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Platelet‐Function Studies in Patients with Glucose‐6‐Phosphate Dehydrogenase Deficiency
Author(s) -
Schwartz Jack P.,
Cooperberg Arthur A.,
Rosenberg Arthur
Publication year - 1974
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1974.tb06793.x
Subject(s) - platelet , chemistry , endocrinology , pentose phosphate pathway , medicine , glucose 6 phosphate dehydrogenase deficiency , dehydrogenase , phospholipid , biochemistry , enzyme , glycolysis , membrane
S ummary . Tests of platelet function were carried out in 17 patients with glucose‐6‐phosphate dehydrogenase (G6PD) deficiency. Despite the clinical absence of defective haemostasis impaired platelet function was observed in all patients studied. This consisted of reduced platelet‐factor 3 (PF 3) availability, a reduced prothrombin‐consumption time, and/or reduced platelet retention in a glass bead column. PF3 assay of freeze‐thawed platelets demonstrated that this reduction of PF3 availability represents a true deficiency rather than defective release. Platelet aggregation with ADP, collagen and adrenaline was normal. These findings suggest that G6PD deficiency, which leads to impaired NADPH production, may cause reduced fatty‐acid and phospholipid synthesis by the platelets resulting in PF3 deficiency. The normal platelet aggregation suggests that energy derived from the hexose‐moaophospliatc shunt is not essential for this function.