Alcohol abuse is generally defined as chronic consumption of more than 80 grams of alcohol per day . This translates into a daily intake of one of the following: approximately 250 mL of hard liquor, more than 500 mL of fortified wine, one bottle (750 mL) of table wine, or 1.5 liters of beer (four 12 ounce cans or bottles).
Alcohol abuse can have a variety of effects on the hematologic system, including macrocytosis with or without anemia, leukopenia, and/or thrombocytopenia. How this occurs is not completely understood. A direct toxic effect on hematopoietic cells, abnormalities in membrane phospholipids, and interference with folate utilization all may be involved [2,3].
The hematologic manifestations of alcohol abuse will be discussed here. The general subject of alcohol-associated disease is discussed separately. (See "Pathogenesis of alcoholic liver disease" and "Clinical manifestations and diagnosis of alcoholic fatty liver disease and alcoholic cirrhosis" and "Ethanol intoxication in adults".)
MECHANISM OF ALCOHOL TOXICITY
The adverse effects of alcohol on hematopoiesis may be mediated in part by metabolites of alcohol (ethanol). Ingested ethanol is metabolized in the liver in part by alcohol dehydrogenase, which oxidizes alcohol to acetaldehyde, while reducing NAD to NADH. (See "Pathogenesis of alcoholic liver disease", section on 'Alcohol metabolism'.)
It has been suggested that acetaldehyde accounts for some of the hematologic toxicity of alcohol [2,3]. Acetaldehyde can produce RBC protein-acetaldehyde adducts , which may generate immune responses against these modified proteins. Indeed, IgA and IgM anti-acetaldehyde-protein adducts have been found in alcoholics with macrocytic red cells . (See 'Macrocytosis' below.)