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Sarcopenia in cirrhosis: from pathogenesis to interventions.

Authors
  • Ebadi, Maryam1
  • Bhanji, Rahima A1
  • Mazurak, Vera C2
  • Montano-Loza, Aldo J3
  • 1 Division of Gastroenterology and Liver Unit, Zeidler Ledcor Centre, University of Alberta, 8540 112 Street NW, Edmonton, AB, T6G 2X8, Canada. , (Canada)
  • 2 Division of Human Nutrition, University of Alberta, Edmonton, AB, Canada. , (Canada)
  • 3 Division of Gastroenterology and Liver Unit, Zeidler Ledcor Centre, University of Alberta, 8540 112 Street NW, Edmonton, AB, T6G 2X8, Canada. [email protected] , (Canada)
Type
Published Article
Journal
Journal of gastroenterology
Publication Date
Oct 01, 2019
Volume
54
Issue
10
Pages
845–859
Identifiers
DOI: 10.1007/s00535-019-01605-6
PMID: 31392488
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Sarcopenia (severe muscle depletion) is a prevalent muscle abnormality in patients with cirrhosis that confers poor prognosis both pre- and post-liver transplantation. The pathogenesis of sarcopenia is multifactorial and results from an imbalance between protein synthesis and breakdown. Nutritional, metabolic, and biochemical abnormalities seen in chronic liver disease alter whole body protein homeostasis. Hyperammonemia, increased autophagy, proteasomal activity, lower protein synthesis, and impaired mitochondrial function play an important role in muscle depletion in cirrhosis. Factors including cellular energy status, availability of metabolic substrates (e.g., branched-chain amino acids), alterations in the endocrine system (insulin resistance, circulating levels of insulin, insulin-like growth factor-1, corticosteroids, and testosterone), cytokines, myostatin, and exercise are involved in regulating muscle mass. A favored atrophy of type II fast-twitch glycolytic fibers seems to occur in patients with cirrhosis and sarcopenia. Identification of muscle biological abnormalities and underlying mechanisms is required to plan clinical trials to reverse sarcopenia through modulation of specific mechanisms. Accordingly, a combination of nutritional, physical, and pharmacological interventions might be necessary to reverse sarcopenia in cirrhosis. Moderate exercise should be combined with appropriate energy and protein intake, in accordance with clinical guidelines. Interventions with branched chain amino acids, testosterone, carnitine, or ammonia-lowering therapies should be considered individually. Various factors such as dose, type, duration of supplementations, etiology of cirrhosis, amount of dietary protein intake, and compliance with supplementation and exercise should be the focus of future large randomized controlled trials investigating both prevention and treatment of sarcopenia in this patient population.

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