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Platelet Storage Pool Deficiency and Prostaglandin Synthesis in Chronic Granulocytic Leukaemia
Author(s) -
Gerrard J. M.,
Stoddard S. F.,
Shapiro R. S.,
Coccia P. F.,
Ramsay N. K. C.,
Nesbit M. E.,
Rao G. H. R.,
Krivit W.,
White J. G.
Publication year - 1978
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.1365-2141.1978.tb05836.x
Subject(s) - platelet , aspirin , thromboxanes , arachidonic acid , chemistry , serotonin , epinephrine , endocrinology , medicine , prostaglandin , biochemistry , thromboxane , enzyme , receptor
S ummary . Platelet function was evaluated in eight patients with chronic granulocytic leukaemia (CGL), seven Ph 1 positive and one Ph 1 negative. Seven of the eight patients’platelets had an absence of the second wave of adrenaline induced aggregation on at least one occasion, while five had impaired collagen aggregation. The platelets of all seven patients with abnormal responses to adrenaline, aggregated with arachidonic acid, thus ruling out a cyclo‐oxygenase deficiency. A marked decrease in the ADP, serotonin, and dense body content of platelets was found in all five patients evaluated. Mixtures of CGL patient platelets with platelets from normal donors who had ingested aspirin gave a normal biphasic response to adrenaline. Normal release of the storage pool contents from aspirin treated platelets was shown by stirring a mixture of CGL platelets and 14 C‐serotonin labelled aspirin treated platelets with adrenaline. The CGL platelets alone or in the mixture produced malondialdehyde in response to adrenaline. These experimental results suggest that CGL platelets have a storage pool deficiency but can synthesize prostaglandins and thromboxanes in response to arachidonic acid and adrenaline.