Hemolytic-uremic syndrome: demonstration of abnormalities of platelet reactivity and insensitivity to prostaglandin I2.
Platelet aggregation and thromboxane synthesis and platelet sensitivity to the antiaggregatory action of prostaglandin I2 were studied serially in a subject suffering from adult hemolytic-uremic syndrome. Platelet aggregation in vitro was defective during the acute phase of the disease and recovered during the convalescent phase. Defective aggregation was not associated with a failure of thromboxane synthesis although it was related to an intrinsic platelet defect rather than an inhibitor in the plasma. The platelets were insensitive to prostaglandin I2, even in the recovery phase of the disease. Furthermore, plasma from the patient rendered normal platelets insensitive to prostaglandin I2 and more sensitive to aggregating agents. It is concluded that the platelet abnormality in hemolytic-uremic syndrome is complex and it combines both an intrinsic platelet abnormality and a plasma component.
D000208:Acute Disease; D004351:Drug Resistance; D011464:Epoprostenol / Q000494:pharmacology*; D005260:Female; D006463:Hemolytic-Uremic Syndrome / Q000097:blood*; D006801:Humans; D066298:In Vitro Techniques; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*; D013929:Thromboxane B2 / Q000096:biosynthesis
D013929:Thromboxane B2; D011464:Epoprostenol