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The Hematological Complications of Alcoholism

People who abuse alcohol1are atrisk for numerous alcohol-relatedmedical Complications , includ-ing those affecting the blood ( , theblood cells as well as proteins presentin the blood plasma) and the bonemarrow, where the blood cells areproduced. (For more information onthe blood s composition and on thevarious types of blood cells and theirproduction, see sidebar, pp. 50 51.)Alcohol s adverse effects on the blood-building, or hematopoietic, system areboth direct and indirect. The directconsequences of excessive alcoholconsumption include toxic effects onthe bone marrow; the blood cell pre-cursors; and the mature red bloodcells (RBC s), white blood cells(WBC s), and platelets. Alcohol sindirect effects include nutritionaldeficiencies that impair the productionand function of various blood cells. These direct and indirect effects ofalcohol can result in serious medicalproblems for the drinker.

to either iron deficiency or excessively high levels of iron in the body. Because iron is essential to RBC functioning, iron deficiency, which is commonly caused by excessive blood loss, can result in anemia. In many alcoholic patients, blood loss and subsequent iron deficiency are caused by gastrointestinal bleeding.

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Transcription of The Hematological Complications of Alcoholism

1 People who abuse alcohol1are atrisk for numerous alcohol-relatedmedical Complications , includ-ing those affecting the blood ( , theblood cells as well as proteins presentin the blood plasma) and the bonemarrow, where the blood cells areproduced. (For more information onthe blood s composition and on thevarious types of blood cells and theirproduction, see sidebar, pp. 50 51.)Alcohol s adverse effects on the blood-building, or hematopoietic, system areboth direct and indirect. The directconsequences of excessive alcoholconsumption include toxic effects onthe bone marrow; the blood cell pre-cursors; and the mature red bloodcells (RBC s), white blood cells(WBC s), and platelets. Alcohol sindirect effects include nutritionaldeficiencies that impair the productionand function of various blood cells. These direct and indirect effects ofalcohol can result in serious medicalproblems for the drinker.

2 For example,anemia2resulting from diminishedRBC production and impaired RBCmetabolism and function can causefatigue, shortness of breath, lighthead-edness, and even reduced mental capac-ity and abnormal heartbeats. A decreasein the number and function of WBC sincreases the drinker s risk of seriousinfection, and impaired platelet produc-tion and function interfere with bloodclotting, leading to symptoms rangingfrom a simple nosebleed to bleeding inthe brain ( , hemorrhagic stroke). Fin-ally, alcohol-induced abnormalities inthe plasma proteins that are required for42 ALCOHOLHEALTH& RESEARCHWORLDThe HematologicalComplications ofAlcoholismHAROLDS. BALLARD, has numerous adverse effects on the various types of blood cells and theirfunctions. For example, heavy alcohol consumption can cause generalizedsuppression of blood cell production and the production of structurally abnormalblood cell precursors that cannot mature into functional cells.

3 Alcoholics frequentlyhave defective red blood cells that are destroyed prematurely, possibly resulting inanemia. Alcohol also interferes with the production and function of white blood cells,especially those that defend the body against invading bacteria. Consequently,alcoholics frequently suffer from bacterial infections. Finally, alcohol adversely affectsthe platelets and other components of the blood-clotting system. Heavy alcoholconsumption thus may increase the drinker s risk of suffering a stroke. KEY WORDS:adverse drug effect; AODE (alcohol and other drug effects); blood function; cell growth anddifferentiation; erythrocytes; leukocytes; platelets; plasma proteins; bone marrow; anemia ;blood coagulation; thrombocytopenia; fibrinolysis; macrophage; monocyte; stroke; bacterialdisease; literature reviewHAROLDS.

4 BALLARD, , is associatechief of hematology and oncology atthe New York Department of VeteransAffairs Medical Center, New York,New this article, the terms chronic alcohol abuse or chronic excessive alcohol consumption refer to theingestion of 1 pint or more of 80- to 90-proof alcohol( , about 11 drinks) per day. However, alcohol-related Hematological problems can occur at muchlower consumption levels. The drinker s risk fordeveloping these problems grows with increasingalcohol the definition of this and other technical termsused in this article, see the central glossary, pp. 93 clotting can lead to the formationof blood clots ( , thrombosis).This article summarizes currentinformation on the consequences ofexcessive alcohol consumption on thebone marrow and on the productionand function of RBC s, WBC s, plate-lets, and plasma SEFFECTS ON THEBONEMARROW AND ONRBCPRODUCTIONA lcohol is the most commonly useddrug whose consequences include thesuppression of blood cell production,or hematopoiesis.

