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Nutrition in the management of hepatic encephalopathy.
Trop Gastroenterol 2003 Apr-Jun; 24(2):59-62TG

Abstract

Nutritional factors play a major role both in the pathogenesis as well as management of hepatic encephalopathy (HE). Physicians treating patients with chronic liver disease often restrict the intake of dietary protein to prevent a rise in blood ammonia levels. The role of protein restriction in patients with chronic hepatic encephalopathy (CHE) has been questioned recently as the efficacy of protein withdrawal in patients with CHE has never been subjected to a controlled trial. Evidence suggests that protein intake plays only a limited role in precipitating encephalopathy. In fact, measures taken to suppress endogenous protein breakdown are more effective than dietary restrictions in reducing the load of amino acids on the decompensated liver. A protein intake of less than 40 g per day, as has been indicated, contributes to a negative nitrogen balance, which along with increased endogenous protein breakdown, worsens encephalopathy. A positive nitrogen balance may have positive effects on encephalopathy. Rather, depressed plasma branched-chain amino acid (BCAA) levels, implicated in the pathogenesis of HE, also supervene in cirrhosis only when malnutrition is present as well. Therefore, the emphasis in the nutritional management of patients with HE should not be on the reduction of protein intake. Instead, the goal should be to promote synthesis by making available ample amounts of amino acids, while instituting other measures to reverse the ongoing catabolism. Different protein sources have varying effects on HE and efforts should be made to identify the most tolerated protein source to prevent malnutrition and maintain these patients on a long-term basis.

Authors+Show Affiliations

Department of Food and Nutrition, MS University, Vadodara.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

14603821

Citation

Srivastava, Nandini, et al. "Nutrition in the Management of Hepatic Encephalopathy." Tropical Gastroenterology : Official Journal of the Digestive Diseases Foundation, vol. 24, no. 2, 2003, pp. 59-62.
Srivastava N, Singh N, Joshi YK. Nutrition in the management of hepatic encephalopathy. Trop Gastroenterol. 2003;24(2):59-62.
Srivastava, N., Singh, N., & Joshi, Y. K. (2003). Nutrition in the management of hepatic encephalopathy. Tropical Gastroenterology : Official Journal of the Digestive Diseases Foundation, 24(2), pp. 59-62.
Srivastava N, Singh N, Joshi YK. Nutrition in the Management of Hepatic Encephalopathy. Trop Gastroenterol. 2003;24(2):59-62. PubMed PMID: 14603821.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nutrition in the management of hepatic encephalopathy. AU - Srivastava,Nandini, AU - Singh,Namrata, AU - Joshi,Y K, PY - 2003/11/8/pubmed PY - 2003/12/3/medline PY - 2003/11/8/entrez SP - 59 EP - 62 JF - Tropical gastroenterology : official journal of the Digestive Diseases Foundation JO - Trop Gastroenterol VL - 24 IS - 2 N2 - Nutritional factors play a major role both in the pathogenesis as well as management of hepatic encephalopathy (HE). Physicians treating patients with chronic liver disease often restrict the intake of dietary protein to prevent a rise in blood ammonia levels. The role of protein restriction in patients with chronic hepatic encephalopathy (CHE) has been questioned recently as the efficacy of protein withdrawal in patients with CHE has never been subjected to a controlled trial. Evidence suggests that protein intake plays only a limited role in precipitating encephalopathy. In fact, measures taken to suppress endogenous protein breakdown are more effective than dietary restrictions in reducing the load of amino acids on the decompensated liver. A protein intake of less than 40 g per day, as has been indicated, contributes to a negative nitrogen balance, which along with increased endogenous protein breakdown, worsens encephalopathy. A positive nitrogen balance may have positive effects on encephalopathy. Rather, depressed plasma branched-chain amino acid (BCAA) levels, implicated in the pathogenesis of HE, also supervene in cirrhosis only when malnutrition is present as well. Therefore, the emphasis in the nutritional management of patients with HE should not be on the reduction of protein intake. Instead, the goal should be to promote synthesis by making available ample amounts of amino acids, while instituting other measures to reverse the ongoing catabolism. Different protein sources have varying effects on HE and efforts should be made to identify the most tolerated protein source to prevent malnutrition and maintain these patients on a long-term basis. SN - 0250-636X UR - https://www.unboundmedicine.com/medline/citation/14603821/Nutrition_in_the_management_of_hepatic_encephalopathy_ L2 - http://www.diseaseinfosearch.org/result/3328 DB - PRIME DP - Unbound Medicine ER -