INFLUENCE OF LIVER-FAILURE, ASCITES, AND ENERGY-EXPENDITURE ON THE RESPONSE TO ORAL NUTRITION IN ALCOHOLIC LIVER-CIRRHOSIS

The influence of liver failure, ascites, and energy expenditure on the response to oral nutrition was assessed in a group of 55 alcoholic ci rrhotic patients. Caloric intake, nutritional status, resting energy e xpenditure (REE), and Child-Pugh score were evaluated before and after 1 mo of oral nutrition. Patients were severely malnourished, 73% had muscular midarm circumference (MMAC) below the 5th percentile of a ref erence population, 51% had triceps skinfold thickness below the 25th p ercentile. Eleven patients were in class A of Child, 19 in class B, an d 25 in class C. Twenty-six patients were nonascitic, whereas ascites was resolved in 10 ascitic patients by the end of the study and 19 pat ients had refractory ascites. Liver damage was more pronounced and did not improve during the study in patients with refractory ascites. Cal oric intake was similar to 40 kcal/kg of body weight and was in the sa me range in the three groups according to Child classification, Fat ma ss (FM) increased, respectively, from 17.4% +/- 1.7% to 19.5% +/- 1.4% , P < 0.01, in Child A patients; from 17.1% +/- 1.4% to 19.3% +/- 1.4% , P < 0.001, in Child B patients; and from 17.6% +/- 1.5% to 18.8% +/- 1.5%, P < 0.05, in Child C patients. The increase in FM was comparabl e in the three groups, whereas MMAC and the creatinine/height ratio di d not change significantly. FM was lower and did not increase in patie nts with refractory ascites. Child C patients were characterized by an increase in the rate of glucose oxidation (P < 0.02) and a decrease i n the rate of lipid oxidation (P < 0.05). High-density lipoprotein cho lesterol and apolipoprotein (Ape) Al were reliable indices of improvem ent of liver function in patients with severe liver failure, ApoA1 was also a marker of improvement of metabolic impairment. With respect to the measured REE/predicted REE ratio calculated according to Harris-B enedict equation (r), 19 patients were considered hypermetabolic (r < 1.1), 30 normometabolic (0.9 < r < 1.1), and 6 hypometabolic (r < 0.9) . An increase in FM correlated with r (P < 0.01) and was more marked i n hypermetabolic patients. In contrast to the other two groups, Child- Pugh score and nutritional status remained unchanged in the hypometabo lic patients. These results show that severe liver failure did not pre clude improvement of nutritional status provided caloric intake was hi gh. In Child C patients, improvement of nutritional status paralleled improvement of liver function and normalization of oxidative metabolis m. Refractory ascites had negative effects on changes m nutritional st atus and liver function. Despite adequate caloric intake to energy req uirements, hypometabolism]las a poor prognosis regarding both nutritio nal status and Liver function. (C) Elsevier Science Inc. 1997.