Platelets and the hemolytic-uremic syndrome.
Clinical studies suggest that the microthrombi characteristically found in hemolytic-uremic syndrome (HUS) may be the consequence of an uncontrolled platelet-endothelial interaction. A defect in prostacyclin production which is corrected by normal plasma may be the fundamental pathogenic mechanism. For this reason, efforts should be made to confirm the recent case reports which suggest that plasma infusion or exchange may be more effective than hemostatic inhibitors in the achievement of clinical remission in HUS.
D000925:Anticoagulants / Q000627:therapeutic use; D001777:Blood Coagulation; D001792:Blood Platelets / Q000502:physiology*; D001803:Blood Transfusion; D001808:Blood Vessels / Q000502:physiology*; D003937:Diagnosis, Differential; D004727:Endothelium / Q000502:physiology; D011464:Epoprostenol / Q000096:biosynthesis; D006463:Hemolytic-Uremic Syndrome / Q000175:diagnosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D010949:Plasma; D010956:Plasmapheresis; D011697:Purpura, Thrombotic Thrombocytopenic / Q000175:diagnosis / Q000473:pathology; D013928:Thromboxane A2 / Q000096:biosynthesis
D000925:Anticoagulants; D013928:Thromboxane A2; D011464:Epoprostenol