dehydrogenase and NADP (in relation to favism and hemolytic anemia) and the Glu487-->Lys mutation (present in one-half of Asians) in aldehyde dehydrogenase (NAD + ) and NAD (in relation to alcohol intolerance, Alzheimer disease and cancer).
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    18. Homocysteine and risk of ischemic heart disease and stroke - A meta-analysis
      Homocysteine Studies Collaboration Ė JAMA, 2002 Oct 23-30;288(16):2015-22 Ė PMID : 12387654
      Context - It has been suggested that total blood homocysteine concentrations are associated with the risk of ischemic heart disease (IHD) and stroke.
      Objective - To assess the relationship of homocysteine concentrations with vascular disease risk.
      Data sources - MEDLINE was searched for articles published from January 1966 to January 1999.
      Relevant studies were identified by systematic searches of the literature for all reported observational studies of associations between IHD or stroke risk and homocysteine concentrations.
      Additional studies were identified by a hand search of references of original articles or review articles and by personal communication with relevant investigators.
      Study selection - Studies were included if they had data available by January 1999 on total blood homocysteine concentrations, sex and age at event.
      Studies were excluded if they measured only blood concentrations of free homocysteine or of homocysteine after a methionine-loading test or if relevant clinical data were unavailable or incomplete.
      Data Extraction - Data from 30 prospective or retrospective studies involving a total of 5073 IHD events and 1113 stroke events were included in a meta-analysis of individual participant data, with allowance made for differences between studies, for confounding by known cardiovascular risk factors and for regression dilution bias.
      Combined odds ratios (ORs) for the association of IHD and stroke with blood homocysteine concentrations were obtained by using conditional logistic regression.
      Data synthesis - Stronger associations were observed in retrospective studies of homocysteine measured in blood collected after the onset of disease than in prospective studies among individuals who had no history of cardiovascular disease when blood was collected.
      After adjustment for known cardiovascular risk factors and regression dilution bias in the prospective studies, a 25% lower usual (corrected for regression dilution bias) homocysteine level (about 3 micromol/L [0.41 mg/L]) was associated with an 11% (OR, 0.89; 95% confidence interval [CI], 0.83-0.96) lower IHD risk and 19% (OR, 0.81; 95% CI, 0.69-0.95) lower stroke risk.
      Conclusions - This meta-analysis of observational studies suggests that elevated homocysteine is at most a modest independent predictor of IHD and stroke risk in healthy populations.
      Studies of the impact on disease risk of genetic variants that affect blood homocysteine concentrations will help determine whether homocysteine is causally related to vascular disease, as may large randomized trials of the effects on IHD and stroke of vitamin supplementation to lower blood homocysteine concentrations.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=12387654&ordinalpos=5&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    19. Homocysteine in Health and Disease
      Ralph Carmel & Donald W. Jacobsen - Cambridge University Press; 1 edition (August 6, 2001) - ISBN-10: 0521653193 / ISBN-13: 978-0521653190
      Review from Joseph Loscalzo, M.D., Ph.D., The New England Journal of Medicine, January 31, 2002 - © 2002 Massachusetts Medical Society : The study of homocysteine and its role in homeostasis and disease has grown considerably over the past decade.
      What began as a series of observations about a rare inborn error of metabolism (homocystinuria) has now evolved into a substantial body of work derived from basic, animal and clinical studies focusing on the central role of homocysteine in the metabolism of sulfur-containing amino acids and its association with common vascular disorders.
      Because of the wide range of investigative perspectives adopted in approaching the role of this deceptively simple amino acid in mammalian biology and pathobiology, the thoughtful and critical integration and synthesis of the available data are a timely and welcome exercise.
      The editors of Homocysteine in Health and Disease attempt to meet this challenge by providing a rigorous and comprehensive overview of the field of homocysteine and hyperhomocysteinemic states.
      The book begins with a fine historical overview by two leading clinical investigators in the field of homocystinuria, which is followed by two sections comprising 18 chapters on biochemistry and physiology and 21 chapters on clinical disorders.
      The first 14 chapters of the first section are well-written, carefully prepared, comprehensive reviews of the complex chemistry and biochemistry of homocysteine (Figure 1).
      They are generally notable for their lack of redundancy, their useful figures and tables and their integrated style, which suggests a careful editorial hand.
      In addition, these chapters provide a rich treasure-trove of biochemical detail that is notably absent from other reviews and textbooks.
      The chapters on physiology are a bit uneven and include only the topics of transport and tissue distribution, renal function and nervous system responses.
      Some additional pathophysiological topics are included in the clinical chapters, where they are covered quite well (e.g., in the chapter on homocysteine and hemostasis by Hajjar and the chapter on homocysteine and cardiovascular physiology by Lentz).
      From the organizational perspective, the editors might have considered including a section on physiology and pathophysiology that incorporated all these topics in a better-integrated fashion.
      Notwithstanding the overall excellence of the first section of the book, one important topic that is not covered in its own chapter is the molecular biologic aspects of homocysteine -- both its role in modulating gene expression and the detailed molecular biology of the genes responsible for regulating its synthesis and metabolism.
      These topics are partially covered in several chapters but are not addressed with the well-integrated, comprehensive approach used to review the chemistry and biochemistry of homocysteine.
      The last 21 chapters offer a marvelous overview of the broad range of pathobiologic processes affected by homocysteine and their role in specific diseases with which hyperhomocysteinemia has been associated.
      The chapter topics range from the genetics of heritable hyperhomocysteinemic states to the relation between B-vitamin-deficiency states and hyperhomocysteinemia.
      These chapters are followed by several others that address the specific associations between homocysteine and largely vascular disorders, including thrombosis in venous beds and atherothrombosis in the coronary, cerebrovascular and peripheral arterial beds.
      In discussing each disorder, the authors are careful not to confuse association with causation, an issue that vexes much of the clinical literature.
      In view of the controversy regarding the direct mechanistic relation of hyperhomocysteinemia to vascular disease, the editors could have done the readers a great service by providing a summary chapter at the end of the book highlighting this important issue and the approach that is actively being pursued toward its resolution.
      Potential approaches to treatment are summarized in the last three chapters, which are reasonably timely, considering the delays that are usual in publishing a textbook of this nature.
      This is a fine textbook that should be of interest to clinicians and basic scientists who are interested in homocysteine and its potential role in a variety of disease states.
      The authors and editors have all made important contributions to this evolving field and, from the perspective of their own investigative experience, offer the reader a clear, comprehensive, authoritative guide to this complex topic.
      Cfr. :
      http://www.amazon.com/Homocysteine-Health-Disease-Ralph-Carmel/dp/0521653193

    20. How many patients are in need of vitamin B12 injections ?
      University of Aarhus - Study ID Numbers : 2005-0198 - Last Updated : June 1, 2007 - Record first received : May 16, 2006 - ClinicalTrials.gov Identifier : NCT00326833 - Health Authority : Denmark : Ethics Committee - ClinicalTrials.gov processed this record on November 14, 2007
      Purpose
      The clinical consequences of vitamin B12 deficiency include megaloblastic anemia and neurological disorders.
      Therefore, a proper and timely diagnosis and treatment is important.
      The use of sensitive biochemical markers such as methylmalonic acid for the diagnosis of vitamin B12 deficiency have increased since the 1980s.
      Consequently, the number of individuals treated with vitamin B12 has increased significantly.
      The objective of this project is to study the actual need for vitamin B12 injections in the group of individuals who have already started treatment.
      In order to investigate this, the investigators stop vitamin B12 treatment in this group and look for signs of vitamin B12 deficiency by monitoring changes in biochemical and hematological markers.
      Furthermore, they will test if the individuals are able to absorb a physiological dose of vitamin B12 using a recently developed absorption test (CobaSorb).
      If a physiological dose can be absorbed, the vitamin B12 injections can be replaced with tablets.
      In the end, the investigators hope to be able to divide the patients into three groups :
      - need life long injections with vitamin B12
      - only need supplementations with a small dose of oral vitamin B12 and
      - no need for further vitamin B12 treatment.
      The perspective is that the new information from this study might be used for a future strategy for vitamin B12 treatment.
      Cfr. :
      -
      http://clinicaltrials.gov/ct/show/NCT00326833;jsessionid=D637A6E99A32AC2CD59
      2580931F024B8?order=13

      -
      http://clinicaltrials.gov/ct/show/NCT00326833;jsessionid=1A574B2DA473019A15230
      60BED57A40E?order=1


    Lees verder : Deel III

     

    17-12-2007 om 22:49 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 0/5 - (0 Stemmen)
    >> Reageer (4)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Vitamine B12 en de relatie met CVS/FM - Deel III
    Klik op de afbeelding om de link te volgen






    Vitamine B12 en de relatie met CVS/FM

    Deel III

    1. Hyperhomocysteinemia and elevated methylmalonic acid indicate a high prevalence of cobalamin deficiency in Asian Indians
      Refsum H, Yajnik CS, Gadkari M, Schneede J, Vollset SE, Orning L et al. - Am J Clin Nutr 2001;74:233-41
      Cfr. :
      http://lib.bioinfo.pl/pmid:11470726

    2. Hyperhomocysteinemia and vitamin B-12 deficiency in elderly using Title IIIc nutrition services
      Johnson MA, Hawthorne NA, Brackett WR, Fischer JG, Gunter EW, Allen RH, Stabler SP, Department of Foods and Nutrition, University of Georgia, Athens, USA - Am J Clin Nutr. 2003 Jan;77(1):211-20 - PMID: 12499344
      Background
      - The effect of the folate food fortification program on the prevalence of hyperhomocysteinemia in the older population with coexisting vitamin B-12 deficiency is not known.
      Objective - The objective was to determine the prevalence of hyperhomocysteinemia and vitamin B-12 deficiency in elderly who were using Title IIIc nutrition services, after folate food fortification in the United States.
      Design - Demographic, nutritional, cognitive, routine diagnostic and serum methylmalonic acid (MMA) and total homocysteine (tHcy) tests were performed in a convenience sample of 103 elderly enrolled in nutrition service programs in rural northeast Georgia.
      A subgroup (n = 27) was treated with vitamin B-12, 2.5 mg and a multivitamin with 400 micro g folic acid, 2 mg vitamin B-6 and 27 mg ferrous fumarate.
      Results - The total cohort included 103 participants (+/- SD age: 76.4 +/- 8.1; 80% female; 68% white, 32% African American).
      Vitamin B-12 deficiency (serum vitamin B-12 < 258 pmol/L and MMA > 271 nmol/L) was present in 23%.
      Mean serum folate was high, 39.3 nmol/L and no subject had serum folate < 6.8 nmol/L.
      Mean tHcy was 17.6 +/- 7.2 micro mol/L in vitamin B-12-deficient subjects and 10.8 +/- 3.6 micro mol/L in those who were nondeficient.
      Determinants of high tHcy were vitamin B-12 deficiency, high serum creatinine and low red blood cell folate.
      Those with vitamin B-12 deficiency were more likely to have poor cognition (58% compared with 20%, P < 0.001) and anemia (38% compared with 18%, P = 0.042).
      High-dose oral B-12 therapy lowered mean MMA and tHcy by 49% and 32%, respectively.
      Conclusion - Vitamin B-12 deficiency was prevalent and was associated with poor cognition, anemia and hyperhomocysteinemia.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    3. Hyperhomocysteinemia correlates with insulin resistance and low-grade systemic inflammation in obese prepubertal children
      Martos R, Valle M, Morales R, CaŮete R, Gavilan MI, SŠnchez-Margalet V, Health Center of Pozoblanco, 14400 Pozoblanco, Cůrdoba, Spain :
      rosariomartos96@yahoo.es - Metabolism. 2006 Jan;55(1):72-7 - PMID: 16324922
      Obesity is an independent risk factor for the development of cardiovascular disease frequently associated with hypertension, dyslipemia, diabetes and insulin resistance.
      Higher homocysteine (Hcy) levels are observed in the hyperinsulinemic obese adults and suggest that Hcy could play a role in the higher risk of cardiovascular disease in obesity.
      We analyzed total Hcy levels in obese prepubertal children and their possible association with both metabolic syndrome and various inflammatory biomarkers and leptin.
      We studied 43 obese children (aged 6-9 years) and an equal number of nonobese children, paired by age and sex.
      The obese subjects presented significantly elevated values for insulin (P = .003), C-reactive protein (P = .033) and leptin (P < .001).
      No significant differences were found in Hcy levels between the obese and nonobese children.
      However, Hcy concentration was significantly higher in the hyperinsulinemic obese children than in the normoinsulinemic group (P = .002).
      Using multivariant regression analysis, in the obese group, corrected for age and sex, the homeostasis model assessment for insulin resistance (P partial = .001) and leptin (P partial = .02) are independent predictive factors for Hcy.
      In the control group, corrected for age and sex, the homeostasis model assessment for insulin resistance (P partial = .005) and leptin (P partial = .031) also are independent predictive factor for Hcy.
      Increased plasma Hcy, particularly in hyperinsulinemic obese children, may be causally involved in the pathogenesis of atherosclerosis and/or cardiovascular disease, both of which are common in obesity.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    4. Impact of government in nutrition epidemiology for nutrition and health policy
      Nitzan Kaluski D - Presented at : 25th ESPEN Congress; September 20, 2003; Cannes, France

