Booze and blood: The effects of acute and chronic alcohol abuse on the hematopoietic system

Clinical Laboratory Science, Jul/Aug 1998 by Heermans, Elizabeth Haile

Acute and chronic alcohol abuse are common conditions in patients admitted to hospitals. Alcohol has widespread direct and indirect effects on the hematologic system which can mimic and/ or obscure other disorders. Leukocyte, erythrocyte, and thrombocyte production and functions are affected directly. Liver damage secondary to alcohol abuse also impacts red blood cells and the hemostatic mechanisms. Nutritional deficiencies are caused not only by poor dietary habits practiced by alcohol abusers, but by the effect of alcohol on the absorption, storage, and utilization of several vitamins. Identifying these numerous effects results in a more comprehensive and clinically accurate understanding of the patient's hematologic status.

ABBREVIATIONS: ADH = alcohol dehydrogenase; ALD = alcoholic liver disease; DIC = disseminated intravascular coagulation; HCT = hematocrit; HGB = hemoglobin; IL-1 = Interleukin1; IL-6 = Interleukin-6; MCH = mean cell hemoglobin; MCHC = mean cell hemoglobin concentration; MCV = mean cell volume; MEOS = microsomal ethanol oxidizing system; NADH = reduced nicotinamide adenine dinucleotide; PLTC = platelet count; PT = prothrombin time; PTT = partial thromboplastin time; RBC = red blood cell count; TNF-alpha = tumor necrosis factor alpha; WBC = white blood cell count.

INDEX TERMS: alcohol and hematopoietic system; alcoholism and hematologic parameters.

Clin Lab Sci 1998;11(4):229

Alcohol abuse is a widespread health problem. Ethanol has been recorded as a factor in 12% to 30% of all hospital admissions, with higher percentages in psychiatric hospital admissions.1,2,3 Although ethanol is toxic to all organs, damage to the liver is particularly significant and has serious consequences for the hematologic and hemostatic systems. Although the changes observed in the hematopoietic system are not part of a diagnostic screen for ethanol abuse, it is important to recognize their effects. Not only may the hematologic picture mimic other conditions, but parameters often change after admission when the patient is no longer drinking.

The impact of ethanol on the hematopoietic system can be divided into direct and indirect effects. Direct effects are primarily seen in the bone marrow and involve the white cell, red cell, and platelet lines. Indirect effects are secondary to metabolic or physiologic alterations resulting in liver disease and to nutritional abnormalities, such as folate deficiency.

Leukopenia, particularly granulocytopenia, may be associated with alcohol abuse.4 This decrease in the white blood cell count appears to be a direct effect of the suppression of granulopoietic factors, as well as an indirect result of associated splenomegaly, infection, and/or impaired nutrition.5 All of these conditions are common in chronic alcohol abusers.

Neutrophil function is also affected by alcohol abuse. Blood ethanol levels of 25 to 100 mg/dL are easily obtained during social drinking (one to four drinks), and have been shown to impair neutrophil adhesion and bactericidal mechanisms, oxidative burst, and degranulation.6,7 This is especially critical in alcoholics with pneumococcal pneumonia, the most common infection associated with alcohol abuse. In one study, the impaired response to streptococcal pneumonia in rats was demonstrable for seven days following ethanol consumption. The effect may last longer than seven days in humans with chronic ethanol intoxication, and may be a significant contributer to mortality. The mortality rate for alcohol abusers with streptococcal pneumonia is 20% to 30%, virtually the same as reported 30 years ago, despite the sophisticated antibiotic therapies developed during this time.7

Both the number and function of lymphocytes, particularly T-- cells, are impaired by ethanol use.8,9 CD4 cell activity is decreased, reflected by the failure of alcoholics to develop expected antibody titers following immunization.1 The concentration of lymphocytes and neutrophils upon hospital admission appears to correlate with outcomes in patients with alcoholic hepatitis and to reflect the improvement in liver status, improvement in nutritional status, and decreased alcohol consumption following the acute illness. Ethanol further appears to impair the communication process between T-cells and macrophages via soluble immune mediators.9 The proinflammatory cytokines, tumor necrosis factor a (TNF-- alpha), Interleukin-1 (IL-1), and IL-6, which are secreted by Kupffer cells, hepatocytes, and liver sinusoidal endothelial cells are all increased in chronic alcohol ingestion.10,11 In alcoholic hepatitis, cytokine concentrations correlated with the severity of the liver disease and revert to normal levels during recovery.11 TNF-alpha has been shown to have a direct effect on the hepatocyte, causing cell injury, as well as resulting in increased neutrophil infiltration in the liver.10 This may be an additional contributory factor in the increased frequency and severity of infections in chronic alcoholics. Stainable iron granules in bone marrow plasma cells have also been noted in alcoholics. This deposition occurs with or without iron overloading, unlike other causes of plasma cell iron uptake, and results from the same biochemical process that causes the formation of ringed sideroblasts.12,13