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Accelerated Improvement of Alcoholic Liver Disease With Enteral Nutrition P. J. KERNS, H. YOUNG, G. GARCIA, ET AL Gastroenterology 102:200–205, 1992
Author(s) -
Demetriou Achilles A.
Publication year - 1992
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/0148607192016003289
Subject(s) - medicine , gastroenterology , parenteral nutrition , ascites , enteral administration , alcoholic liver disease , alcoholic hepatitis , hepatic encephalopathy , prothrombin time , liver disease , creatinine , hepatology , cirrhosis
This is a prospective study that compares the effects of tube feeding to those of a regular diet in patients with alcohol‐induced liver disease. Study inclusion criteria were a clinical diagnosis of acute liver disease (ALD), serum bilirubin greater than 51 μmol/L, and one of the following: albumin less than 30 g/L, prothrombin time 4 seconds or greater over control, presence of ascites on physical examination. Fifty‐two patients met the inclusion criteria; however, 21 patients were excluded from the study because of the following reasons: objection to the length of the study, refusal of nasoduodenal tube placement, continuing gastrointestinal bleeding, elevated serum creatinine (>221 μmol/L), and inability to give informed consent. Thirty‐one patients were randomly assigned to either a regular diet control group (n = 15) or a tubefed treatment group (n = 16). Patients in the treatment group received, in addition to a regular diet, Isocal HCN (Mead Johnson, Evansville, Ind) tube feeding formula that provided 167 kJ/kg and 1.5 g/kg of ideal body weight protein. The enteral supplement was delivered via an 8F nasoduodenal tube (Keofeed, IVAC Corp, San Diego, Calif). Sodium (2 g) and fluid (1500 mL) restrictions were imposed, if clinically indicated, by the presence of peripheral edema or ascites. Demographic, clinical, and laboratory features of the two groups were similar at the time of randomization. Three patients from each group dropped out of the study. Patients were observed in the hospital for 28 days. Comparisons of encephalopathy, antipyrine clearance, metabolic rate, and biochemical parameters were performed weekly during the 4‐week hospital stay between the two groups. Complete nutrition assessment and periodic monitoring were carried out in all patients (indirect calorimetry, anthropometrics, 24‐hour urine urea, and creatinine measurements). Calorie counts were performed three times weekly. No statistically significant differences in clinical course and outcome (mortality, renal insufficiency, diarrhea, gastrointestinal bleeding, ascites) between the two groups were noted. However, the mean grade of encephalopathy over the initial week of treatment improved in the treatment group of patients (from 1.1 to 0.4; p <.02), whereas patients in the control group did not experience such an improvement (from 0.7 to 0.9; p value not significant). The median encephalopathy scores improved more rapidly in the treatment group compared with the control group. A 49% decrease in serum bilirubin was noted in the treatment group at 2 weeks and 79% at 4 weeks, compared with 12% and 22% decrease (p <.05 to.01), respectively, in the control group. Antipyrine elimination improved significantly more rapidly in the treatment group (improving the t 1/2 by 40% at 2 weeks) than in the control group (5% t 1/2 improvement at 2 weeks; p <.02). Control patients lost weight during the study period (from 78 to 72 kg; p <.05), whereas patients in the treatment group did not experience a significant weight loss (from 74 to 72 kg; p value not significant). The nutrition intake of the two groups differed markedly, with the treatment group receiving 200% the calories and protein consumed by the control group ( p <.01).