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In vivo platelet activation in beta-thalassemia major reflected by
increased platelet-thromboxane urinary metabolites
A Eldor, F Lellouche, A Goldfarb, EA Rachmilewitz and J Maclouf
Department of Hematology, Hadassah University Hospital, Jerusalem, Israel.
Increased frequency of thromboembolic events has been recently observed in
patients with beta-thalassemia major (TM). Platelet function anomalies
including impaired aggregation, increased circulating aggregates, and our
finding of shortened platelet survival indicate that platelets may be
involved in the hypercoagulability in thalassemia. Consequently, we used a
technique based on thin layer chromatography purification and enzyme
immunoassay to measure urinary metabolites of thromboxane A2 (TXA2) and
prostacyclin (PGI2) in nine splenectomized patients with beta-TM regularly
transfused, five non- splenectomized patients with beta-thalassemia
intermedia (TI), and 20 healthy individuals. A significant 4- to 10-fold
increase was observed in the urinary excretion of 2,3-dinor-TXB2,
11-dehydro-TXB2 and 2,3- dinor-6-keto-PGF1 alpha in patients with TM and TI
as compared with healthy controls. No significant differences were found in
the concentrations of these metabolites between TM and TI patients. Six TM
patients received a very low dose of aspirin (20 mg/day) for 7 days. A
significant decrease was observed in the urinary concentrations of 2,3-
dinor-TXB2 and 11-dehydro-TXB2 derived from platelets. However, the levels
of urinary 2,3-dinor-6-keto-PGF1 alpha reflecting vascular production and
TXB2 and 6-keto-PGF1 alpha originating from the kidney were not
significantly changed. These results are consistent with those of increased
in vivo production of TXA2 because of endogenous platelet activation.
Volume 77,
Issue 8,
pp. 1749-1753,
04/15/1991
Copyright © 1991 by The American Society of Hematology
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