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Thrombocytopathy in Preleukaemia: Association with a Defect of Thromboxane A 2 Activity
Author(s) -
Russell N. H.,
Keenan J. P.,
Bellingham A. J.
Publication year - 1979
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.1365-2141.1979.tb05876.x
Subject(s) - platelet , adenosine diphosphate , radioimmunoassay , thromboxane a2 , arachidonic acid , thromboxane , thromboxane b2 , medicine , chemistry , endocrinology , platelet aggregation , biochemistry , enzyme
S ummary . 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. Malonyldialdehyde (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 A 2 (TxA 2 ) were very low in both patients. Production of thromboxane B 2 (TxB 2 ) assessed by thin layer chromatographic separation of the metabolites of [I‐ 14 C]AA and by radioimmunoassay, was normal. These abnormalities of platelet function appear to be due to the production of TxA 2 with a low biological activity.