[Alcohol-induced disorders of the hematopoietic system]

Alcohol has a variety of pathologic effects on hematopoiesis. It directly damages erythroid precursors, thereby contributing to macrocytosis and the anemic state of chronic alcoholics. Megaloblastic anemia in chronic alcoholism results from a combination of nutritional deficiency and the effect of ethanol as a folate antagonist. Experimental studies suggest that alcohol may disturb hepatic folate metabolism. Ethanol induces sideroblastic anemia, perhaps by direct interference with heme synthesis. Further, chronic ingestion of alcohol can lead to various types of hemolytic anemia caused by alterations in the erythrocyte membrane lipids which occur in association with alcoholic liver disease. Alcohol directly suppresses platelet formation and decreases the platelet life span. These two mechanisms contribute to thrombocytopenia which is a common complication to chronic alcoholism. Since ethanol also interferes with platelet function, prolongation of bleeding the time is common at all stages of alcoholism. Chronic ingestion of alcohol is associated with a diminished marrow granulocyte reserve and may lead to neutrocytopenia. Ethanol-induced dysfunction of granulocytes, monocyte-macrophages and T-lymphocytes undoubtedly contributes to the predisposition to infection observed in alcoholics. In contrast to alcohol-induced changes in liver, heart and central nervous system, hematopoietic disorders are reversible after alcohol withdrawal.