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Subnormal platelet response to thromboxane A 2 in a patient with chronic myeloid leukaemia
Author(s) -
Okuma Minoru,
Takayama Hiroshi,
Uchino Haruto
Publication year - 1982
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.1365-2141.1982.tb02804.x
Subject(s) - platelet , ristocetin , chemistry , thromboxane , arachidonic acid , endocrinology , medicine , adenosine diphosphate , epinephrine , thrombin , thrombocytosis , incubation , thromboxane b2 , serotonin , platelet aggregation , biochemistry , receptor , enzyme
S ummary . A new type of acquired platelet dysfunction was found in a chronic myeloid leukaemia patient with petechiae and thrombocytosis. Platelet aggregation induced by arachidonic acid (AA), collagen and A23187 was decreased, secondary aggregation by ADP and epinephrine was defective and ristocetin‐induced aggregation was completely reversible. No platelet ATP was released by AA and collagen. Only high concentrations of AA (≤ 2 mM) induced minimal reversible aggregation. 14 C‐serotonin uptake by the platelet and platelet adenine nucleotide contents were normal. Normal AA metabolism was demonstrated by thin‐layer radiochromatographic analysis of the metabolites of 14 C‐AA and the determination of thiobarbituric acid reactive substances produced by the incubation of AA or thrombin with the platelets. Minimal reversible aggregation was observed when patient's platelet‐rich plasma was added to a reaction mixture in which thromboxane A 2 (TXA 2 ) had been generated. TXA 2 produced by patient's platelets showed normal platelet‐aggregating activity. These results suggest that a subnormal platelet response to TXA 2 is included as a mechanism for this acquired hypofunction of the platelet.