5 Because its toxiceffects are dose dependent, however,significantly impaired hematopoiesisusually occurs only in people withsevere Alcoholism , who also may sufferfrom nutritional deficiencies of folicacid and other vitamins that play a rolein blood cell development. Chronicexcessive alcohol ingestion reduces thenumber of blood cell precursors in thebone marrow and causes characteristicstructural abnormalities in these cells,resulting in fewer-than-normal or non-functional mature blood cells. As aresult, alcoholics may suffer frommoderate anemia , characterized byenlarged, structurally abnormal RBC s;mildly reduced numbers of WBC s,especially of neutrophils; and moder-ately to severely reduced numbers ofplatelets. Although this generalizedreduction in blood cell numbers ( ,pancytopenia) usually is not progres-sive or fatal and is reversible with ab-stinence, complex aberrations ofhematopoiesis can develop over timethat may cause bone marrow abnormalitiesoccurring in severe alcoholics affectthe RBC precursor cells.

6 These abnor-malities most prominently includeprecursors containing fluid-filledcavities ( , vacuoles) or characteris-tic iron of Vacuoles in RBCP recursorsThe most striking indication of alco-hol s toxic effects on bone marrowcells is the appearance of numerouslarge vacuoles in early RBC precursorcells. It is unknown whether thesevacuoles affect the cell s function andthus the drinker s health; however,their appearance generally is consid-ered an indicator of excessive vacuoles usuallyappear in the pronormoblasts 5 to 7days following the initiation of heavyalcohol consumption. Moreover, thevacuoles on average disappear after 3to 7 days of abstinence, although insome patients they persist for up to a lesser extent, vacuoles alsodevelop in the granulocyte precursorsof alcoholics. This finding is notspecifically alcohol related, however,because other events that interferewith WBC production ( , infec-tions) may induce similar structuralchanges in the granulocyte precise mechanism underly-ing vacuole development in bloodcell precursors currently is analyses of early bloodcell precursors grown in tissue cul-ture suggest that when the cells areexposed to a wide range of alcoholconcentrations, the membrane sur-rounding each cell is damaged.

7 Thesealterations in membrane structure mayplay an influential role in AnemiaOne component of RBC s is hemo-globin, an iron -containing substancethat is essential for oxygen , however, the iron is notincorporated properly into the hemo-globin molecules. Instead, it is con-verted into a storage form calledferritin, which can accumulate in RBCprecursors, often forming granules thatencircle the cell s nucleus. These fer-ritin-containing cells, which are calledringed sideroblasts, cannot matureVOL. 21, NO. 1, 199743 Hematological Complications of AlcoholismALCOHOL SEFFECTS ONIRONMETABOLISMIn addition to interfering with the proper absorption of iron into thehemoglobin molecules of red blood cells (RBC s), alcohol use can leadto either iron deficiency or excessively high levels of iron in the iron is essential to RBC functioning, iron deficiency , which iscommonly caused by excessive blood loss, can result in anemia .

8 In manyalcoholic patients, blood loss and subsequent iron deficiency are causedby gastrointestinal bleeding. iron deficiency in alcoholics often is diffi-cult to diagnose, however, because it may be masked by symptoms ofother nutritional deficiencies ( , folic acid deficiency ) or by coexistingliver disease and other alcohol-related inflammatory conditions. For anaccurate diagnosis, the physician must therefore exclude folic aciddeficiency and evaluate the patient s iron stores in the bone , alcohol abuse can increase iron levels in the body. Forexample, iron absorption from the food in the gastrointestinal tract maybe elevated in alcoholics. iron levels also can rise from excessiveingestion of iron -containing alcoholic beverages, such as red wine. Theincreased iron levels can cause hemochromatosis, a condition character-ized by the formation of iron deposits throughout the body ( , in theliver, pancreas, heart, joints, and gonads).

9 Moreover, patients whosechronic alcohol consumption and hemochromatosis have led to livercirrhosis are at increased risk for liver commonly, vacuole development in pronor-moblasts also can occur after treatment with theantibiotic chloramphenicol. The two conditions caneasily be distinguished, however, because in contrastto the alcohol-induced vacuolation, chloramphenicol-induced vacuolation is accompanied by the disappear-ance of virtually all later RBC into functional RBC s. As aresult, the number of RBC s in theblood declines and patients developanemia. Many patients also have somecirculating RBC s that contain ferritingranules called Pappenheimer presence of these cells in theblood serves as an indicator of sider-oblastic anemia and can prompt thephysician to perform a bone marrowexamination to confirm the anemia is a commoncomplication in severe alcoholics:Approximately one-third of thesepatients contain ringed sideroblastsin their bone marrow.

10 Alcohol maycause sideroblastic anemia by interfer-ing with the activity of an enzyme thatmediates a critical step in hemoglobinsynthesis. (For information on othereffects of alcohol on iron metabolism,see box, p. 43) Abstinence can reversethis effect: The ringed sideroblastsgenerally disappear from the bonemarrow within 5 to 10 days, and RBCproduction resumes. In fact, excessnumbers of young RBC s called retic-ulocytes can accumulate temporarilyin the blood, indicating higher-than-normal RBC AnemiaBlood cell precursors require folicacid and other B vitamins for theircontinued production. Under condi-tions of folic acid deficiency , precur-sor cells cannot divide properly andlarge immature and nonfunctionalcells ( , megaloblasts) accumulatein the bone marrow as well as in thebloodstream. This impaired hema-topoiesis affects mainly RBC s, butalso WBC s and platelets.


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