    5. Increased concentrations of homocysteine in the cerebrospinal fluid in patients with fibromyalgia and chronic fatigue syndrome
      Regland B, Andersson M, Abrahamsson L, Bagby J, Dyrehag LE, Gottfries CG, Institute of Clinical Neuroscience, GŲteborg University, Sweden - Scand J Rheumatol. 1997;26(4):301-7 - PMID: 9310111
      Twelve outpatients, all women, who fulfilled the criteria for both fibromyalgia and chronic fatigue syndrome were rated on 15 items of the Comprehensive Psychopathological Rating Scale (CPRS-15).
      These items were chosen to constitute a proper neurasthenic subscale.
      Blood laboratory levels were generally normal.
      The most obvious finding was that, in all the patients, the homocysteine (HCY) levels were increased in the cerebrospinal fluid (CSF).
      There was a significant positive correlation between CSF-HCY levels and fatiguability and the levels of CSF-B12 correlated significantly with the item of fatiguability and with CPRS-15.
      The correlations between vitamin B12 and clinical variables of the CPRS-scale in this study indicate that low CSF-B12 values are of clinical importance.
      Vitamin B12 deficiency causes a deficient remethylation of HCY and is therefore probably contributing to the increased homocysteine levels found in our patient group.
      We conclude that increased homocysteine levels in the central nervous system characterize patients fulfilling the criteria for both fibromyalgia and chronic fatigue syndrome.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    6. Insulin resistance and endothelial function are improved after folate and vitamin B12 therapy in patients with metabolic syndrome - Relationship between homocysteine levels and hyperinsulinemia
      Setola E, Monti LD, Galluccio E, Palloshi A, Fragasso G, Paroni R, Magni F, Sandoli EP, Lucotti P, Costa S, Fermo I, Galli-Kienle M, Origgi A, Margonato A, Piatti P, Cardiovascular and Metabolic Rehabilitation Unit, Rehabilitation and Functional Reeducation Division, Scientific Institute H. San Raffaele, Italy - Eur J Endocrinol. 2004 Oct;151(4):483-9 - PMID: 15476449
      Objective
      - The purpose of this study was (a) to study whether a folate and vitamin B12 treatment, aimed at decreasing homocysteine levels, might ameliorate insulin resistance and endothelial dysfunction in patients with metabolic syndrome according to the National Cholesterol Education Program-Adult Treatment Panel-III criteria and (b) to evaluate whether, under these metabolic conditions, there is a relationship between hyperhomocysteinemia and insulin resistance.
      Design and methods - A double-blind, parallel, identical placebo-drug, randomized study was performed for 2 months in 50 patients.
      Patients were randomly allocated to two groups.
      In group 1, patients were treated with diet plus placebo for 2 months.
      In group 2, patients were treated with diet plus placebo for 1 month, followed by diet plus folic acid (5 mg/day) plus vitamin B12 (500 microg/day) for another month.
      Results - In group 2, folate treatment significantly decreased homocysteine levels by 27.8% (12.2+/-1.2 vs 8.8+/-0.7 micromol/l; P<0.01).
      A significant decrement was observed for insulin levels (19.9+/-1.7 vs 14.8+/-1.6 microU/ml; P<0.01) accompanied by a 27% reduction in the homeostasis model assessment levels.
      A positive relationship was found between the decrement of homocysteine and insulin levels (r=0.60; P<0.002).
      In parallel, endothelial dysfunction significantly improved in the treated group, since post-ischemic maximal hyperemic vasodilation increased by 29.8% and cGMP by 13.6% while asymmetrical dimethylarginine levels decreased by 21.7%.
      On the contrary, in group 1 patients, treated with placebo, no changes were shown in any of the variables.
      Conclusions - Folate and vitamin B12 treatment improved insulin resistance and endothelial dysfunction, along with decreasing homocysteine levels, in patients with metabolic syndrome, suggesting that folic acid has several beneficial effects on cardiovascular disease risk factors.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    7. Is testing for clinical cobalamin deficiency truly unreliable ?
      Carmel R, Solomon LR - Correspondence : Ralph Carmel, Department of Medicine, New York Methodist Hospital, 506 Sixth St, Brooklyn, NY 11215 :
      rac9001@nyp.org - Blood. 2005 Aug 1;106(3):1136-8; author reply 1137-8 - PMID: 16033957
      Cobalamin and metabolite assays' sensitivities depend greatly on whether the tested patients have clinical abnormalities (95%-99% sensitivities) or not (< 70% for cobalamin, but data and criteria vary).1,2
      In his report of massive diagnostic failures in even symptomatic cobalamin deficiency, Solomon misperceives what failed.3
      The likeliest initial culprit is a defective cobalamin assay.
      Overlapping the study's time period, we reported that the ADVIA Centaur (Bayer Diagnostics, Tarrytown, NY) assay produced falsely normal results in 16 of 22 cobalamin-deficient sera that had consistently subnormal levels by 2 radioisotopic assays.4
      Assay error best explains Solomon's truly unprecedented claims that just 5 (14%!) of 37 patients with symptomatic deficiency had cobalamin levels less than 200 ng/L or that as many as 20 (54%) of 37 could have had levels more than 300 ng/L.
      As to metabolite data, the pretreatment values were very inconsistent and frequently jumped the divide between normal and abnormal.
      Left unexamined were whether assay or patient fluctuation was responsible and if variability rather than therapy explained the (unreplicated) posttreatment improvements.
      Equally puzzling was the tendency of results to be less, not more, abnormal in presumably deficient patients than in nondeficient ones.
      The clinical and therapeutic diagnoses raise concerns too.
      Hematologic findings, which lacked individual complete blood count (CBC) details, were surprisingly insubstantial.
      Only 2 of 37 patients had anemia, 1 of whom incongruously "responded" to cobalamin without changing mean corpuscular volume; 6 others (75% of hematologically abnormal patients) had mild macrocytosis without anemia, something that more often reflects alcoholism,5 which, being often both unrecognized and fluctuating, can confound therapeutic assessments; and blood smears were not examined for hypersegmentation, a major failing given the study's goals and controversial findings.
      Neurologic information was sketchy and the appendices suggest diagnostic alternatives; patient 3, for example, closely mimics a reported patient whose alcohol-induced neurologic and other abnormalities were mistakenly deemed cobalamin responsive.6
      Further suggesting subclinical or no deficiency rather than clinical deficiency in many patients was the near-absence of the characteristically extreme metabolite elevations of clinical deficiency1 (eg, methylmalonic acid > 1000 nM) and the rarity of abnormal Schilling test results7 (only 4 of 12 were abnormal, while the 5 positive intrinsic factor antibody results seem artifacts of cobalamin injection8 because, among other things, the 2 patients also given Schilling tests had incompatibly normal absorption).
      The proposal of overwhelming, structural diagnostic inadequacy in symptomatically cobalamin-deficient patients, therefore, seems attributable instead to the more prosaic and remediable failures of manufacturers and clinical laboratories, compounded by an uncertain diagnostic mix of study patients.
      An important subtext, too, is the confusing cobalamin cutpoint inflation peppering the data and that the paper promotes.
      As discussed elsewhere,9 the growing impact on clinical diagnosis and management of this inflation, paradoxically derived from data in subclinical deficiency, has drawbacks that have not been thoroughly examined.
      Clinicians may minimize potential diagnostic confusion by carefully distinguishing clinical from subclinical cobalamin deficiency, despite their overlaps.9 (Tab1)
      Clinical deficiency is a relatively uncommon medical disease, usually easily diagnosed, typically relentless and requiring urgent treatment; subclinical deficiency is a common biochemical abnormality, often less easily diagnosed and usually having a still-undefined course and therapeutic imperatives.7,9
      Cfr. :
      http://bloodjournal.hematologylibrary.org/cgi/content/full/106/3/1136-a

    8. Laboratory diagnosis of vitamin B12 and folate deficiency - A guide for the primary care physician
      Snow CF, Division of Primary Care, Santa Clara Valley Medical Center, San Jose, Calif., USA - Arch Intern Med. 1999 Jun 28;159(12):1289-98 - PMID: 10386505
      At one time, the diagnosis of a deficiency of vitamin B12 or folate was considered to be relatively straightforward.
      As knowledge has accumulated, the limitations of such tests as serum vitamin level measurements and the Schilling test have become apparent.
      With the development of newer tests, atypical and subclinical deficiency states have been recognized.
      In this review, available tests used in the diagnosis of vitamin B12 and folate deficiency are discussed and a rational approach to the diagnosis of these deficiency states is presented.
      Cfr. :
      -
      http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=10386505&cmd=showdetailview&indexed=google
      -
      http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&dopt=AbstractPlus&list_uids=10386505

    9. Long-term effects of vitamin B(12), folate and vitamin B(6) supplements in elderly people with normal serum vitamin B(12) concentrations
      Henning BF, Tepel M, Riezler R, Naurath HJ Ė Gerontology 2001;47(1):30-5
      Cfr. :
      http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowAbstract&ProduktNr=224091&Ausgabe=227949&ArtikelNr=52767

    10. Mechanisms of dairy modulation of adiposity
      Michael B. Zemel, Departments of Nutrition and Medicine, The University of Tennessee, Knoxville, TN 37996 :
      mzemel@utk.edu Ė Symposium : 'Dairy Product Components and Weight Regulation©', 2003 - The American Society for Nutritional Sciences J. Nutr. 133:252S-256S, January 2003
      Dietary calcium plays a pivotal role in the regulation of energy metabolism, in that we have found high calcium diets to attenuate adipocyte lipid accretion and weight gain during periods of overconsumption of an energy-dense diet and to increase lipolysis and preserve thermogenesis during caloric restriction, thereby markedly accelerating weight loss.
      Our studies of the agouti gene in obesity and insulin resistance demonstrate a key role for intracellular Ca2+ in regulating adipocyte lipid metabolism and triglyceride storage, with increased intracellular Ca2+, resulting in stimulation of lipogenic gene expression and lipogenesis and suppression of lipolysis, resulting in adipocyte lipid filling and increased adiposity.
      Moreover, we have recently demonstrated that the increased calcitriol produced in response to low calcium diets stimulates Ca2+ influx in human adipocytes and thereby promotes adiposity.
      Accordingly, suppressing calcitriol levels by increasing dietary calcium is an attractive target for the prevention and management of obesity.
      In support of this concept, transgenic mice expressing the agouti gene specifically in adipocytes (a humanlike pattern) respond to low calcium diets with accelerated weight gain and fat accretion, whereas high calcium diets markedly inhibit lipogenesis, accelerate lipolysis, increase thermogenesis and suppress fat accretion and weight gain in animals maintained at identical caloric intakes.
      Further, low calcium diets impede body fat loss, whereas high calcium diets markedly accelerate fat loss in transgenic mice subjected to caloric restriction.
      Notably, dairy sources of calcium exert markedly greater effects in attenuating weight and fat gain and accelerating fat loss.
      This augmented effect of dairy vs. supplemental calcium is likely attributable to additional bioactive compounds in dairy that act synergistically with calcium to attenuate adiposity; among these are angiotensin converting enzyme inhibitory peptides, which limit angiotensin II production and thereby limit angiotensin II stimulation of adipocyte lipogenesis.
      These concepts are confirmed by both epidemiological and clinical data, which similarly demonstrate that dairy products exert a substantially greater effect on both fat loss and fat distribution compared to an equivalent amount of supplemental calcium.
      Cfr. :
      http://jn.nutrition.org/cgi/content/full/133/1/252S

    11. Mild transcobalamin I (haptocorrin) deficiency and low serum cobalamin concentrations
      Carmel R. - Clin Chem 2003;49:1367-74
      Cfr. :
      http://www.clinchem.org/cgi/content/full/49/8/1367

    12. Modern approaches to the investigation of vitamin B12 deficiency
      Ward PC. - Clin Lab Med 2002;22:435-45
      Cfr. :
      http://grande.nal.usda.gov/ibids/index.php?mode2=detail&origin=ibids_references&therow=719927

    13. Multiple sclerosis and vitamin B12 metabolism
      Reynolds EH, Maudsley Hospital, London, UK - J Neuroimmunol. 1992 Oct;40(2-3):225-30 - PMID: 1430153
      Multiple sclerosis (MS) is occasionally associated with vitamin B12 deficiency.
      Recent studies have shown an increased risk of macrocytosis, low serum and/or CSF vitamin B12 levels, raised plasma homocysteine and raised unsaturated R-binder capacity in MS.
      The aetiology of the vitamin B12 deficiency in MS is often uncertain and a disorder of vitamin B12 binding or transport is suspected.
      The nature of the association of vitamin B12 deficiency and MS is unclear but is likely to be more than coincidental.
      There is a remarkable similarity in the epidemiology of MS and pernicious anaemia.
      Vitamin B12 deficiency should always be looked for in MS.
      The deficiency may aggravate MS or impair recovery.
      There is evidence that vitamin B12 is important for myelin synthesis and integrity but further basic studies are required.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=1430153&ordinalpos=25&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    14. Neural-tube defects are associated with low concentrations of cobalamin (vitamin B12) in amniotic fluid
      Steen MT, Boddie AM, Fisher AJ, Macmahon W, Saxe D, Sullivan KM, Dembure PP, Elsas LJ, Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30322, USA Prenat Diagn. 1998 Jun;18(6):545-55 - PMID: 9664599
      While folate supplementation reduces the risk of recurrent neural-tube defects (NTD), both folate and cobalamin deficiencies may be independent risk-factors for neural-tube defects.
      Folate-dependence and impaired remethylation of homocysteine are implicated as mechanisms for NTD.
      There are few references reported for folate, cobalamin, homocysteine and methionine in the fetal compartment.
      This case-controlled pilot study of amniotic fluid (AF) samples derived from 16 NTD pregnancies and 64 age-matched controls quantities total homocysteine (tHcy), total cysteine (tCys), folate, cobalamin (B12) and methionine.
      Only decreased AF B12 concentrations were found (150 pg/ml versus 540 pg/ml, P < 0.02).
      Since cobalamin, folate and homocysteine participate in the remethylation of homocysteine, via methyl transfer from 5-methyltetrahydrofolate to B12, to methionine, we compared ratios of these methionine synthase (EC 2.1.1.13)-related intermediates.
      The ratio of B12/folate for NTD versus controls was 48 (34-90) versus 126 (123-182), P < 0.001.
      The ratio of methionine/(folate x tHcy) was 1.4 (1.2-2.2) versus 2.7 (2.4-3.3), P < 0.001.
      We conclude that AF from pregnancies with NTD have lower B12 concentrations and that ratios of product to substrate(s) of homocysteine remethylation suggest impaired methionine synthase in the fetal compartment through the early second trimester.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    15. Neurologic aspects of cobalamin deficiency
      Healton EB, Savage DG, Brust JC, Garrett TJ, Lindenbaum J, Department of Neurology, Columbia-Presbyterian Medical Center, New York, NY 10032 - Medicine (Baltimore). 1991 Jul;70(4):229-45 - PMID: 1648656
      We reviewed 153 episodes of cobalamin deficiency involving the nervous system that occurred in 143 patients seen over a recent 17-year period at 2 New York City hospitals.
      Pernicious anemia was the most common underlying cause of the deficiency.
      Neurologic complaints, most commonly paresthesias or ataxia, were the first symptoms of Cbl deficiency in most episodes.
      The median duration of symptoms before diagnosis and treatment with vitamin B12 was 4 months, although long delays in diagnosis occurred in some patients.
      Diminished vibratory sensation and proprioception in the lower extremities were the most common objective findings.
      A wide variety of neurologic symptoms and signs were encountered, however, including ataxia, loss of cutaneous sensation, muscle weakness, diminished or hyperactive reflexes, spasticity, urinary or fecal incontinence, orthostatic hypotension, loss of vision, dementia, psychoses and disturbances of mood.
      Multiple neurologic syndromes were often seen in a single patient.
      In 42 (27.4%) of the 153 episodes, the hematocrit was normal and in 31 (23.0%), the mean corpuscular volume was normal.
      Neutropenia and thrombocytopenia were unusual even in anemic patients.
      In nonanemic patients in whom diagnosis was delayed, neurologic progression frequently occurred although the hematocrit remained normal.
      In 27 episodes, the serum cobalamin concentration was only moderately decreased (in the range of 100-200 pg/ml) and in 2 the serum level was normal.
      Neurologic impairment, as assessed by a quantitative severity score, was judged to be mild in 99 episodes, moderate in 39 and severe in 15.
      Severity of neurologic dysfunction before treatment was clearly related to the duration of symptoms prior to diagnosis.
      In addition, the hematocrit correlated significantly with severity, independent of the longer duration of symptoms in nonanemic patients.
      Four patients experienced transient neurologic exacerbations soon after beginning treatment with cyanocobalamin, with subsequent recovery.
      Followup evaluation was adequate to assess the neurologic response to vitamin B12 therapy in 121 episodes.
      All patients responded and in 57 (47.1%), recovery was complete, with no remaining symptoms or findings on examination.
      The severity score was reduced by 50% or greater after treatment in 91% of the episodes.
      Residual long-term moderate or severe neurologic disability was noted following only 7 (6.3%) episodes.
      The extent of neurologic involvement after treatment was strongly related to that before therapy as well as to the duration of symptoms.
      The percent improvement over baseline neurologic status after treatment was inversely related to duration of symptoms and hematocrit.
      Some evidence of response was always seen during the first 3 months of treatment .../...
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=1648656&ordinalpos=1&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    16. Neurology - 4th. Ed
      Mumenthaler, M. en Mattle, H - Thieme Medical Publishers (4th edition), 2004 - ISBN : 9781588900456 / 9783135239040 - p. 442
      Cfr. :
      http://www.thieme.com/SID2389280558719/productsubpages/pubid-848078832.html

