Thrombocytopathy in preleukaemia: association with a defect of thromboxane A2 activity.
Platelet aggregation and the platelet prostaglandin pathway have been investigated in two patients with preleukaemic states who had a haemorrhagic tendency but a normal platelet count. In both patients platelet aggregation induced by collagen adenosine diphosphate (ADP) and arachidonic acid (AA) were abnormal. Malonyldiadehyde (MDA) production from exogenous AA was normal in both patients thus excluding cyclo-oxygenase deficiency. The platelet aggregating and rabbit aorta contracting activities of thromboxane A2 (TxA2) were very low in both patients. Production of thromboxane B2 (TxB2) assessed by thin layer chromatographic separation of the metabolites of [1(-14)C]AA and by radioimmunoassay, was normal. These abnormalities of platelet function appear to be due to the production of TxA2 with a low biological activity.
D000227:Adenine Nucleotides / Q000097:blood; D001791:Blood Platelet Disorders / Q000209:etiology*; D001792:Blood Platelets / Q000032:analysis; D005260:Female; D006801:Humans; D008297:Male; D010974:Platelet Aggregation; D011289:Preleukemia / Q000150:complications*; D013928:Thromboxane A2 / Q000502:physiology*; D013929:Thromboxane B2 / Q000097:blood; D013931:Thromboxanes / Q000502:physiology*
D000227:Adenine Nucleotides; D013931:Thromboxanes; D013929:Thromboxane B2; D013928:Thromboxane A2