The reports of Tagnon and co-workers1 and others in the early 1950's suggested that the hemorrhagic syndrome that occurs in some patients with carcinoma of the prostate is due to fibrinolysis. However, Rapaport and Chapman,2 in 1959 and others since then have clearly shown that the mechanism in most, if not all, cases is disseminated intravascular coagulation, not fibrinolysis. It is now apparent that the condition is not caused by release from the prostate of a tissue activator of fibrinolysis, as was originally thought, but rather by the dissemination of procoagulant material into the circulating blood.
Possibly as the result of the earlier misconception regarding the pathogenesis of the bleeding tendency in patients with carcinoma of the prostate, the thought has persisted that the severe generalized bleeding syndrome occasionally encountered following transurethral resection of the prostate for benign adenoma is also caused by fibrinolysis.3 In a recent