    17. Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis
      Lindenbaum J, Healton EB, Savage DG, Brust JC, Garrett TJ, Podell ER et al. - N Engl J Med 1988;318:1720-8
      Cfr. :
      http://content.nejm.org/cgi/content/abstract/318/26/1720

    18. Neuropsychiatric disturbances in presumed late-onset cobalamin C disease
      Roze E, Gervais D, Demeret S, Ogier de Baulny H, Zittoun J, Benoist JF, Said G, Pierrot-Deseilligny C, Bolgert F, Service de Neurologie 1, Groupe Hospitalier Pitiť-SalpÍtriŤre, Paris, France - Arch Neurol. 2003 Oct;60(10):1457-62 - PMID: 14568819
      Background - Combined methylmalonic aciduria and homocystinuria cobalamin C type (cobalamin C disease) is an inborn metabolic disorder consisting of an impaired intracellular synthesis of the 2 active forms of vitamin B12 (cobalamin), namely, adenosylcobalamin and methylcobalamin, that results in increased levels of methylmalonic acid and homocysteine in the blood and urine.
      Most patients present in the first year of life with systemic, hematological and neurological abnormalities.
      Late-onset forms are rare and had not been comprehensively characterized.
      They could be easily misdiagnosed.
      Objective - To describe clinical and biochemical features of the disease in 2 siblings affected with presumed late-onset cobalamin C disease.
      Design - Case report and review of the literature.
      Setting - Neurological intensive care unit of a university hospital.
      Observation - We describe 2 patients with neurological deterioration due to presumed cobalamin C disease.
      A 16-year-old girl was initially seen with psychosis and severe progressive neuropathy requiring mechanical ventilatory support and her 24-year-old sister had a 2-year disease course of subacute combined degeneration of the spinal cord.
      A metabolic workup displayed increased methylmalonic acid levels, severe hyperhomocysteinemia and low plasma methionine levels.
      The diagnosis was then confirmed by demonstration of impaired synthesis of adenosylcobalamin and methylcobalamin in cultured skin fibroblasts and Epstein-Barr virus-infected lymphocytes.
      Under specific treatment the younger sister's condition dramatically improved.
      Conclusions - Although complementation studies have not been conducted, it is most likely these patients had cobalamin C disease.
      This study emphasizes the possibility of late-onset disease with purely neurological manifestations.
      Left untreated, this treatable condition can lead to death or irreversible damage to the nervous system.
      Screening for intracellular vitamin B12 dysmetabolism should, therefore, be considered in the investigation of adults with unexplained neurological disease, particularly when they are initially seen with a clinical picture suggestive of vitamin B12 deficiency.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    19. Neutrophil nuclear segmentation in mild cobalamin deficiency - Relation to metabolic tests of cobalamin status and observations on ethnic differences in neutrophil segmentation
      Carmel R, Green R, Jacobsen DW, Qian GD, Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033, USA - Am J Clin Pathol. 1996 Jul;106(1):57-63 - PMID: 8701933
      Neutrophil hypersegmentation is considered the most sensitive peripheral blood cell marker of cobalamin deficiency.
      However, its diagnostic value in the mild deficiency states that accompany most low cobalamin levels and its relation to metabolic test of cobalamin status are unknown.
      The authors compared neutrophil lobe averages and percent neutrophils with 5 or more lobes (%5+ lobes) in 169 subjects with their mean corpuscular volume (MCV) and serum cobalamin, methylmalonic acid (MMA), homocysteine and folate levels and, in 65 cases, with the deoxyuridine suppression test (dUST).
      Only 9 subjects had hypersegmentation by lobe average and 20 subjects by %5+ lobes.
      They were not more often cobalamin-deficient than subjects without hypersegmentation.
      Moreover, only one of 34 subjects with dUST results diagnostic for cobalamin deficiency had neutrophil hypersegmentation.
      Both indices of neutrophil segmentation in the 169 subjects correlated significantly with homocysteine levels.
      They also showed weak inverse correlation with cobalamin levels, but did not correlate with MMA, folate or MCV values.
      Cobalamin therapy for 6 months did not significantly change neutrophil lobe averages in 35 subjects with mild deficiency, compared with 8 nondeficient controls and only marginally improved the %5+ lobes.
      A surprising, incidental observation was that blacks had significantly greater neutrophil segmentation by both criteria than did whites and others.
      This difference was unrelated to cobalamin or folate status.
      Our results indicate that dUST abnormalities precede all morphologic changes of deficiency, including hypersegmentation.
      Although a tendency exists for neutrophil segmentation to increase very slightly as some serum values, especially homocysteine, start to worsen in mild cobalamin deficiency, the metabolic changes precede overt hypersegmentation.
      Neutrophil nuclear segmentation is insufficiently sensitive in relation to metabolic evidence of deficiency to be used as a clinical tool in the diagnosis of mild cobalamin deficiency.
      Cfr. :
      http://grande.nal.usda.gov/ibids/index.php?mode2=detail&origin=ibids_references&therow=105923

    20. New studies support utility of Axis-Shield Active-B12 test
      08/06/07
      Cfr. :
      http://www.axis-shield.com/index.cfm?action=newsdetail&newsid=128

    21. Obese Children and Adolescents A Risk Group for Low Vitamin B12 Concentration 
      Orit Pinhas-Hamiel, MD; Noa Doron-Panush, RD; Brian Reichman, MD; Dorit Nitzan-Kaluski, MD, MPH, RD; Shlomit Shalitin, MD; Liat Geva-Lerner, MD Arch Pediatr Adolesc Med. 2006;160:933-936
      Cfr. :
      http://archpedi.ama-assn.org/cgi/content/abstract/160/9/933

    22. Ontwikkelingsachterstand bij borstgevoede kinderen door ontoereikend dieet van de moeder 
      A.Baatenburg de Jong, J.Bekhof, P.Zwart, V.J.Langenhorst en R.J.Roorda Ned Tijdschr Geneeskd. 2006 4 maart;150(9) - PMID: 16553042
      Two infant boys of 7 and 12 months respectively who presented with symptoms of failure to thrive and developmental delay were diagnosed with vitamin B12 deficiency.
      This deficiency is a rare condition in infants living in developed countries.
      It does occur, however, in infants who are breastfed by mothers with an inadequate diet.
      Both of the children studied were breastfed by vegetarian mothers.
      Following vitamin suppletion, both children showed signs of recovery.
      The importance of considering vitamin deficiencies in similar infants presenting with failure to thrive is emphasized.
      Moreover, maternal dietary habits in breastfed children should be checked.
      To prevent irreversible neurological damage, early recognition of any nutritional deficiencies is important.Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=16553042&dopt=AbstractPlus

    23. Overweight children and adolescents - A risk group for iron deficiency
      Nead KG, Halterman JS, Kaczorowski JM, Auinger P, Weitzman M - Pediatrics. 2004;114:104-108

    24. Patients must learn about B12 which can be low regardless of diet
      Rose Ann Fuhrman
      Cfr. :
      http://roseannster.googlepages.com/home

    25. Performance of the serum cobalamin assay for diagnosis of cobalamin deficiency
      Matchar DB, McCrory DC, Millington DS, Feussner JR - Am J Med Sci. 1994;308: 276-283


    Lees verder : Deel IV

    17-12-2007 om 22:41 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 2/5 - (2 Stemmen)
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Vitamine B12 en de relatie met CVS/FM - Deel IV
    Klik op de afbeelding om de link te volgen


     



    Vitamine B12 en de relatie met CVS/FM

    Deel IV


    1. Pernicious Anaemia 
      Ban-Hock T.O.H and F. Alderuccio Autoimmunity, 2004 Vol. 00 (0), pp. 1-5
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&dopt=AbstractPlus&list_uids=15518059

    2. Pernicious anemia - The expected findings of very low serum cobalamin levels, anemia and macrocytosis are often lacking
      Carmel, R - Arch Intern Med. 1988;148: 1712-1714
      When patients are examined for possible cobalamin deficiency, great stress is often placed on the presence or absence of macrocytosis and anemia and on how low the serum cobalamin level is.
      The present study, however, shows that only 45 (64%) of 70 consecutively diagnosed patients with pernicious anemia, the most common cause of cobalamin deficiency, had very low cobalamin levels (less than 74 pmol/L [or less than 100 ng/L]).
      Anemia was absent in 13 (19%) of the patients and macrocytosis was absent in 23 (33%) of the patients; such absence was particularly common when cobalamin levels were only slightly or moderately low (74 to 184 pmol/L).
      Coexisting iron deficiency was responsible for the absence of macrocytosis in nine patients.
      Of the ten patients with neither anemia nor macrocytosis, neurological disturbance was prominent in six, including four whose only noticeable abnormality was cerebral.
      These observations indicate that macrocytosis and anemia, two classic features of pernicious anemia, may be overstressed in our diagnostic approach.
      All subnormal serum cobalamin results are best viewed as pathological until proved otherwise.
      Emphasis on only very low cobalamin levels risks delaying the diagnosis of pernicious anemia in a substantial proportion of cases, particularly in those without anemia or macrocytosis.
      Cfr. :
      http://www.mdconsult.com/das/citation/body/84037169-2/jorg=journal&source=MI&sp=14454421&sid=0/N/14454421/1.html#abs

