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Intravenous Prostacyclin in Thrombotic Thrombocytopenic Purpura

GARRET A. FITZGERALD, M.D.; RICHARD L. MAAS, A.B.; RICHARD STEIN, M.D.; JOHN A. OATES, M.D.; and L. JACKSON ROBERTS, M.D.
[+] Article and Author Information

Grant support: in part by grant GM 15431 from the U. S. Department of Health and Human Services. Dr. Oates is the Joe and Morris Werthan Professor of Investigative Medicine.

▸Requests for reprints should be addressed to Garret A. FitzGerald, M.D.; Division of Clinical Pharmacology, Department of Pharmacology, Vanderbilt University Medical School; Nashville, TN 37232.


Nashville, Tennessee


© 1981 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1981;95(3):319-322. doi:10.7326/0003-4819-95-3-319
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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.

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