GARRET A. FITZGERALD, M.D.; RICHARD L. MAAS, A.B.; RICHARD STEIN, M.D.; JOHN A. OATES, M.D.; L. JACKSON ROBERTS, M.D.
A therapeutic trial of prostacyclin (PGI2) was done in a patient with thrombotic thrombocytopenic purpura resistant to treatment with antiplatelet drugs and plasmapheresis. Despite marked thrombocytopenia and continued treatment with aspirin, sulfinpyrazone, and dipyridamole, the urinary excretion of 2,3-dinor-thromboxane B2, a major thromboxane urinary metabolite, was within the normal range (90.3 to 368 pg/mg creatinine) at 96 pg/mg creatinine. Because of its potent antiaggregatory properties and the possibility of a defect in endogenous PGI2 production in thrombotic thrombocytopenic purpura, synthetic PGI2 (4 to 10 ng/kg-1 · min-1) was infused intravenously, first for 72 hours and then continuously for 18 days. Prostacyclin markedly reduced the excretion of 2,3-dinor-thromboxane B2, and the platelet count rose steadily to reach 100 000/mm3 by the eighth day of the second infusion. The patient remains in clinical remission, on no therapy, 7 months later. A controlled evaluation of PGI2 in thrombotic thrombocytopenic purpura is warranted. Apparent therapeutic failure in previous cases may have resulted from inadequate prolongation of PGI2 infusion.
FITZGERALD GA, MAAS RL, STEIN R, et al. Intravenous Prostacyclin in Thrombotic Thrombocytopenic Purpura. Ann Intern Med. 1981;95:319–322. doi: 10.7326/0003-4819-95-3-319
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Published: Ann Intern Med. 1981;95(3):319-322.
Cardiology, Coagulopathies, Coronary Risk Factors, Hematology/Oncology, Hypertension.
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