    3. Plasma homocysteine and lipoprotein (a) levels in Turkish patients with metabolic syndrome
      Guven A, Inanc F, Kilinc M, Ekerbicer H, Department of Cardiology, School of Medicine, Kahramanmaras Sutcu Imam University, Kahramanmaras, Turkey - Heart Vessels. 2005 Nov;20(6):290-5 - PMID: 16314912
      High serum total homocysteine (tHcy) and lipoprotein (a) [Lp(a)] levels are independent risk factors for cardiovascular disease.
      In this study, we examined the relationship of tHcy and Lp(a) levels with the components of metabolic syndrome.
      Fifty-one patients diagnosed with metabolic syndrome (median age : 38 [range 25-48] years) and 50 healthy subjects (median age : 35 [26-48] years) were included in the study.
      We used the National Cholesterol Education Program criteria to define metabolic syndrome.
      Total tHcy concentrations were measured by using an IMX (Abbott Diagnostics, Abbott Park, IL, USA). Lipoprotein (a) was measured by immunonephelometry using Behring nephrometer method (Behring BN 100, Behring, Germany).
      Total homocysteine and Lp(a) levels were found to be higher in the metabolic syndrome group than in the control group (tHcy : 24.2 vs 13.4 micromol/l, P < 0.01 and Lp(a) : 34.9 vs 15.8 mg/dl, P < 0.01).
      Vitamin B12 levels were lower in the metabolic syndrome group than in the control group (214 pg/ml vs 247 pg/ml, P < 0.01).
      In partial correlation, tHcy and Lp(a) concentrations were unrelated to metabolic syndrome or to the components of metabolic syndrome, including fasting serum triglycerides, HDL-cholesterol, fasting glucose, blood pressure or body mass index.
      tHcy levels were strongly related only to the vitamin B12 concentration.
      The risk of cardiovascular disease is higher in patients with metabolic syndrome compared with the normal population.
      High tHcy and Lp(a) levels should be evaluated in this group of patients in addition to the evaluation of the parameters of metabolic syndrome.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    4. Plasma vitamin B-12 concentrations relate to intake source in the Framingham Offspring study
      Tucker KL, Rich S, Rosenberg I, Jacques P, Dallal G, Wilson PW, Selhub J, Jean Mayer Human Nutrition Research Center on Aging at Tufts University, Boston MA 02111, USA.
      tucker@hnrc.tufts.edu - Am J Clin Nutr. 2000 Feb;71(2):514-22 - PMID: 10648266
      Background - Low vitamin B-12 status is prevalent among the elderly, but few studies have examined the association between vitamin B-12 status and intake.
      Objective - We hypothesized that vitamin B-12 concentrations vary according to intake source.
      Design - Plasma concentrations and dietary intakes were assessed cross-sectionally for 2999 subjects in the Framingham Offspring Study.
      The prevalence of vitamin B-12 concentrations <148, 185, and 258 pmol/L was examined by age group (26-49, 50-64, and 65-83 y), supplement use and the following food intake sources : fortified breakfast cereal, dairy products and meat.
      Results - Thirty-nine percent of subjects had plasma vitamin B-12 concentrations <258 pmol/L, 17% had concentrations <185 pmol/L and 9% had concentrations <148 pmol/L, with little difference between age groups.
      Supplement users were significantly less likely than non-supplement-users to have concentrations <185 pmol/L (8% compared with 20%, respectively).
      Among non-supplement-users, there were significant differences between those who consumed fortified cereal >4 times/wk (12%) and those who consumed no fortified cereal (23%) and between those in the highest and those in the lowest tertile of dairy intake (13% compared with 24%, respectively), but no significant differences by meat tertile.
      Regression of plasma vitamin B-12 on log of intake, by source, yielded significant slopes for each contributor adjusted for the others.
      For the total group, b = 40.6 for vitamin B-12 from vitamin supplements.
      Among non-supplement-users, b = 56.4 for dairy products, 35.2 for cereal, and 16.7 for meat.
      Only the meat slope differed significantly from the others.
      Conclusions - In contrast with previous reports, plasma vitamin B-12 concentrations were associated with vitamin B-12 intake.
      Use of supplements, fortified cereal and milk appears to protect against lower concentrations.
      Further research is needed to investigate possible differences in bioavailability.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    5. Polymorphisms in the transcobalamin gene - Association with plasma homocysteine in healthy individuals and vascular disease patients
      Lievers KJ, Afman LA, Kluijtmans LA, Boers GH, Verhoef P, den Heijer M, Trijbels FJ, Blom HJ, Departments of Pediatrics, Division of Endocrinology, University Medical Center Nijmegen, 6500 HB Nijmegen, The Netherlands - Clin Chem. 2002 Sep;48(9):1383-9 - PMID: 12194912
      Background
      - Hyperhomocysteinemia is an independent risk factor for cardiovascular disease (CVD).
      Intracellular vitamin B(12) deficiency may lead to increased plasma total homocysteine (tHcy) concentrations and because transcobalamin (TC) is the plasma transporter that delivers vitamin B(12) to cells, genetic variation in the TC gene may affect intracellular vitamin B(12) availability and, consequently, tHcy concentrations.
      Methods - We examined five sequence variants, i.e., I23V, G94S, P259R, S348F and R399Q, in the TC gene as possible determinants of tHcy and, concordantly, as possible risk factors for CVD in 190 vascular disease patients and 601 controls.
      We also studied potential effect-modification of vitamin B(12) by genotype.
      Results - In individuals with high vitamin B(12), 259PP individuals had lower tHcy concentrations than 259PR and 259RR individuals.
      Homozygous 23VV individuals had lower fasting tHcy concentrations than their 23IV and 23II peers.
      None of the genotypes defined by the three other sequence variants showed an association with tHcy concentrations, nor was any TC genotype associated with an increased CVD risk.
      Conclusions - In individuals in the highest quartile of the vitamin B(12) distribution (>299 pmol/L), tHcy concentrations are lower in 259PP homozygotes than in 259PR and 259RR individuals.
      Therefore, 259PP individuals, who represent >25% of the general population, may be more susceptible to reduction of plasma tHcy concentrations by increasing the vitamin B(12) status.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    6. Prevalence of anemia in persons 65 years and older in the United States - Evidence for a high rate of unexplained anemia
      Guralnik JM, Eisenstaedt RS, Ferrucci L, Klein HG, Woodman RC, Laboratory of Epidemiology, Demography, and Biometry, National Institute on Aging, 7201 Wisconsin Ave, Rm 3C-309, Bethesda, MD 20815, USA - Blood. 2004 Oct 15;104(8):2263-8. Epub 2004 Jul 6 - PMID: 15238427
      Clinicians frequently identify anemia in their older patients, but national data on the prevalence and causes of anemia in this population in the United States have been unavailable.
      Data presented here are from the noninstitutionalized US population assessed in the third National Health and Nutrition Examination Survey (1988-1994).
      Anemia was defined by World Health Organization criteria; causes of anemia included iron, folate and B(12) deficiencies, renal insufficiency, anemia of chronic inflammation (ACI), formerly termed anemia of chronic disease and unexplained anemia (UA).
      ACI by definition required normal iron stores with low circulating iron (less than 60 microg/dL).
      After age 50 years, anemia prevalence rates rose rapidly, to a rate greater than 20% at age 85 and older.
      Overall, 11.0% of men and 10.2% of women 65 years and older were anemic.
      Of older persons with anemia, evidence of nutrient deficiency was present in one third, ACI or chronic renal disease or both was present in one third and UA was present in one third.
      Most occurrences of anemia were mild; 2.8% of women and 1.6% of men had hemoglobin levels lower than 110 g/L (11 g/dL).
      Therefore, anemia is common, albeit not severe, in the older population and a substantial proportion of anemia is of indeterminate cause.
      The impact of anemia on quality of life, recovery from illness, and functional abilities must be further investigated in older persons.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    7. Role of cobalamin intake and atrophic gastritis in mild cobalamin deficiency in older Dutch subjects
      van Asselt DZ, de Groot LC, van Staveren WA, Blom HJ, Wevers RA, Biemond I, Hoefnagels WH, Department of Geriatric Medicine, University Hospital Nijmegen, The Netherlands.
      D.vanAsselt@czzoger.azn.nl - Am J Clin Nutr. 1998 Aug;68(2):328-34 - PMID: 9701190
      Background - The reason for the high prevalence of mild cobalamin (vitamin B-12) deficiency in the elderly is poorly understood.
      Objective - We aimed to determine the reason for this high prevalence.
      Design - We examined cobalamin intake, the presence and severity of atrophic gastritis, the presence of Helicobacter pylori infection and plasma cobalamin and methylmalonic acid (MMA) concentrations in 105 healthy, free-living, older subjects aged 74-80 y.
      Results - Mild cobalamin deficiency, ie, low to low-normal plasma cobalamin concentrations (< 260 pmol/L) and elevated plasma MMA concentrations (> 0.32 micromol/L), were found in 23.8% of subjects; 25.7% of subjects were not cobalamin deficient (plasma cobalamin > or = 260 pmol/L and plasma MMA < or = 0.32 micromol/L).
      Six subjects (5.8%), including 1 with mild cobalamin deficiency, had dietary cobalamin intakes below the Dutch recommended dietary intake of 2.5 microg/d.
      Mildly cobalamin-deficient subjects had lower total (diet plus supplements) cobalamin intakes (median: 4.9 microg/d; 25th and 75th percentiles: 3.9, 6.4) than did non-cobalamin-deficient subjects (median: 6.3 microg/d; 25th and 75th percentiles: 5.4, 7.9) (P = 0.0336), mainly because of less frequent use of cobalamin supplements (8% compared with 29.6%; chi2 = 3.9, P = 0.048).
      Atrophic gastritis was found in 32.4% of the total study group: mild to moderate in 19.6% and severe in 12.7%.
      The prevalence of severe atrophic gastritis, but not mild-to-moderate atrophic gastritis, was higher in mildly cobalamin-deficient subjects (25%) than in non-cobalamin-deficient subjects (3.7%) (chi2 = 4.6, P = 0.032).
      The prevalence of immunoglobulin G antibodies to H. pylori was similar in mildly cobalamin-deficient subjects (54.2%) and in non-cobalamin-deficient subjects (44.4%) (chi2 = 0.5, P = 0.5).
      Conclusions - The high prevalence of mild cobalamin deficiency in healthy, free-living, older Dutch subjects could be explained by inadequate cobalamin intake or severe atrophic gastritis in only 28% of the study population.
      Other mechanisms explaining mild cobalamin deficiency in older people must be sought.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    8. Screening for vitamin B-12 and folate deficiency in older persons
      Clarke R, Refsum H, Birks J, Evans JG, Johnston C, Sherliker P, Ueland PM, Schneede J, McPartlin J, Nexo E, Scott JM, Clinical Trial Service Unit, University of Oxford, Oxford, United Kingdom.
      robert.clarke@ctsu.ox.ac.uk - Am J Clin Nutr. 2003 May;77(5):1241-7 - PMID: 12716678
      Background - Vitamin B-12 deficiency is usually accompanied by elevated concentrations of serum total homocysteine (tHcy) and methylmalonic acid (MMA).
      Folate deficiency also results in elevated tHcy.
      Measurement of these metabolites can be used to screen for functional vitamin B-12 or folate deficiency.
      Objective - We assessed the prevalence of vitamin B-12 and folate deficiency in a population-based study (n = 1562) of older persons living in Oxford City, United Kingdom.
      Design - We postulated that, as vitamin B-12 or folate concentrations declined from adequate to impaired levels, tHcy (or MMA) concentrations would increase.
      Individuals were classified as being at high risk of vitamin B-12 deficiency if they had low vitamin B-12 (< 150 pmol/L) or borderline vitamin B-12 (150-200 pmol/L) accompanied by elevated MMA (> 0.35 micromol/L) or tHcy (> 15.0 micromol/L).
      Individuals were classified as being at high risk of folate deficiency if they had low folate (< 5 nmol/L) or borderline folate (5-7 nmol/L) accompanied by elevated tHcy (> 15 micromol/L).
      Results - Cutoffs of 15.0 micro mol/L for tHcy and 0.35 micro mol/L for MMA identified persons with normal or elevated concentrations.
      Among persons aged 65-74 and >or= 75 y, respectively, approximately 10% and 20% were at high risk of vitamin B-12 deficiency.
      About 10% and 20%, respectively, were also at high risk of folate deficiency.
      About 10% of persons with vitamin B-12 deficiency also had folate deficiency.
      Conclusion - Use of tHcy or MMA among older persons with borderline vitamin concentrations may identify those at high risk of vitamin B-12 deficiency who should be considered for treatment.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=12716678&ordinalpos=6&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    9. Sensitivity of serum methylmalonic acid and total homocysteine determinations for diagnosing cobalamin and folate deficiencies
      Savage DG, Lindenbaum J, Stabler SP, Allen RH, Department of Medicine, Columbia University, College of Physicians and Sugeons, Columbia-Presbyterian Medical Center, New York, New York 10032 - Am J Med. 1994 Mar;96(3):239-46 - PMID: 8154512
      Purpose - Patients with cobalamin (vitamin B12) deficiency usually lack many of the classic features of severe megaloblastic anemia; because of the low diagnostic specificity of decreased serum cobalamin levels, demonstrating the deficiency unequivocally is often difficult.
      We examined the sensitivity of measuring serum concentrations of methylmalonic acid and total homocysteine for diagnosing patients with clear-cut cobalamin deficiency and compared the results with those of patients with clear-cut folate deficiency.
      Patienst and methods - Serum metabolites were measured for all patients seen from 1982 to 1989 at two university hospitals who met the criteria for cobalamin and folate deficiency states and for such patients seen from 1968 to 1981 from whom stored sera were available.
      In all, 406 patients had 434 episodes of cobalamin deficiency and 119 patients had 123 episodes of folate deficiency.
      Criteria for deficiency states included serum vitamin levels, hematologic and neurologic findings and responses to therapy.
      Responses were documented in 97% of cobalamin-deficient patients and 76% of folate-deficient patients.
      Metabolite levels were measured by modified techniques using capillary-gas chromatography and mass spectrometry.
      Results - Most of the cobalamin-deficient patients had underlying pernicious anemia; two thirds were blacks or Latinos.
      Hematocrits were normal in 28% and mean cell volumes in 17%. Of the 434 episodes of cobalamin deficiency, 98.4% of serum methylmalonic acid levels and 95.9% of serum homocysteine levels were elevated (greater than 3 standard deviations above the mean in normal subjects).
      Only one patient had normal levels of both metabolites.
      Serum homocysteine levels were increased in 91% of the 123 episodes of folate deficiency.
      Methylmalonic acid was elevated in 12.2% of the folate-deficient patients; in all but one, the elevation was attributable to renal insufficiency or hypovolemia.
      Conclusions - For the cobalamin-deficient patients, measuring serum metabolite concentrations proved to be a highly sensitive test of deficiency.
      We conclude that normal levels of both methylmalonic acid and total homocysteine rule out clinically significant cobalamin deficiency with virtual certainty.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    10. Short-term variability of plasma homocysteine measurement
      Garg UC, Zheng J, Folsom AR et al. - Clin Chem. 1997;43: 141-145
      Cfr. :
      http://www.clinchem.org/cgi/reprint/43/1/141.pdf

    11. Signs of impaired cognitive function in adolescents with marginal cobalamin status
      Louwman MW, van Dusseldorp M, van de Vijver FJ, Thomas CM, Schneede J, Ueland PM, Refsum H, van Staveren WA, Division of Human Nutrition and Epidemiology, Wageningen Agricultural University, Netherlands - Am J Clin Nutr. 2000 Sep;72(3):762-9 - PMID: 10966896
      Background - Lack of cobalamin may lead to neurologic disorders, which have been reported in strict vegetarians.
      Objective - The objective of this study was to investigate whether cognitive functioning is affected in adolescents (aged 10-16 y) with marginal cobalamin status as a result of being fed a macrobiotic diet up to an average age of 6 y.
      Design - Data on dietary intake, psychological test performance and biochemical variables of cobalamin status were collected from 48 adolescents who consumed macrobiotic (vegan type) diets up to the age of 6 y, subsequently followed by lactovegetarian or omnivorous diets and from 24 subjects (aged 10-18 y) who were fed omnivorous diets from birth onward.
      Thirty-one subjects from the previously macrobiotic group were cobalamin deficient according to their plasma methylmalonic acid concentrations.
      Seventeen previously macrobiotic subjects and all control subjects had normal cobalamin status.
      Results - The control subjects performed better on most psychological tests than did macrobiotic subjects with low or normal cobalamin status.
      A significant relation between test score and cobalamin deficiency (P: = 0.01) was observed for a test measuring fluid intelligence (correlation coefficient: -0.28; 95% CI: -0.48, -0.08).
      This effect became more pronounced (P: = 0.003) within the subgroup of macrobiotic subjects (correlation coefficient: -0.38; 95% CI: -0.62, - 0.14).
      Conclusions - Our data suggest that cobalamin deficiency, in the absence of hematologic signs, may lead to impaired cognitive performance in adolescents.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    12. Studies on a radioassay for intrinsic factor antibody - Comparison of methods and false positive results due to elevated serum B12 levels
      Muckerheide MM, Wolfman JA, Rohde DA, McManamy GE - Am J Clin Pathol. 1984 Sep;82(3):300-4 - PMID: 6465096
      Availability of a kit method (Corning Immo Phase IFAB) for intrinsic factor antibody (IFAB) has made it possible for a routine radioimmunoassay (RIA) laboratory to test for the antibody, thereby providing another aid in diagnosing pernicious anemia.
      Comparison of data from a charcoal method with the kit method was favorable, each method detecting 35 (74%) positives and 12 (26%) negatives of 47 pernicious anemia patients.
      Compared with a charcoal method study the kit method had fewer false positives due to elevated serum B12.
      False positive results occurred for only 24 hours after a 1-mg injection of B12 and results remained negative the following seven days.
      The authors' studies supported the manufacturer's statement that results are unreliable when the serum B12 level exceeds 3,500 pg/ml.
      Clinical experience with the Corning Immo Phase IFAB test and false positive results is summarized.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=6465096&cmd=showdetailview&indexed=google

    13. The importance of hyperhomocysteinemia as a risk factor for diseases - An overview
      Herrmann W, Department of Clinical Chemistry/Central Laboratory, University Hospital of the Saarland, Homburg/Saar, Germany :
      kchwher@med-rz.uni-sb.de - Clin Chem Lab Med. 2001 Aug;39(8):666-74 - PMID: 11592431
      Hyperhomocysteinemia is the result of a disturbed methionine metabolism.
      It results from enzyme and/or vitamin deficiency.
      Epidemiological studies have proven, that hyperhomocysteinemia is a risk factor for atherosclerotic cardiovascular diseases, stroke, peripheral arterial occlusive disease and venous thrombosis.
      Conflicting results come from prospective studies.
      Trials which are now in progress may clarify the "causality" of high homocysteine concentrations and will assess the value of homocysteine-lowering therapy.
      The induction of the atherogenic process by hyperhomocysteinemia seems to be associated with an alteration of endothelial and smooth muscle cell function leading to an accelerated formation of reactive oxygen species.
      An increased endothelial expression of adhesion molecules will then lead to an enhanced deposition of oxidized LDL in the vessel wall with the formation of foam cells.
      Additionally, hyperhomocysteinemia interferes with the coagulation system and thus also has prothrombotic effects.
      There is a high prevalence of hyperhomocysteinemia as a sign of a vitamin deficiency in elderly subjects which strongly increases with age.
      Elderly people have a high frequency of vitamin B12 deficiency which can be diagnosed more reliably by the measurement of serum methylmalonic acid (MMA) level than by serum vitamin B12.
      Subjects following a strict vegetarian diet also have a high prevalence of hyperhomocysteinemia caused by functional vitamin B12 deficiency (increased MMA level).
      Last but not least, hyperhomocysteinemia is a factor in the pathogenesis of neural tube defects and pre-eclampsia.
      An early diagnosis of vitamin B12 deficiency is important for the prevention of neurological damages.
      Homocysteine should be measured in patients with a history of atherothrombotic vessel diseases, in patients with diabetes or hyperlipidemia, in renal patients, in obese subjects, in elderly people, in postmenopausal women and in early pregnancy.
      A specific diagnosis of an underlying vitamin deficiency is important for adequate treatment.
      Individuals with homocysteine level >12 micromol/l should increase and/or supplement their dietary intake of vitamins.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=11592431&cmd=showdetailview&indexed=google

