Why the study?
Is the in vivo biosynthesis of prostacyclin and thromboxane A2 altered in patients with chronic idiopathic thrombocytopenic purpura compared to controls?
Is the in vivo biosynthesis of prostacyclin and thromboxane A2 altered in patients with chronic idiopathic thrombocytopenic purpura compared to controls?
Patients with chronic ITP exhibit enhanced in vivo biosynthesis of prostacyclin and thromboxane A2, suggesting platelet cyclooxygenase hyperactivity.
Supports platelet COX hyperactivity in chronic ITP; leaves open effects on bleeding or thrombotic risk pending prospective studies.
The production of thromboxane A2 (TxA2) and prostacyclin (PGI2) was studied in patients with chronic idiopathic thrombocytopenic purpura (10 patients) compared to central thrombocytopenia (five patients) and healthy subjects (10 subjects). This production was monitored by the assay of urinary 2,3-dinor-TxB2 and 2,3-dinor-6-keto-PGF1 alpha as respective breakdown products of TxA2 and PGI2 by stable isotope dilution assays employing negative ion-chemical gas-chromatography-mass-spectrometry. Evidence is presented for the existence of an enhanced PGI2 and TxA2 urinary excretion in the group of idiopathic thrombocytopenic purpura (ITP) patients. Moreover, production of serum TxB2 per platelet was decreased in ITP group. These results provide arguments for an in vivo platelet cyclooxygenase hyperactivity during chronic ITP.
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Rousson et al. (1989) studied this question.
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