Nocturnal nutritional supplementation improves total body protein status of patients with liver cirrhosis: a randomized 12-month trial.

UNLABELLED: Patients with liver cirrhosis exhibit early onset of gluconeogenesis after short-term fasting. This accelerated metabolic reaction to starvation may underlie their increased protein requirements and muscle depletion. A randomized controlled trial was conducted to test the hypothesis that provision of a late-evening nutritional supplement over a 12-month period would improve body protein stores in patients with cirrhosis. A total of 103 patients (68 male, 35 female; median age 51, range 28-74; Child-Pugh grading: 52A, 31B, 20C) were randomized to receive either daytime (between 0900 and 1900 hours) or nighttime (between 2100 and 0700 hours) supplementary nutrition (710 kcal/day). Primary etiology of liver disease was chronic viral hepatitis (67), alcohol (15), cholestatic (6), and other (15). Total body protein (TBP) was measured by neutron activation analysis at baseline, 3, 6, and 12 months. Total daily energy and protein intakes were assessed at baseline and at 3 months by comprehensive dietary recall. As a percentage of values predicted when well, TBP at baseline was similar for the daytime (85 +/- 2[standard error of the mean]%) and nighttime (84 +/- 2%) groups. For the nighttime group, significant increases in TBP were measured at 3 (0.38 +/- 0.10 kg, P = 0.0004), 6 (0.48 +/- 0.13 kg, P = 0.0007), and 12 months (0.53 +/- 0.17 kg, P = 0.003) compared to baseline. For the daytime group, no significant changes in TBP were seen. Daily energy and protein intakes at 3 months were higher than at baseline in both groups (P < 0.0001), and these changes did not differ between the groups. CONCLUSION: Provision of a nighttime feed to patients with cirrhosis results in body protein accretion equivalent to about 2 kg of lean tissue sustained over 12 months. This improved nutritional status may have important implications for the clinical course of these patients.

Dietary protein intakes in patients with hepatic encephalopathy and cirrhosis: current practice in NSW and ACT.

OBJECTIVE: To ascertain whether current practice in teaching hospitals in New South Wales and the Australian Capital Territory delivers adequate dietary protein in the management of malnutrition in adults with cirrhosis, in accordance with European Society for Clinical Nutrition and Metabolism (ESPEN) guidelines for nutrition in liver disease. STUDY DESIGN: Cross-sectional study of dietitians using a self-administered, mail-back survey. SETTING: Teaching hospitals in NSW and the ACT treating patients with cirrhosis. PARTICIPANTS: Dietitians seeing patients with cirrhosis in the 12 months prior to completing the survey. MAIN OUTCOME MEASURES: Current dietary protein prescription practice for patients with cirrhosis (with and without hepatic encephalopathy); use of nutritional supplements and enteral feeding for malnourished patients with cirrhosis. RESULTS: Dietitians following the ESPEN guidelines were in the minority: 36% of the dietitians recommended an adequate protein intake for patients with hepatic encephalopathy. Sixty-four per cent of the dietitians had received referrals from the medical team requesting inappropriate protein-restricted diets for patients without hepatic encephalopathy. Seventy-eight per cent of the dietitians requested clarification of the recommended nutritional management of patients with cirrhosis. CONCLUSION: Many medical and dietetic staff inappropriately restrict protein intake of patients with cirrhosis.

Regulation of the growth hormone receptor/binding protein, insulin-like growth factor ternary complex system in human cirrhosis.

BACKGROUND/AIMS: The liver is the central organ of the endocrine growth hormone/insulin-like growth factor I (GH/IGF-I) axis and cirrhosis effects a state of acquired GH resistance. Low IGF-I levels are associated with adverse clinical outcomes in cirrhotic patients and may be pathogenic to the complications of cirrhosis. We examined the impact of cirrhosis on hepatic mRNA and serum protein levels for the GH receptor (GHR)/binding protein (GHBP), IGF-I, IGF binding protein (IGFBP)-3 and the acid-labile subunit (ALS). METHODS: Fifty patients with cirrhosis were studied and liver tissue was obtained from 18. Gene expression was assessed by Northern analysis and serum protein levels by immunoassay. RESULTS: In cirrhotic liver GHR mRNA and GH binding to microsomal membranes were decreased by 61 and 56%, respectively. Serum GHBP levels were decreased only in severe disease, not correlating with GHR mRNA or GH binding. Hepatic IGF-I and ALS mRNA were significantly decreased by 84 and 68%, respectively, in parallel with serum protein, suggesting transcriptional regulation. Hepatic IGFBP-3 mRNA was unchanged but low serum IGFBP-3 suggested post-transcriptional regulation. CONCLUSIONS: The decreased mRNA and serum levels for the GH-dependent, hepatocyte produced proteins IGF-I and ALS confirm the importance of GH receptor loss to the GH resistance of cirrhosis.