    14. The kidney in vitamin B12 and folate homeostasis: characterization of receptors for tubular uptake of vitamins and carrier proteins
      Birn H, Department of Cell Biology, Institute of Anatomy, University of Aarhus, Bldg. 234, DK-8000 Aarhus C, Denmark :
      hb@ana.au.dk - Am J Physiol Renal Physiol. 2006 Jul;291(1):F22-36 - PMID: 16760376
      Over the past 10 years, animal studies have uncovered the molecular mechanisms for the renal tubular recovery of filtered vitamin and vitamin carrier proteins.
      Relatively few endocytic receptors are responsible for the proximal tubule uptake of a number of different vitamins, preventing urinary losses.
      In addition to vitamin conservation, tubular uptake by endocytosis is important to vitamin metabolism and homeostasis.
      The present review focuses on the receptors involved in renal tubular recovery of folate, vitamin B12 and their carrier proteins.
      The multiligand receptor megalin is important for the uptake and tubular accumulation of vitamin B12.
      During vitamin load, the kidney accumulates large amounts of free vitamin B12, suggesting a possible storage function.
      In addition, vitamin B12 is metabolized in the kidney, suggesting a role in vitamin homeostasis.
      The folate receptor is important for the conservation of folate, mediating endocytosis of the vitamin.
      Interaction between the structurally closely related, soluble folate-binding protein and megalin suggests that megalin plays an additional role in the uptake of folate bound to filtered folate-binding protein.
      A third endocytic receptor, the intrinsic factor-B12 receptor cubilin-amnionless complex, is essential to the renal tubular uptake of albumin, a carrier of folate.
      In conclusion, uptake is mediated by interaction with specific endocytic receptors also involved in the renal uptake of other vitamins and vitamin carriers.
      Little is known about the mechanisms regulating intracellular transport and release of vitamins and whereas tubular uptake is a constitutive process, this may be regulated, e.g., by vitamin status.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    15. The marker of cobalamin deficiency, plasma methylmalonic acid, correlates to plasma creatinine
      Hvas AM, Juul S, Gerdes LU, NexÝ E, Department of Haematology, AAS, Aarhus University Hospital, Aarhus, Denmark :
      Anne_Mette.Hvas@aas.auh.dk - J Intern Med. 2000 Apr;247(4):507-12 - PMID: 10792566
      Objective - To examine the relationship between the two diagnostic tests, plasma methylmalonic acid and plasma cobalamins and their association with plasma creatinine, age and sex.
      Design - Cross-sectional study of simultaneous laboratory measurements.
      Setting - County of Aarhus, Denmark.
      Subjects - Records on 1689 patients who had their first plasma methylmalonic acid measurement during 1995 and 1996 and who had a simultaneous measurement of plasma cobalamins.
      Plasma creatinine values measured within a week of measurements of plasma methylmalonic acid and plasma cobalamins were available for 1255 of the patients.
      Main outcome measures - Predictors of variation in plasma methylmalonic acid; plasma cobalamins, plasma creatinine, age and sex.
      Results - Plasma methylmalonic acid was positively correlated with plasma creatinine, even for plasma creatinine within the normal range.
      These associations remained in a multiple regression analysis.
      For plasma cobalamins below 200 pmol L-1, there was a strong negative correlation between plasma methylmalonic acid and plasma cobalamins, whilst the association was weak for higher plasma cobalamin levels.
      Plasma methylmalonic acid increased and plasma cobalamins decreased with age.
      Conclusions - The strong correlation between plasma methylmalonic acid and plasma creatinine suggests that plasma creatinine - also within the normal range - must be taken into consideration when interpreting plasma methylmalonic acid.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    16. The The Massachusetts General Hospital Handbook of Neurology
      Alice W Flaherty, Natalia S Rost - Lippincott Williams & Wilkins (2 edition), April 1, 2007 Ė ISBN-10 : 0781751373 / ISBN-13 : 978-0781751377
      Now in its revised, updated Second Edition, this pocket-sized handbook is a practical quick-reference guide to the diagnosis and management of neurologic diseases.
      It presents specific management recommendations in a succinct outline format and includes protocols, step-by-step tests and procedures, and treatment algorithms.
      This handbook is unique in its inclusion of material from related disciplines such as general medicine, cardiology, psychiatry, neurosurgery, neuroanatomy and radiology.
      The authors offer guidance in using contemporary neuroimaging techniques in diagnosis.
      Cfr. :
      http://www.amazon.com/Massachusetts-General-Hospital-Handbook-Neurology/dp/0781751373/ref=pd_sim_b_title_1

    17. Total homocysteine and its predictors in Dutch children
      van Beynum IM, den Heijer M, Thomas CM, Afman L, Oppenraay-van Emmerzaal D, Blom HJ, Department of Pediatrics, Radboud University Nijmegen Medical Centre, Nijmegen, Netherlands :
      i.vanbeynum@cukz.umcn.nl - Am J Clin Nutr. 2005 May;81(5):1110-6 - PMID: 15883436
      Background - Vitamin status, methylenentetrahydrofolate reductase (MTHFR) genotype, age, sex and lifestyle factors are all predictors of total homocysteine (tHcy) concentrations in adults.
      Limited data are available about the influence of these factors on tHcy in children.
      Objective - The objective was to describe tHcy and its predictors in Dutch children.
      Design - A sample of 234 white children aged 0-19 y was analyzed cross-sectionally.
      Results - The geometric mean tHcy concentrations were 5.1 (95% CI: 4.6, 5.6), 4.6 (4.2, 5.1), 6.2 (5.6, 6.9), 7.3 (6.7, 8.0) and 8.7 (7.9, 9.6) micromol/L in the 0-1, 2-5, 6-10, 11-14, and 15-19 y groups, respectively.
      Plasma folate and vitamin B-12 concentrations decreased markedly with age.
      The inverse association between tHcy and plasma folate seen at all ages was stronger than that between tHcy and plasma vitamin B-12.
      A negative association of plasma folate with tHcy was confined to folate concentrations <20 nmol/L.
      Homozygosity for the MTHFR 677C-->T polymorphism was identified in 8.2% of the children.
      The homocysteine concentration did not differ significantly between the MTHFR genotypes.
      Conclusions - This study provided age-specific data regarding tHcy concentrations and their predictors in the whole range of childhood.
      The tHcy concentration increased as a function of age in both sexes.
      Plasma folate was a concentration-dependent predictor of tHcy.
      The MTHFR 677C-->T polymorphism played a minor role in determining tHcy concentrations in children.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    18. Transcobalamin II 775G>C polymorphism and indices of vitamin B12 status in healthy older adults
      Miller JW, Ramos MI, Garrod MG, Flynn MA, Green R, Department of Medical Pathology, School of Medicine, University of California, Davis, CA 95817, USA :
      jwmiller@ucdavis.edu - Blood. 2002 Jul 15;100(2):718-20 - PMID: 12091374 (erratum in : Blood 2002 Nov 15;100(10):3483)
      A common polymorphism (775G>C) in the vitamin B12 transport protein, transcobalamin II (TCII), has been identified in which proline replaces arginine at codon 259.
      We determined the influence of TCII genotype on indices of B12 status, including total serum B12, the amount of B12 bound to TCII (holoTCII), methylmalonic acid and homocysteine, in 128 healthy older adults (ages 40-88 years).
      Mean total B12 and homocysteine concentrations were not significantly different among the 3 genotypes.
      Mean holoTCII concentration was significantly higher in those subjects homozygous for the proline form of TCII (PP) compared with those homozygous for the arginine form (RR) and heterozygotes (PR) (P <or=.006).
      In addition, mean methylmalonic acid concentrations were significantly lower in the PP and PR groups compared with the RR group (P <or=.02).
      The PP genotype may be more efficient in delivering B12 to tissues, resulting in enhanced B12 functional status.
      TCII genotype may thus influence susceptibility to B12 deficiency.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez


    Lees verder Deel V

    17-12-2007 om 22:31 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 0/5 - (0 Stemmen)
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Vitamine B12 en de relatie met CVS/FM - Deel V
    Klik op de afbeelding om de link te volgen  





    Vitamine B12 en de relatie met CVS/FM

    Deel V

    1. Treatment of depression - Time to consider folic acid and vitamin B12
      Coppen A, Bolander-Gouaille C, MRC Neuropsychiatric Research Laboratory, Epsom, Surrey, UK :
      acoppen@globalnet.co.uk - J Psychopharmacol. 2005 Jan;19(1):59-65 - PMID: 15671130
      We review the findings in major depression of a low plasma and particularly red cell folate, but also of low vitamin B12 status.
      Both low folate and low vitamin B12 status have been found in studies of depressive patients and an association between depression and low levels of the two vitamins is found in studies of the general population.
      Low plasma or serum folate has also been found in patients with recurrent mood disorders treated by lithium.
      A link between depression and low folate has similarly been found in patients with alcoholism.
      It is interesting to note that Hong Kong and Taiwan populations with traditional Chinese diets (rich in folate), including patients with major depression, have high serum folate concentrations.
      However, these countries have very low life time rates of major depression.
      Low folate levels are furthermore linked to a poor response to antidepressants and treatment with folic acid is shown to improve response to antidepressants.
      A recent study also suggests that high vitamin B12 status may be associated with better treatment outcome.
      Folate and vitamin B12 are major determinants of one-carbon metabolism, in which S-adenosylmethionine (SAM) is formed.
      SAM donates methyl groups that are crucial for neurological function.
      Increased plasma homocysteine is a functional marker of both folate and vitamin B12 deficiency.
      Increased homocysteine levels are found in depressive patients.
      In a large population study from Norway increased plasma homocysteine was associated with increased risk of depression but not anxiety.
      There is now substantial evidence of a common decrease in serum/red blood cell folate, serum vitamin B12 and an increase in plasma homocysteine in depression.
      Furthermore, the MTHFR C677T polymorphism that impairs the homocysteine metabolism is shown to be overrepresented among depressive patients, which strengthens the association.
      On the basis of current data, we suggest that oral doses of both folic acid (800 microg daily) and vitamin B12 (1 mg daily) should be tried to improve treatment outcome in depression.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    2. Unreliability of current assays to detect cobalamin deficiency : "nothing gold can stay"
      Ralph Green - Blood 2005 105: 910-911
      Cfr. :
      -
      http://home.hetnet.nl/~hindrikdejong/Solomon-blood-2005-inl.pdf
      -
      http://www.direct.bl.uk/bld/PlaceOrder.do?UIN=163026534&ETOC=RN&from=searchengine

    3. Update on cobalamin, folate and homocysteine
      Carmel R, Green R, Rosenblatt DS, Watkins D, New York Methodist Hospital, Brooklyn, NY 11215, USA - Hematology Am Soc Hematol Educ Program. 2003;:62-81 -PMID: 14633777
      Three topics affecting cobalamin, folate and homocysteine that have generated interest, activity and advances in recent years are discussed.
      These are :
      (I). the application of an expanded variey of tools to the diagnosis of cobalamin deficiency and how these affect and are affected by our current understanding of deficiency;
      (II). the nature of the interaction between homocysteine and vascular disease and how the relationship is affected by vitamins; and
      (III). the improved understanding of relevant genetic disorders and common genetic polymorphisms and how these interact with environmental influences.
      The diagnostic approach to cobalamin deficiency now allows better diagnosis of difficult and atypical cases and more confident rejection of the diagnosis when deficiency does not exist.
      However, the process has also become a complex and sometimes vexing undertaking.
      Part of the difficulty derives from the lack of a diagnostic gold standard among the many available tests, part from the overwhelming numerical preponderance of patients with subclinical deficiency (in which isolated biochemical findings exist without clinical signs or symptoms) among the cobalamin deficiency states and part from the decreased availability of reliable tests to identify the causes of a patient's cobalamin deficiency and thus a growing deemphasis of that important part of the diagnostic process.
      In Section I, Dr. Carmel discusses the tests, the diagnostic issues and possible approaches to the clinical evaluation.
      It is suggested no single algorithm fits all cases, some of which require more biochemical proof than others and that differentiating between subclinical and clinical deficiency, despite their overlap, may be a helpful and practical point of departure in the evaluation of patients encountered in clinical practice.
      The arguments for and against a suggested expansion of the cobalamin reference range are also weighed.
      The epidemiologic data suggest that homocysteine elevation is a risk factor for vascular and thrombotic disease.
      In Section II, Dr. Green notes that the interactions of metabolism and clinical risk are not well understood and a causative relationship remains unproven despite new reports that lowering homocysteine levels may reduce vascular complications.
      Genetic and acquired influences may interact in important ways that are still being sorted out.
      The use of vitamins, especially folate, often reduces homocysteine levels but also carries potential disadvantages and even risks.
      Folate fortification of the diet and supplement use have also markedly reduced the frequency of folate deficiency and cobalamin deficiency is now the more common deficiency state, especially among the elderly.
      Although genetic disorders are rare, they illuminate important metabolic mechanisms and pose diagnostic challenges, especially when clinical presentation occurs later in life.
      In Section III, Drs. Rosenblatt and Watkins use selected disorders to illustrate the subject. Imerslund-Gršsbeck syndrome, a hereditary disorder of cobalamin absorption at the ileal level, demonstrates genetic heterogeneity.
      Finnish patients show mutation of the gene for cubilin, the multiligand receptor for intrinsic factor.
      Surprisingly, Norwegian and other patients have been found recently to have mutations of the AMN (amnionless) gene, mutations that are lethal in mice at the embryonic stage.
      Two disorders of cobalamin metabolism, cblG and cblE, are now known to arise from mutations of the methionine synthase and methionine synthase reductase genes, respectively.
      These disorders feature megaloblastic anemia and neurologic manifestations.
      The folate disorder selected for illustration, methylenetetrahydrofolate reductase (MTHFR) deficiency, paradoxically causes neurological problems but no megaloblastic anemia.
      This rare deficiency is the most common inborn error of folate metabolism.
      It is distinct from the very common MTHFR gene polymorphisms, mutations that cause mild to moderate reductions in MTHFR activity but no direct clinical manifestations.
      The MTHFR polymTHFR polymorphisms, especially the 677C-->T mutation, may contribute to vascular and birth defect risks, while reducing the risk of certain malignancies, such as colon cancer.
      These polymorphisms and those of genes for other enzymes and proteins related to cobalamin, folate and homocysteine metabolism may be important role players in frequent interactions between genes and the environment.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=14633777&ordinalpos=1&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    4. Visual failure caused by vitamin B12 deficiency optic neuropathy
      Larner AJ, Walton Centre for Neurology and Neurosurgery, Lower Lane, Fazakerley, Liverpool, UK :
      a.larner@thewaltoncentre.nhs.uk - Int J Clin Pract. 2004 Oct;58(10):977-8 - PMID: 15587778
      Optic neuropathy is a rare but recognised complication of vitamin B12 deficiency, which may proceed to visual failure if not diagnosed early enough.
      Clues to the possible diagnosis include a history of, or risk factors for, pernicious anaemia or previous resective gastrointestinal surgery.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    5. Vitamin B-12 Mystery Is Solved - Enzyme structure reveals that one vitamin is cannibalized to make another
      Celia Arnaud - Chemical & Engineering News - ISSN 0009-2347 - © 2007 American Chemical Society
      Cfr. :
      http://pubs.acs.org/cen/news/85/i13/8513notw1.html

