Effect of alcoholism on hemostasis.

Ample data exist indicating that alcoholism profoundly affects the hemostatic mechanism. In alcoholic patients without cirrhosis, the primary effect is on the blood platelet. Both quantitative and qualitative abnormalities appear during ethanol ingestion. Alcohol-related thrombocytopenia appears to be due to a combination of events: an increased rate of platelet destruction leading to decreased platelet survival and ineffective thrombopoiesis resulting in decreased effective platelet production. The qualitative abnormalities are also multiple and include decreased platelet aggregation, release, and procoagulant activity and decreased storage pool nucleotides, cyclic AMP, and MAO activity. The functional and metabolic abnormalities are associated with striking disturbances in ultrastructural morphology. These defects cause prolongation of the bleeding time and place affected patients at risk for hemorrhagic complications. The relationship between the quantitative abnormalities and the occurrence of thrombocytopenia is obscure, although their severity appears to increase in parallel. The various defects are readily corrected after cessation of drinking. Hence, their long-term significance, absent development of cirrhosis, is questionable. In alcoholic patients with cirrhosis, both platelet abnormalities and coagulation defects may be present. Which predominates in severity varies with each individual. Due to the chronicity of the underlying clinical state, the duration of the defects is more likely to be prolonged if not permanent. In addition, owing to the mechanism of their development, treatment or correction of the defects is difficult and of transitory benefit.