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A Qualitative Platelet Defect in Severe Vitamin B12 Deficiency: Response, Hyperresponse, and Thrombosis After Vitamin B12 Therapy

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Aided by a grant from the American Medical Association Education and Research Foundation, Chicago, Illinois.

▸Requests for reprints should be addressed to Peter H. Levine, M.D., New England Medical Center Hospital, 171 Harrison Ave., Boston, MA 02111.

Boston, Massachusetts

Ann Intern Med. 1973;78(4):533-539. doi:10.7326/0003-4819-78-4-533
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Three patients with vitamin B12 deficiency had profound qualitative platelet abnormalities: lack of secondary aggregation (release reaction) with ADP stimulation, total lack of aggregation in response to standard amounts of epinephrine or collagen, and, in two patients, bleeding times of more than 20 minutes. Vitamin B12 therapy corrected all these defects. Serial studies, after vitamin B12 administration, showed increased platelet aggregation response in two of the patients, when compared with 60 healthy controls. All three developed increased platelet factor 3 availability. One patient developed evidence of arterial and venous thrombi at this time, with no thrombocytosis. A retrospective chart review suggests that thrombotic episodes during recovery from vitamin B12 deficiency are not rare. The platelet apparently is one of the cells of the body that are susceptible to metabolic abnormality in severe vitamin B12 deficiency. Platelet function may be extremely important in the pathogenesis of both hemorrhage and thrombosis.





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