    6. Vitamin B12 & Cophins
      University of New England, Biddeford, ME - July 1-6, 2007 Ė Chair :
      Wilfred A. Van Der Donk - Vice Chair : Bernhard Kraeutler

      Cfr. :
      https://www.grc.org/programs.aspx?year=2007&program=vitamin

    7. Vitamin B12 and folate serum levels in newly admitted psychiatric patients
      Lerner V, Kanevsky M, Dwolatzky T, Rouach T, Kamin R, Miodownik C, Division of Psychiatry, Ministry of Health Mental Health Center, Faculty of Health Sciences Ben-Gurion University of the Negev, Be'er-Sheva, Israel :
      lernervld@yahoo.com - Clin Nutr. 2006 Feb;25(1):60-7. Epub 2005 Oct 10 - PMID: 16216392
      Background & aims - Deficiencies of cobalamin and folate may play a causal role in the development or exacerbation of psychiatric illnesses.
      We compared cobalamin and folate levels in newly admitted psychiatric patients to mentally healthy controls and assessed their correlation with various psychiatric conditions.
      Methods - All patients consecutively admitted to a psychiatric hospital were examined for serum cobalamin and folate levels.
      Controls were obtained from a population with no known mental illness.
      Values were considered to be below normal if cobalamin was <223 pg/ml and folate <3.1 ng/ml.
      Results - The 224 newly admitted patients did not differ significantly from controls, both with regard to the mean cobalamin level and to the prevalence of lower than normal levels.
      About 30% of patients had low folate values compared to 2.5% in the control group (P<0.0001).
      Mean folate level in controls was significantly higher than in patients (P<0.0001), where a positive correlation was found between low folate levels and depression.
      Conclusions - The results of our study suggest that folate levels be assessed in patients admitted to psychiatric wards, especially in those with depression.
      Further study is needed to evaluate the role of folate and cobalamin in psychiatric illness.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16216392&ordinalpos=1&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    8. Vitamin B12 and its relationship to age of onset of multiple sclerosis
      Sandyk R, Awerbuch GI, NeuroCommunication Research Laboratories, Danbury, CT 06811 - Int J Neurosci. 1993 Jul-Aug;71(1-4):93-9 - PMID: 8407160
      Attention has been focused recently on the association between vitamin B12 metabolism and the pathogenesis of multiple sclerosis (MS).
      Several recent reports have documented vitamin B12 deficiency in patients with MS.
      The etiology of this deficiency in MS is unknown.
      The majority of these patients do not have pernicious anemia and serum levels of the vitamin are unrelated to the course or chronicity of the disease.
      Moreover, vitamin B12 does not reverse the associated macrocytic anemia nor are the neurological deficits of MS improved following supplementation with vitamin B12.
      It has been suggested that vitamin B12 deficiency may render the patient more vulnerable to the putative viral and/or immunologic mechanisms widely suspected in MS.
      In the present communication, we report that serum vitamin B12 levels in MS patients are related to the age of onset of the disease.
      Specifically, we found in 45 MS patients that vitamin B12 levels were significantly lower in those who experienced the onset of first neurological symptoms prior to age 18 years (N = 10) compared to patients in whom the disease first manifested after age 18 (N = 35).
      In contrast, serum folate levels were unrelated to age of onset of the disease.
      As vitamin B12 levels were statistically unrelated to chronicity of illness, these findings suggest a specific association between the timing of onset of first neurological symptoms of MS and vitamin B12 metabolism.
      In addition, since vitamin B12 is required for the formation of myelin and for immune mechanisms, we propose that its deficiency in MS is of critical pathogenetic significance.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    9. Vitamin B12 could be a "master key" in the regulation of multiple pathological processes
      Volkov I, Press Y, Rudoy I, Department of Family Medicine, Faculty of Health Sciences, Ben-Gurion University of the Negev, Israel :
      r0019@zahav.net.il - J Nippon Med Sch. 2006 Apr;73(2):65-9 - PMID: 16641529
      Multifunctional systems must maintain homeostasis.
      Man is an ideal example of a system that constantly aspires to attain optimal regulation, even under the stress of severe disease.
      We assume that there are universal, interchangeable (as required) biologically active substances that regulate the system and try to keep it in balance.
      We propose that one of these substances is vitamin B12.
      Why vitamin B12? The list of organs and body systems in which vitamin B12 plays a functional role is constantly being added to.
      Vitamin B12 affects the normal growth of children, the peripheral and central nervous systems, bone marrow, skin, mucous membranes, bones and vessels.
      It is possible that even when the serum cobalamin level is normal, treatment with vitamin B12 could correct defects caused by other biologically active substances.
      We call this phenomenon the "Master Key" effect.
      We suggest that this "Master Key" concept can be tested by treating diseases, such as recurrent stomatitis, various forms of hyperpigmentation, trophic ulcers and burns, with vitamin B12, even if the B12 serum level is normal.
      MeSH Terms :
      -
      Animals
      -
      Avitaminosis/complications
      -
      Cardiovascular Diseases/prevention & control
      -
      Dogs
      -
      Growth/physiology
      -
      Humans
      -
      Infant
      -
      Male
      -
      Nervous System Diseases/drug therapy
      -
      Skin Diseases/etiology
      -
      Vitamin B 12/physiology*
      -
      Vitamin B 12/therapeutic use
      Substances :
      -
      Vitamin B 12
      Cfr. : http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=16641529&dopt=Citation

    10. Vitamin B12 deficiency - Is it underestimated in pregnant women ?
      Glew RH, McCarthy DM, VanderJagt DJ, Department of Biochemistry and Molecular Biology, University of New Mexico Health Sciences Center, Albuquerque, NM, USA - Acta Obstet Gynecol Scand. 2006;85(2):241-2 - PMID: 16532922
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    11. Vitamin B12 deficiency (C. Robert)
      Robert C. OH, CPT, MC, USA, U.S. Army Health Clinic, Darmstadt, Germany & David L. Brown, MAJ, MC, USA, Madigan Army Medical Center, Fort Lewis, Washington - Am Fam Physician 2003;67:979-86,993-4
      Cfr. :
      http://www.aafp.org/afp/20030301/979.html

    12. Vitamin B12 deficiency (Natural Health)
      Natural Health DOC
      Various degrees of Vitamin B12 deficiency begins with vague symptoms of ill health as it can take years to develop.
      It is known that Vitamin B12 absorption decreases with age and it is thought by some that Vitamin B12 absorption ceases at approximately age 60 - other facts state that 15% of adults over the age of 65 have Vitamin B12 deficiency.
      Senility and Alzheimer's symptoms have been confused with Vitamin B12 deficiency.
      It is important to note that folic acid deficiency can mimic Vitamin B12 deficiency.
      You can have serum tests for both Vitamin B12 and Folic Acid deficiencies at local laboratories with a prescription from your doctor.
      There is also a test called MMA (methylmalonic acid) which you can get information about online at : Lab Tests Online that can be used to test for Vitamin B12 deficiency.
      If you feel you have a possible Vitamin B12 or Folic Acid deficiency and you want to avoid testing, consider supplementing with the supplements listed below that best fits your needs.
      Vitamin B12 deficiency symptoms can be :
      - shortness of breath
      - sore tongue
      - jaundice (yellow skin or eyes)
      - pale lips, tongue and gums
      - appetite loss and weight loss
      - difficulty keeping balance
      - psychiatric disorders (disorientation, confusion, mental slowness, memory problems, depression, dementia)
      - numbness and hands and feet
      - arm and leg weakness
      - inadequate myelin synthesis resulting in neurological disorders
      - lack of DNA synthesis due to thymidylate deficiency
      - disrupted methyl folate recycling creating folate deficiency which can result in death of hematopoietic cells in bone marrow
      - lack of growth in children
      - anemias
      - poor muscle coordination.
      Vitamin B12 - What can lead to its deficiency
      - lack of hydrochloric acid in the stomach
      - rapid passage of half-digested food through the intestines (laxatives etc. might be the cause)
      - decreased absorptive area through congestive buildup or digestive tract removal surgeries
      - envelopment of the Vitamin B12 by fat droplets or abnormal intestinal bacteria
      - increased age
      - gastric acid-blocking agents
      - nutritional deficiencies caused by poor diet
      - malabsorption syndromes (Celiac disease, Crohn's disease)
      - gastrointestinal causes (dyspepsia, reoccurring peptic ulcers, diarrhea)
      - intestinal parasitic infections
      - chronic alcoholism.
      Some diseases that responded to vitamin B12 therapy
      - Parisian doctors tried Vitamin B12 for multiple sclerosis and reported great improvement in those patients who toke the Vitamin B12
      - South African physicians used Vitamin B12 in treating the neuritis of chronic alcoholism and diabetes mellitus with a 'dramatic response' in our 9 out of 11 cases
      - Pennsylvania doctor gave Vitamin B12 to patients with osteoarthritis and osteoporosis. Of the 33 cases of osteoarthritis, 20 patients had obtained results within a week. The two cases of osteoporosis were without symtoms by the end of the third week
      - Issue of Journal of American Medical Association reports on the use of Vitamin B12 in France for multiple sclerosis, spastic paraplegia, cerebellar atrophy, polyneuritis, Korsakoff psychosis (a disorder frequently caused by alcoholism resulting in hallucination etc.) and spinocerebellar disorders
      - A group of Ohio scientists working with a number of undernourished children at a Fresh Air Camp and Hospital gave 11 of the children Vitamin B12. Five of them responded dramatically and within a few weeks had surpassed in growth and physical efficiency well-nourished children of their own age
      - Barnett Sure of the University of Arkansas indicates that, in laboratory animals, the success of reproduction and lactation is assured by a diet containing ample Vitamin B12 and folic acid, whereas control animals on the same diet, minus these two B vitamins, could not bear litter successfully of nurse their young.
      Cfr. :
      http://healthy-information.naturalhealthdoc.net/NUTRITIONAL-HEALTH-INFORMATION/Vitamin-B12-Information/Vitamin-B12-Deficiency.htm

    13. Vitamin B12 deficiency can mimic multiple sclerosis - Report of two cases 
      Iwona Kurkowska-Jastrzebska, Wojciech Wicha, Anna Czlonkowska Case Rep Clin Pract Rev, 2006; 7: 64-68
      Cfr. :
      http://journals.indexcopernicus.com/fulltxt.php?ICID=449522

    14. Vitamin B12 deficiency in children and adolescents
      Sonja A. Rasmussen, MD, MS, Paul M. Fernhoff, MD, and Kelley S. Scanlon, PhD, RD - J Pediatr 2001;138:10-7
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    15. Vitamin B12 deficiency in dementia and cognitive impairment - The effects of treatment on neuropsychological function
      Rebecca Eastley, Gordon K. Wilcock, Romola S. Bucks - International Journal of Geriatric Psychiatry Volume 15, Issue 3, Date: March 2000, Pages: 226-233
      Cfr. :
      http://www3.interscience.wiley.com/cgi-bin/abstract/70500054/ABSTRACT

    16. Vitamin B12 in low back pain - A randomised, double-blind, placebo-controlled study
      Mauro GL, Martorana U, Cataldo P, Brancato G, Letizia G, Clinica Ortopedica e Traumatologica con Fisioterapia e Medicina dello Sport, Universitŗ degli Studi di Palermo, Italy - Eur Rev Med Pharmacol Sci. 2000 May-Jun;4(3):53-8 - PMID: 11558625
      Objectives - The objective of this double-blind randomised, placebo-controlled study was to examine the efficacy and safety intramuscular vitamin B12 (Tricortin 1000) in the treatment of low back pain in patients with mechanical or irritative lumbago.
      Methods - 60 patients aged between 18 and 65 years with lumbago or sciatic neuritis of mechanical origin without need for surgical procedures were enrolled.
      Patients had to present with a proven medical history for back pain (lasting from 6 months to 5 years) and a pain intensity [as evaluated with a Visual Analogic Scale (VAS)] equal or greater than 60 mm.
      Efficacy primary end-point was evaluated by means of a visual analogic scale (VAS) and a Disability Questionnaire (DQ).
      Consumption of paracetamol during the study period was the secondary efficacy end-point.
      Results - Both treatment groups experienced a sharp decrease in pain and disability.
      However, comparison between groups at the end of the treatment period showed a statistically significant difference in favour of the active treatment both for VAS and DQ (p < 0.0001 and p < 0.0002, respectively).
      Consumption of paracetamol proved significantly higher in the placebo group than in the active treatment (p < 0.0001).
      Conclusions - The efficacy and safety of parenteral Vitamin B12 in alleviating low back pain and related disability and in decreasing the consumption of paracetamol was confirmed in patients with no signs of nutritional deficiency.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    17. Vitamin B12 metabolism and massive-dose methyl vitamin B12 therapy in Japanese patients with multiple sclerosis
      Kira J, Tobimatsu S, Goto I Intern Med. 1994 Feb;33(2):82-6
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    18. Vitamin B12 metabolism in multiple sclerosis
      Reynolds EH, Bottiglieri T, Laundy M, Crellin RF, Kirker SG, Department of Neurology, King's College Hospital, London, England - Arch Neurol. 1992 Jun;49(6):649-52 - PMID: 1596201
      We have previously described 10 patients with multiple sclerosis (MS) and unusual vitamin B12 deficiency.
      We have therefore studied vitamin B12 metabolism in 29 consecutive cases of MS, 17 neurological controls and 31 normal subjects.
      Patients with MS had significantly lower serum vitamin B12 levels and significantly higher unsaturated R-binder capacities than neurological and normal controls and they were significantly macrocytic compared with normal controls.
      Nine patients with MS had serum vitamin B12 levels less than 147 pmol/L and, in the absence of anemia, this subgroup was significantly macrocytic and had significantly lower red blood cell folate levels than neurological and normal controls.
      Nine patients with MS had raised plasma unsaturated R-binder capacities, including three patients with very high values.
      There is a significant association between MS and disturbed vitamin B12 metabolism.
      Vitamin B12 deficiency should always be looked for in patients with MS.
      The cause of the vitamin B12 disorder and the nature of the overlap with MS deserve further investigation.
      Coexisting vitamin B12 deficiency might aggravate MS or impair recovery from MS.

