Platelet dysfunction in myeloproliferative syndromes.
The most common abnormality of the platelets in 43 patients with a variety of myeloproliferative syndromes was impaired or absent aggregation when stimulated with collagen and adrenaline. Eight unselected cases studied in more detail showed a normal prostaglandin synthesis pathway as evidenced by normal aggregation with arachidonic acid and the production of normal amounts of malonyldialdehyde. Mixing experiments with aspirin-tested platelets showed correction of the abnormal adrenaline and collagen responses and confirmed that the nature of the defect was different from that induced by aspirin. Stimulation of "myeloproliferative" platelets with thrombin after blocking the prostaglandin pathway with aspirin resulted in reduced aggregation, indicating either a deficiency of the storage pool of adenine nucleotides in the platelets or an abnormality of a membrane receptor for thrombin.
D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D008315:Malondialdehyde / Q000378:metabolism; D008433:Mathematics; D009196:Myeloproliferative Disorders / Q000378:metabolism / Q000503:physiopathology*; D010974:Platelet Aggregation; D011453:Prostaglandins / Q000096:biosynthesis / Q000378:metabolism
D011453:Prostaglandins; D008315:Malondialdehyde; D001241:Aspirin