Alcoholic Liver Disease - Electrolyte Imbalances

3/31/00 (Brady)

Group: Friday Interns

RE: A 38 year old female with increasing weakness, diarrhea, and chills. 

Question:  What changes in electrolytes can be anticipated in alcoholic liver disease?

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Unique Identifier: 94192944

Authors: Lieber CS.

Institution: Section of Liver Disease and Nutrition, Bronx VA Medical Center, New York.

Abstract: This article reviews current concepts on the pathogenesis and treatment of alcoholic liver disease. It has been known: that the hepatotoxicity of ethanol results from alcohol dehydrogenase-mediated excessive generation of hepatic: nicotinamide adenine dinucleotide, reduced form, and acetaldehyde. It is now recognized that acetaldehyde is also: produced by an accessory (but inducible) microsomal pathway that additionally generates oxygen radicals and activates: many xenobiotics to toxic metabolites, thereby explaining the increased vulnerability of heavy drinkers to industrial: solvents, anesthetics, commonly used drugs, over-the-counter medications, and carcinogens. The contribution of gastric: alcohol dehydrogenase to the first-pass metabolism of ethanol and alcohol-drug interactions is discussed. Roles for: hepatitis C, cytokines, sex, genetics, and age are now emerging. Alcohol also alters the degradation of key nutrients,: thereby promoting deficiencies as well as toxic interactions with vitamin A and beta carotene. Conversely, nutritional: deficits may affect the toxicity of ethanol and acetaldehyde, as illustrated by the depletion in glutathione, ameliorated by: S-adenosyl-L-methionine. Other "supernutrients" include polyunsaturated lecithin, shown to correct the alcohol-induced: hepatic phosphatidylcholine depletion and to prevent alcoholic cirrhosis in nonhuman primates. Thus, a better: understanding of the pathology induced by ethanol is now generating improved prospects for therapy. [References:: 274]

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Unique Identifier: 89260615

Authors: Diehl AM.

Institution: Gastroenterology-Hepatology Division, Georgetown University, Washington DC.

Abstract: Liver injury may develop in some people who consume alcohol. The pathogenesis of liver damage in such subjects: remains obscure. Major histopathologic features of alcohol-associated liver injury include steatosis, steatonecrosis, and: cirrhosis. The clinical manifestations of alcoholic liver disease are nonspecific and range from asymptomatic: hepatomegaly to stigmata of portal hypertension with advanced parenchymal failure. The severity of the clinical: presentation and the degree of aminotransferase elevation correlate poorly with the liver histopathology, particularly in: patients who continue to drink alcohol. Short-term mortality of such patients is best predicted by a composite of clinical: and laboratory parameters that are influenced by alcohol consumption as well as by liver disease. Long-term: prognosis is determined by residual damage to vital organs (that is, whether or not cirrhosis has developed) and whether: or not the patient continues to drink. Current therapy of alcoholic liver disease includes abstinence and correction of: nutritional deficiencies. Other therapies are experimental and are best utilized in the setting of controlled clinical trials.: [References: 131]