      Cfr. :
      -
      http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=1596201&cmd=showdetailview&indexed=google
      -
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=1430153&ordinalpos=3&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    19. Vitamin B12, demyelination, remyelination and repair in multiple sclerosis
      Miller A, Korem M, Almog R, Galboiz Y. J Neurol Sci 2005 Jun 15;233(1-2):93-7
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15896807&ordinalpos=2&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    20. Vitamin B12, folic acid and the nervous system
      Reynolds E, Institute of Epileptology, King's College, Denmark Hill Campus, Cutcombe Road, London, SE5 6PJ, UK :
      reynolds@buckles.u-net.com - Lancet Neurol. 2006 Nov;5(11):949-60 - PMID: 17052662
      There are many reasons for reviewing the neurology of vitamin-B12 and folic-acid deficiencies together, including the intimate relation between the metabolism of the two vitamins, their morphologically indistinguishable megaloblastic anaemias and their overlapping neuropsychiatric syndromes and neuropathology, including their related inborn errors of metabolism.
      Folates and vitamin B12 have fundamental roles in CNS function at all ages, especially the methionine-synthase mediated conversion of homocysteine to methionine, which is essential for nucleotide synthesis and genomic and non-genomic methylation.
      Folic acid and vitamin B12 may have roles in the prevention of disorders of CNS development, mood disorders and dementias, including Alzheimer's disease and vascular dementia in elderly people.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17052662&ordinalpos=1&itool=
      EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

    21. Vitamin Intervention for Stroke Prevention (VISP) trial - Rationale and design
      Spence JD, Howard VJ, Chambless LE, Malinow MR, Pettigrew LC, Stampfer M, Toole JF, Robarts Research Institute, London, Ont., Canada - Neuroepidemiology. 2001 Feb;20(1):16-25 - PMID: 11174041
      Elevated plasma levels of homocyst(e)ine [H(e)] are surprisingly common and strongly associated with endothelial dysfunction and a marked increase in vascular risk.
      Treatment with a combination of folic acid, pyridoxine (vitamin B6) and cobalamin (vitamin B12) reduces plasma H(e) levels in most cases, restores endothelial function and regresses carotid plaque, but there is no evidence that such treatment will reduce clinical events.
      The Vitamin Intervention for Stroke Prevention (VISP) study is a double-masked, randomized, multicenter clinical trial designed to determine if, in addition to best medical/surgical management, high-dose folic acid, vitamin B6 and vitamin B12 supplements will reduce recurrent stroke compared to lower doses of these vitamins.
      Patients at least 35 years old with a nondisabling ischemic stroke within 120 days,and screening plasma H(e) > the 25th percentile of benchmark population data are eligible.
      Secondary endpoints are myocardial infarction or fatal coronary heart disease.
      This paper describes the design and rationale of the study.
      Cfr. :
      http://www.ncbi.nlm.nih.gov/sites/entrez

    22. Vitamin Puzzle Solved By MIT Biologists
      Biology / Biochemistry News, 27 Mar 2007
      Cfr. :
      http://www.medicalnewstoday.com/articles/65927.php

    23. World Congress on Hyperhomocysteinemia - 6th Conference on Homocysteine Metabolism - SaarbrŁcken (Duitsland), 5 -9 juni 2007
      Cfr. :
      http://homocysteine-conference.org/hyperhomocysteinemia-conference-2007.htm
       

    17-12-2007 om 22:21 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 2/5 - (1 Stemmen)
    >> Reageer (0)


    Blog als favoriet !

    Gastenboek

    Druk op onderstaande knop om een berichtje achter te laten in mijn gastenboek


    Foto

    Raadpleeg steeds je arts !
    Inhoud blog
  • Tijd om afscheid te nemen...
  • Fibromyalgie in het kort
  • Leden ME/CVS Vereniging unaniem tegen CBO-voorstel
  • Blood donation, XMRV & chronic fatigue syndrome
  • Illness duration and coping style in chronic fatigue syndrome
  • Review confirms PTSD in Gulf vets - Panel finds many reports of multisymptom illnesses
  • M.E. (cvs) - Richtlijnen voor psychiaters - Deel I
  • M.E. (cvs) - Richtlijnen voor psychiaters - Deel II
  • M.E. (cvs) - Richtlijnen voor psychiaters - Deel III
  • M.E. (cvs) - Richtlijnen voor psychiaters - Deel IV
  • M.E. (cvs) - Richtlijnen voor psychiaters - Deel V
  • M.E. (cvs) - Richtlijnen voor psychiaters - Deel VI
  • M.E. (cvs) - Richtlijnen voor psychiaters - Deel VII
  • M.E. (cvs) - Richtlijnen voor psychiaters - Deel VIII
  • M.E. (cvs) - Richtlijnen voor psychiaters - Deel IX
  • M.E. (cvs) - Richtlijnen voor psychiaters - Deel X
  • M.E. (cvs) - Richtlijnen voor psychiaters - Deel XI
  • When do symptoms become a disease ?
  • Burnout
  • Gepest ? - Zet de juiste stappen
  • Voldoet jouw werkplek aan de ARBO-normen ?
  • Chiropractie - Vrijspraak voor Simon Singh in smaadzaak
  • ME/CVS ? - Werk mee aan onderzoek naar tegemoetkoming chronisch zieken !
  • Magical Medicine - How to make a disease disappear
  • A new hypothesis of chronic fatigue syndrome - Co-conditioning theory
  • A light in the darkness - Good news ahead for XMRV ?
  • Zomertijd - Help je biologische klok
  • Beter van de bedrijfsarts
  • De invloed van economisering op het werk van artsen
  • Chronisch Vermoeidheidssyndroom (IOCOB)
  • Gezond brein, gezonde darmen
  • A retrospective review of the sleep characteristics in patients with chronic fatigue syndrome and fibromyalgia
  • Opdracht voor het volgende kabinet : afschaffing van het UWV
  • Test maakt validering pijn bij ME/CVS patienten mogelijk
  • Surprise discovery that HIV retrovirus hides in bone marrow offers new hope for eradication
  • A doctor's roadmap for dealing with the problems of ME/CFS
  • De Terug Plezant Club
  • Het retrovirus XMRV - Waar of niet waar ?
  • Being homebound with chronic fatigue syndrome - A multidimensional comparison with outpatients
  • Oplaaiende symptomen ME patient verraden ontstekingsreactie
  • UWV : 'ME/CVS is ziekte in zin van arbeidsongeschiktheid'
  • Een succesverhaal met Vistide in de strijd tegen ME/CVS - Een verhaal over herstel
  • Depressie
  • Hoe stressvol is je leven ?
  • Making the diagnosis of CFS/ME in primary care - A qualitative study
  • A new system of evaluating fibromyalgia and chronic fatigue
  • Nijmeegs onderzoek haalt CVS-doorbraak onderuit
  • Psychotherapie bij depressie overschat
  • Secrets of novel retrovirus unfolding
  • XMRV : 'missing link' bij ME/CVS ?
  • Reeves, hoofd van CDC CVS onderzoeksprogramma, gaat weg
  • Constant agony of an ME sufferer
  • Canon van de geneeskunde in Nederland
  • Dr. Frank dieet
  • Defeatism is undermining evidence that chronic fatigue syndrome can be treated
  • Cellular and molecular mechanisms of interaction between the neuroendocrine and immune systems under chronic fatigue syndrome in experiment
  • Zo zorg je voor weerstand - Houd je lichaam in optimale conditie
  • Fibromyalgie Vlaanderen Nederland - Dr. Bauer
  • Bussemaker komt terug op erkenning CVS
  • Postexertional malaise in women with chronic fatigue syndrome - Laboratioriumonderzoek bevestigt inspanningsintolerantie bij ME/CVS
  • Ze vertelden stervende dochter dat ze een leugenaar was - Interview met ME moeder Criona Wilson
  • Bijwerkingen antidepressiva erger dan gedacht
  • Bereken je BMI
  • Host range and cellular tropism of the human exogenous gammaretrovirus XMRV
  • The Brain Boosting B-12 - Hydroxocobalamin
  • Vertaling Canadese criteria ME/CVS
  • Slapeloosheid & osteopathie
  • Het Advies- en meldpunt ziekteverzuim en arbeidsongeschiktheid
  • Association between serum ferritin [stored iron] level and fibromyalgia syndrome
  • Dr. Mikovits XMRV Seminar (videos)
  • Zorgen voor een ander (2010) - Antwoorden op veelgestelde vragen
  • Herwin je veerkracht - Omgaan met chronische vermoeidheid en pijn
  • Je eten bepaalt je slaap
  • Dierenleed
  • ME/CVS erkend als chronische ziekte
  • Understanding fibromyalgia pain
  • Hyperalgesia in chronic fatigue syndrome
  • Wegwijzer psychische problemen
  • Positieve psychologie
  • Fietsen in de sneeuw...
  • Tips tegen de koude
  • Failure to detect the novel retrovirus XMRV in chronic fatigue syndrome
  • Nieuwe behandeling VermoeidheidCentrum zeer effectief
  • Een Zalig Kerstfeest en een gezond en voorspoedig 2010 !
  • Taming stressful thoughts
  • Burn-out - Werken tot je erbij neervalt - Deel I
  • Burn-out - Werken tot je erbij neervalt - Deel II
  • Canadese kriteria voor kinderen ook geschikt om onderscheid te maken tussen "milde" en "ernstige" gevallen
  • Stop met piekeren
  • Gedumpt, wat nu ? - Deel I
  • Gedumpt, wat nu ? - Deel II
  • Making a Difference in ME/CFS (Chronic Fatigue Syndrome) and FM
  • Psychotherapie - Van theorie tot praktijk
  • Fibromyalgie, waardevolle dagbesteding en werk - Deel I
  • Fibromyalgie, waardevolle dagbesteding en werk - Deel II
  • Fibromyalgie
  • Europees instrument spoort fibromyalgie op
  • Gezinsgeluk heeft positieve invloed op werk
  • Cognitieve gedragstherapie bij depressie
  • Nooit meer hetzelfde...
  • Rugklachten en RSI beroepsziekten nummer 1
  • SOS ! Hulp voor ouders
  • Dr. Nancy Klimas opens new Chronic Fatigue Center
  • The dramatic story of microbiologist Elaine DeFreitas' discovery
  • Fibromyalgie - Genezing is mogelijk - Gratis boek !
  • Verdedig je tegen wintervirussen
  • 7 geheimen die vrouwen verzwijgen
  • Eťn op de twee Belgen krijgt ooit last van reuma
  • Wie langdurig ziek wordt heeft nood aan informatie
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel I
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel II
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel III
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel IV
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel V
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel VI
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel VII
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel VIII
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel IX
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel X
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XI
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XII
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XIII
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XIV
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XV
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XVI
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XVII
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XVIII
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XIX
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XX
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XXI
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XXII
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XXIII
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XXIV
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XXV
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XXVI
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XXVII
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XXVIII
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XXIX
  • Doe een wens... - Make a wish...
  • 7 geheimen die mannen verzwijgen
  • Snel weer aan het werk - Bedrijfsartsen op bres voor arbeidsongeschikten - Deel XXX
  • Fibromyalgie - Genezing is mogelijk - GRATIS !
  • Af en toe een geheim is juist gezond
  • FM/CVS en verzekeringen - Info voor thesis
  • Mogelijke doorbraak MS-behandeling
  • Wees een winterdepressie voor
  • Vitamine B12-tekort - Een mogelijke oorzaak van Chronische vermoeidheid ? - Deel I
  • Vitamine B12-tekort - Een mogelijke oorzaak van Chronische vermoeidheid ? - Deel II
  • The Guaifenesin Story
  • A virus linked to chronic fatigue syndrome - Dr. Nancy Klimas interviews
  • Don't wait for a cure to appear
  • Gezonde chocoladeletters van Sinterklaas
  • Oorzaken van puisten
  • Sporten beter dan pauzeren bij RSI
  • Alles voor het goeie doel !!
  • Gewoon gelukkig zijn...
  • Chronic Fatigue Syndrome - La b√™te noire of the Belgian Health Care System
  • Persoonlijkheidstests
  • Vaccinatie risicogroepen H1N1
  • Geopereerd Prof. Johann Bauer - Een update (Greta)
  • Weersfactoren oorzaak van hoofdpijn
  • Infection as one possible cause of fibromyalgia - Part I
  • Infection as one possible cause of fibromyalgia - Part II
  • Infection as one possible cause of fibromyalgia - Part III
  • Infection as one possible cause of fibromyalgia - Part IV
  • Infection as one possible cause of fibromyalgia - Part V
  • Infection as one possible cause of fibromyalgia - Part VI
  • Infection as one possible cause of fibromyalgia - Part VII
  • Infection as one possible cause of fibromyalgia - Part VIII
  • Infection as one possible cause of fibromyalgia - Part IX
  • Challenges to conventional thinking about mind and body
  • What is CFS and what is ME ?
  • CVS-Referentiecentra - Opheffing en sluiting
  • Heb ik voldoende ontspanning ?
  • 7 tips tegen een overactieve blaas
  • Wallen en kringen onder de ogen
  • Recovered CFS/ME Patient Goes to Washington, D.C.
  • Chronische vermoeidheid zit niet tussen de oren
  • Dr. Bauer heeft mijn leven gered
  • Has your marriage been damaged by fibromyalgia or chronic fatigue syndrome ?
  • Vijf grootste bedreigingen gezondheid
  • Onbegrepen lage rugpijn beter te behandelen
  • Je beste antistresstip
  • Sufferers of chronic fatigue see life as a balancing act
  • Te hard gewerkt...
  • Prof. Dr. Johann Brauer op mijn blog
  • Geopereerd Prof. Johann Bauer
  • Is de griepprik gevaarlijk ?
  • Griep en verkoudheid - Deel I
  • Griep en verkoudheid - Deel II
  • Support the 500 Professionals of the IACFS/ME
  • Slanker met je hartritme
  • Enzym veroorzaakt gevolgen slaaptekort
  • Now we can get down to business
  • XMRV and chronic fatigue syndrome
  • Verslaving is een behandelbare hersenziekte
  • Kopstukken filosofie - Oktober 2009
  • Gek op je werk
  • Fikse schadevergoeding om antidepressivum
  • ME/CFS patients have retrovirus (XMRV) on YouTube

