Ancrod in systemic lupus erythematosus with thrombosis. Clinical and fibrinolysis effects.
A patient with systemic lupus erythematosus had severe hypertension, rapidly worsening renal failure, and multiple successive thrombotic cerebrovascular and retinal lesions develop. In a kidney biopsy specimen luminal thrombi were demonstrated in arteries and arterioles, without vasculitic or inflammatory changes. The patient's plasma was markedly deficient in both prostacyclin stimulating factor (PSF) and vascular plasminogen activator (VPA), and also contained a potent inhibitor of in vitro urokinase-induced fibrinolysis. Treatment with ancrod resulted in striking reversal of the progressive renal damage and clinical recovery from the thrombotic cerebrovascular and retinal lesions. This clinical improvement was associated with improved renal histologic appearance, correction of the PSF and VPA deficiencies, and disappearance of the urokinase inhibitor. Possible mechanisms of action of ancrod are discussed.
D058186:Acute Kidney Injury / Q000209:etiology; D000328:Adult; D000721:Ancrod / Q000494:pharmacology / Q000627:therapeutic use*; D001706:Biopsy; D011464:Epoprostenol / Q000097:blood; D005260:Female; D005341:Fibrinolysin / Q000037:antagonists & inhibitors; D005342:Fibrinolysis / Q000187:drug effects*; D006801:Humans; D006973:Hypertension / Q000209:etiology; D002542:Intracranial Embolism and Thrombosis / Q000188:drug therapy* / Q000209:etiology; D007668:Kidney / Q000473:pathology; D008180:Lupus Erythematosus, Systemic / Q000150:complications*; D010960:Plasminogen Activators / Q000097:blood; D012164:Retinal Diseases / Q000188:drug therapy* / Q000209:etiology; D013927:Thrombosis / Q000188:drug therapy* / Q000209:etiology; D014568:Urokinase-Type Plasminogen Activator / Q000037:antagonists & inhibitors
D011464:Epoprostenol; D000721:Ancrod; D010960:Plasminogen Activators; D005341:Fibrinolysin; D014568:Urokinase-Type Plasminogen Activator