Anemia can result from hemorrhage, hemolysis, or bone marrow hypoplasia. Megaloblastic anemia, usually a result of folate deficiency, has been observed in 20-40% of seriously ill, hospitalized alcoholic patients and in up to 4% of ambulatory alcoholics. Alcohol inhibits absorption of folate. There is not a strong correlation between megaloblastic anemia and the presence of liver disease. Alcohol also has a direct toxic effect on the bone marrow, which results in a transient sideroblastic anemia. Reticulocytosis commonly occurs as part of recovery from alcohol toxicity (Lee, 1999). Transient thrombocytopenia is found after consumption of large quantities of alcohol, especially in binge drinkers (Hardin, 2001).
Leukopenia is less common, resulting from the same mechanisms of toxic and nutritional factors already mentioned. Hypersplenism, an irreversible complication, may also contribute to leukopenia, thrombocytopenia, and anemia.
Bone marrow recovery with resolution of leukopenia usually occurs after 1-2 weeks of abstinence.
Alcohol also affects both thrombotic and coagulation functions. In particular, the cascade of clotting proteins is impeded as a result of diminished production of the vitamin K-dependent clotting factors (prothrombin, VII, IX, and X). Fibrinolysis, and occasionally disseminated intravascular coagulation may also occur. Transient thrombocytopenia is found after consumption of large quantities of alcohol, especially in binge drinkers (Hardin, 2001).
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