Nutrition in end-stage liver disease: principles and practice.

D a alnutrition is commonly seen in both alcoholic and nonalcoholic liver disease1–3 and has been hown to adversely affect outcome (see Figure 1).4,5 By efinition, it occurs when diet does not provide adequate alories and protein to maintain nutritional status or the ody is unable to fully absorb or utilize food eaten econdary to liver disease. Despite the obvious relevance, linical research in this field is surprisingly limited and alnutrition is frequently underdiagnosed in clinical ractice.6 The prevalence of malnutrition in cirrhosis is as high s 65%–90%.1–3 Evidence concerning the impact of etiolgy (of cirrhosis) on malnutrition is conflicting. Some tudies have shown no difference in prevalence and seerity of malnutrition in patients with viraland alcoholelated cirrhosis who were abstinent.2,7,8 Others have hown that alcoholic cirrhosis was associated with a oorer nutritional state compared with virus-associated irrhosis.9 Active alcoholism is a major cause of malnurition per se and could contribute to the earlier develpment observed.10 Protein depletion and reduced musle function are common in cirrhosis, particularly in men nd patients with alcoholic liver disease.11 The reason for he male preponderance is unknown and is not related to ypermetabolism or reduced energy and protein intake.11 he reduced levels of testosterone observed in male paients with cirrhosis12 may contribute to decreased proein anabolism, but this requires further investigation. he largest studies on prevalence and severity have been he Veterans Affairs Cooperative Studies in 1984 and 993, which focused on alcoholic hepatitis.13,14 These nd other studies showed that the severity of malnutriion correlated with that of the liver disease and the evelopment of serious complications such as hepatic ncephalopathy, ascites, hepatorenal syndrome, postransplantation outcome, and mortality.15–18 Also, shorterm survival is reduced in parallel with severity of malutrition.19 The majority of patients in these pivotal tudies had advanced liver disease; however, more sophisicated methods of analysis (neutron activation analysis r intracellular/extracellular body water) have shown that ignificant losses of body cell mass may occur in Child A irrhosis.20 In this review, we examine the mechanisms underlying alnutrition in chronic liver disease, the assessment ethods available, and the role of nutritional therapy advice, supplementation, enteral or parenteral) in the arious stages of chronic liver disease. Acute liver failure nd transplantation and the emerging data on probiotics re considered separately.