    Foto

    Archief per week
  • 12/04-18/04 2010
  • 05/04-11/04 2010
  • 29/03-04/04 2010
  • 22/03-28/03 2010
  • 15/03-21/03 2010
  • 08/03-14/03 2010
  • 01/03-07/03 2010
  • 22/02-28/02 2010
  • 15/02-21/02 2010
  • 08/02-14/02 2010
  • 01/02-07/02 2010
  • 25/01-31/01 2010
  • 18/01-24/01 2010
  • 04/01-10/01 2010
  • 28/12-03/01 2010
  • 21/12-27/12 2009
  • 14/12-20/12 2009
  • 07/12-13/12 2009
  • 30/11-06/12 2009
  • 23/11-29/11 2009
  • 16/11-22/11 2009
  • 09/11-15/11 2009
  • 02/11-08/11 2009
  • 19/10-25/10 2009
  • 12/10-18/10 2009
  • 05/10-11/10 2009
  • 28/09-04/10 2009
  • 21/09-27/09 2009
  • 14/09-20/09 2009
  • 07/09-13/09 2009
  • 31/08-06/09 2009
  • 10/08-16/08 2009
  • 27/07-02/08 2009
  • 20/07-26/07 2009
  • 06/07-12/07 2009
  • 22/06-28/06 2009
  • 15/06-21/06 2009
  • 08/06-14/06 2009
  • 01/06-07/06 2009
  • 25/05-31/05 2009
  • 18/05-24/05 2009
  • 11/05-17/05 2009
  • 04/05-10/05 2009
  • 27/04-03/05 2009
  • 20/04-26/04 2009
  • 13/04-19/04 2009
  • 30/03-05/04 2009
  • 23/03-29/03 2009
  • 16/03-22/03 2009
  • 09/03-15/03 2009
  • 02/03-08/03 2009
  • 23/02-01/03 2009
  • 16/02-22/02 2009
  • 09/02-15/02 2009
  • 02/02-08/02 2009
  • 26/01-01/02 2009
  • 19/01-25/01 2009
  • 12/01-18/01 2009
  • 05/01-11/01 2009
  • 22/12-28/12 2008
  • 15/12-21/12 2008
  • 08/12-14/12 2008
  • 01/12-07/12 2008
  • 24/11-30/11 2008
  • 17/11-23/11 2008
  • 10/11-16/11 2008
  • 03/11-09/11 2008
  • 27/10-02/11 2008
  • 20/10-26/10 2008
  • 13/10-19/10 2008
  • 06/10-12/10 2008
  • 29/09-05/10 2008
  • 22/09-28/09 2008
  • 15/09-21/09 2008
  • 08/09-14/09 2008
  • 01/09-07/09 2008
  • 25/08-31/08 2008
  • 18/08-24/08 2008
  • 11/08-17/08 2008
  • 04/08-10/08 2008
  • 28/07-03/08 2008
  • 21/07-27/07 2008
  • 14/07-20/07 2008
  • 30/06-06/07 2008
  • 23/06-29/06 2008
  • 16/06-22/06 2008
  • 09/06-15/06 2008
  • 02/06-08/06 2008
  • 26/05-01/06 2008
  • 19/05-25/05 2008
  • 12/05-18/05 2008
  • 05/05-11/05 2008
  • 28/04-04/05 2008
  • 21/04-27/04 2008
  • 14/04-20/04 2008
  • 07/04-13/04 2008
  • 31/03-06/04 2008
  • 24/03-30/03 2008
  • 17/03-23/03 2008
  • 10/03-16/03 2008
  • 03/03-09/03 2008
  • 25/02-02/03 2008
  • 18/02-24/02 2008
  • 11/02-17/02 2008
  • 04/02-10/02 2008
  • 28/01-03/02 2008
  • 21/01-27/01 2008
  • 14/01-20/01 2008
  • 07/01-13/01 2008
  • 31/12-06/01 2008
  • 24/12-30/12 2007
  • 17/12-23/12 2007
  • 10/12-16/12 2007
  • 03/12-09/12 2007
  • 26/11-02/12 2007
  • 19/11-25/11 2007
  • 12/11-18/11 2007
  • 05/11-11/11 2007
  • 29/10-04/11 2007
  • 22/10-28/10 2007
  • 15/10-21/10 2007
  • 08/10-14/10 2007
  • 01/10-07/10 2007
  • 24/09-30/09 2007
  • 17/09-23/09 2007
  • 10/09-16/09 2007
  • 03/09-09/09 2007
  • 27/08-02/09 2007
  • 20/08-26/08 2007
  • 13/08-19/08 2007
  • 06/08-12/08 2007
  • 30/07-05/08 2007
  • 23/07-29/07 2007
  • 16/07-22/07 2007
  • 09/07-15/07 2007
  • 18/06-24/06 2007
  • 11/06-17/06 2007
  • 04/06-10/06 2007
  • 28/05-03/06 2007
  • 21/05-27/05 2007
  • 14/05-20/05 2007
  • 07/05-13/05 2007
  • 30/04-06/05 2007
  • 23/04-29/04 2007
  • 16/04-22/04 2007
  • 09/04-15/04 2007
  • 02/04-08/04 2007
  • 26/03-01/04 2007
  • 19/03-25/03 2007
  • 12/03-18/03 2007
  • 05/03-11/03 2007
  • 26/02-04/03 2007
  • 19/02-25/02 2007
  • 12/02-18/02 2007
  • 05/02-11/02 2007
  • 29/01-04/02 2007
  • 22/01-28/01 2007
  • 15/01-21/01 2007
  • 08/01-14/01 2007
  • 18/12-24/12 2006
  • 11/12-17/12 2006
  • 04/12-10/12 2006
  • 27/11-03/12 2006
  • 20/11-26/11 2006
  • 13/11-19/11 2006
  • 06/11-12/11 2006
  • 30/10-05/11 2006
  • 23/10-29/10 2006
  • 16/10-22/10 2006
  • 09/10-15/10 2006
  • 02/10-08/10 2006
  • 25/09-01/10 2006
  • 18/09-24/09 2006
  • 11/09-17/09 2006
  • 04/09-10/09 2006
  • 28/08-03/09 2006
  • 07/08-13/08 2006
  • 31/07-06/08 2006
  • 24/07-30/07 2006
  • 03/07-09/07 2006
  • 26/06-02/07 2006
  • 19/06-25/06 2006
  • 12/06-18/06 2006
  • 29/05-04/06 2006
  • 22/05-28/05 2006
  • 15/05-21/05 2006
  • 08/05-14/05 2006
  • 01/05-07/05 2006
  • 24/04-30/04 2006
  • 17/04-23/04 2006
  • 10/04-16/04 2006
  • 27/03-02/04 2006
  • 20/03-26/03 2006
  • 13/03-19/03 2006
  • 06/03-12/03 2006
  • 27/02-05/03 2006
  • 20/02-26/02 2006
  • 13/02-19/02 2006
  • 06/02-12/02 2006
  • 30/01-05/02 2006
  • 23/01-29/01 2006
  • 16/01-22/01 2006
  • 09/01-15/01 2006
  • 26/12-01/01 2006
  • 19/12-25/12 2005
  • 12/12-18/12 2005
  • 05/12-11/12 2005
  • 28/11-04/12 2005
  • 21/11-27/11 2005
  • 14/11-20/11 2005
  • 07/11-13/11 2005
  • 24/10-30/10 2005
  • 17/10-23/10 2005
  • 10/10-16/10 2005
  • 03/10-09/10 2005
  • 26/09-02/10 2005
  • 19/09-25/09 2005
  • 12/09-18/09 2005
  • 05/09-11/09 2005
  • 29/08-04/09 2005
  • 22/08-28/08 2005
  • 15/08-21/08 2005
  • 08/08-14/08 2005
  • 01/08-07/08 2005
  • 25/07-31/07 2005
  • 04/07-10/07 2005
  • 27/06-03/07 2005
  • 20/06-26/06 2005
  • 13/06-19/06 2005
  • 06/06-12/06 2005
  • 30/05-05/06 2005
  • 23/05-29/05 2005
  • 16/05-22/05 2005
  • 09/05-15/05 2005
  • 02/05-08/05 2005
  • 25/04-01/05 2005
  • 18/04-24/04 2005
  • 11/04-17/04 2005
  • 29/11-05/12 1999
  • 29/12-04/01 1970

    Foto

  • 12/04-18/04 2010
  • 05/04-11/04 2010
  • 29/03-04/04 2010
  • 22/03-28/03 2010
  • 15/03-21/03 2010
  • 08/03-14/03 2010
  • 01/03-07/03 2010
  • 22/02-28/02 2010
  • 15/02-21/02 2010
  • 08/02-14/02 2010
  • 01/02-07/02 2010
  • 25/01-31/01 2010
  • 18/01-24/01 2010
  • 04/01-10/01 2010
  • 28/12-03/01 2010
  • 21/12-27/12 2009
  • 14/12-20/12 2009
  • 07/12-13/12 2009
  • 30/11-06/12 2009
  • 23/11-29/11 2009
  • 16/11-22/11 2009
  • 09/11-15/11 2009
  • 02/11-08/11 2009
  • 19/10-25/10 2009
  • 12/10-18/10 2009
  • 05/10-11/10 2009
  • 28/09-04/10 2009
  • 21/09-27/09 2009
  • 14/09-20/09 2009
  • 07/09-13/09 2009
  • 31/08-06/09 2009
  • 10/08-16/08 2009
  • 27/07-02/08 2009
  • 20/07-26/07 2009
  • 06/07-12/07 2009
  • 22/06-28/06 2009
  • 15/06-21/06 2009
  • 08/06-14/06 2009
  • 01/06-07/06 2009
  • 25/05-31/05 2009
  • 18/05-24/05 2009
  • 11/05-17/05 2009
  • 04/05-10/05 2009
  • 27/04-03/05 2009
  • 20/04-26/04 2009
  • 13/04-19/04 2009
  • 30/03-05/04 2009
  • 23/03-29/03 2009
  • 16/03-22/03 2009
  • 09/03-15/03 2009
  • 02/03-08/03 2009
  • 23/02-01/03 2009
  • 16/02-22/02 2009
  • 09/02-15/02 2009
  • 02/02-08/02 2009
  • 26/01-01/02 2009
  • 19/01-25/01 2009
  • 12/01-18/01 2009
  • 05/01-11/01 2009
  • 22/12-28/12 2008
  • 15/12-21/12 2008
  • 08/12-14/12 2008
  • 01/12-07/12 2008
  • 24/11-30/11 2008
  • 17/11-23/11 2008
  • 10/11-16/11 2008
  • 03/11-09/11 2008
  • 27/10-02/11 2008
  • 20/10-26/10 2008
  • 13/10-19/10 2008
  • 06/10-12/10 2008
  • 29/09-05/10 2008
  • 22/09-28/09 2008
  • 15/09-21/09 2008
  • 08/09-14/09 2008
  • 01/09-07/09 2008
  • 25/08-31/08 2008
  • 18/08-24/08 2008
  • 11/08-17/08 2008
  • 04/08-10/08 2008
  • 28/07-03/08 2008
  • 21/07-27/07 2008
  • 14/07-20/07 2008
  • 30/06-06/07 2008
  • 23/06-29/06 2008
  • 16/06-22/06 2008
  • 09/06-15/06 2008
  • 02/06-08/06 2008
  • 26/05-01/06 2008
  • 19/05-25/05 2008
  • 12/05-18/05 2008
  • 05/05-11/05 2008
  • 28/04-04/05 2008
  • 21/04-27/04 2008
  • 14/04-20/04 2008
  • 07/04-13/04 2008
  • 31/03-06/04 2008
  • 24/03-30/03 2008
  • 17/03-23/03 2008
  • 10/03-16/03 2008
  • 03/03-09/03 2008
  • 25/02-02/03 2008
  • 18/02-24/02 2008
  • 11/02-17/02 2008
  • 04/02-10/02 2008
  • 28/01-03/02 2008
  • 21/01-27/01 2008
  • 14/01-20/01 2008
  • 07/01-13/01 2008
  • 31/12-06/01 2008
  • 24/12-30/12 2007
  • 17/12-23/12 2007
  • 10/12-16/12 2007
  • 03/12-09/12 2007
  • 26/11-02/12 2007
  • 19/11-25/11 2007
  • 12/11-18/11 2007
  • 05/11-11/11 2007
  • 29/10-04/11 2007
  • 22/10-28/10 2007
  • 15/10-21/10 2007
  • 08/10-14/10 2007
  • 01/10-07/10 2007
  • 24/09-30/09 2007
  • 17/09-23/09 2007
  • 10/09-16/09 2007
  • 03/09-09/09 2007
  • 27/08-02/09 2007
  • 20/08-26/08 2007
  • 13/08-19/08 2007
  • 06/08-12/08 2007
  • 30/07-05/08 2007
  • 23/07-29/07 2007
  • 16/07-22/07 2007
  • 09/07-15/07 2007
  • 18/06-24/06 2007
  • 11/06-17/06 2007
  • 04/06-10/06 2007
  • 28/05-03/06 2007
  • 21/05-27/05 2007
  • 14/05-20/05 2007
  • 07/05-13/05 2007
  • 30/04-06/05 2007
  • 23/04-29/04 2007
  • 16/04-22/04 2007
  • 09/04-15/04 2007
  • 02/04-08/04 2007
  • 26/03-01/04 2007
  • 19/03-25/03 2007
  • 12/03-18/03 2007
  • 05/03-11/03 2007
  • 26/02-04/03 2007
  • 19/02-25/02 2007
  • 12/02-18/02 2007
  • 05/02-11/02 2007
  • 29/01-04/02 2007
  • 22/01-28/01 2007
  • 15/01-21/01 2007
  • 08/01-14/01 2007
  • 18/12-24/12 2006
  • 11/12-17/12 2006
  • 04/12-10/12 2006
  • 27/11-03/12 2006
  • 20/11-26/11 2006
  • 13/11-19/11 2006
  • 06/11-12/11 2006
  • 30/10-05/11 2006
  • 23/10-29/10 2006
  • 16/10-22/10 2006
  • 09/10-15/10 2006
  • 02/10-08/10 2006
  • 25/09-01/10 2006
  • 18/09-24/09 2006
  • 11/09-17/09 2006
  • 04/09-10/09 2006
  • 28/08-03/09 2006
  • 07/08-13/08 2006
  • 31/07-06/08 2006
  • 24/07-30/07 2006
  • 03/07-09/07 2006
  • 26/06-02/07 2006
  • 19/06-25/06 2006
  • 12/06-18/06 2006
  • 29/05-04/06 2006
  • 22/05-28/05 2006
  • 15/05-21/05 2006
  • 08/05-14/05 2006
  • 01/05-07/05 2006
  • 24/04-30/04 2006
  • 17/04-23/04 2006
  • 10/04-16/04 2006
  • 27/03-02/04 2006
  • 20/03-26/03 2006
  • 13/03-19/03 2006
  • 06/03-12/03 2006
  • 27/02-05/03 2006
  • 20/02-26/02 2006
  • 13/02-19/02 2006
  • 06/02-12/02 2006
  • 30/01-05/02 2006
  • 23/01-29/01 2006
  • 16/01-22/01 2006
  • 09/01-15/01 2006
  • 26/12-01/01 2006
  • 19/12-25/12 2005
  • 12/12-18/12 2005
  • 05/12-11/12 2005
  • 28/11-04/12 2005
  • 21/11-27/11 2005
  • 14/11-20/11 2005
  • 07/11-13/11 2005
  • 24/10-30/10 2005
  • 17/10-23/10 2005
  • 10/10-16/10 2005
  • 03/10-09/10 2005
  • 26/09-02/10 2005
  • 19/09-25/09 2005
  • 12/09-18/09 2005
  • 05/09-11/09 2005
  • 29/08-04/09 2005
  • 22/08-28/08 2005
  • 15/08-21/08 2005
  • 08/08-14/08 2005
  • 01/08-07/08 2005
  • 25/07-31/07 2005
  • 04/07-10/07 2005
  • 27/06-03/07 2005
  • 20/06-26/06 2005
  • 13/06-19/06 2005
  • 06/06-12/06 2005
  • 30/05-05/06 2005
  • 23/05-29/05 2005
  • 16/05-22/05 2005
  • 09/05-15/05 2005
  • 02/05-08/05 2005
  • 25/04-01/05 2005
  • 18/04-24/04 2005
  • 11/04-17/04 2005
  • 29/11-05/12 1999
  • 29/12-04/01 1970

    Foto

    Willekeurig SeniorenNet Blogs
    omaatje
    blog.seniorennet.be/omaatje
    Foto


    Blog tegen de regels? Meld het ons!
    Gratis blog op http://blog.seniorennet.be - SeniorenNet Blogs, eenvoudig, gratis en snel jouw eigen blog!