Abstract

Advanced liver disease is associated with a persistent inflammatory state, derived from abnormal bacterial translocation from the gut, which may contribute to the development of sarcopenia in cirrhosis. We aim to document the association of chronic inflammation and bacterial translocation with the presence of sarcopenia in cirrhosis. We prospectively followed cirrhotic patients aged 18–70 years with medically refractory ascites at a single tertiary care center in Toronto, Canada. The baseline data included patient demographic variables, the presence of bacterial DNA in serum/ascitic fluid, systemic inflammatory response syndrome (SIRS) status, and nutritional assessment. Thirty-one patients were enrolled, 18 (58.1%) were sarcopenic, 9 (29%) had bacterial DNA in serum and ascites fluid. The mean MELD score was 11.5 ± 4.0 (6–23). Sarcopenic and non-sarcopenic patients did not differ significantly in their baseline MELD scores, caloric intake, resting energy expenditure, the incidence of bacterial translocation, or SIRS. While sarcopenia was not linked to increased hospital admissions or death, it was strongly associated with increased episodes of acute kidney injury (3 vs. 0, p = 0.05). This pilot study did not demonstrate an association between sarcopenia and SIRS or bacterial translocation. These results should be confirmed in future larger studies, encompassing a greater number of chronic inflammation events and quantifying levels of bacterial DNA.

Highlights

  • Sarcopenia, or loss of muscle mass, is a common complication of advanced liver disease, occurring in 40–68% of cirrhotic patients [1,2]

  • The presence of sarcopenia in this population has been implicated as a risk factor for serious adverse outcomes of liver disease, including an increased incidence of overt and minimal hepatic encephalopathy [3], longer hospital stays [4], and reduced survival, both pre- [5] and post- liver transplantation [6]

  • High levels of inflammatory markers have been found to inversely correlate with muscle mass and strength [15] and to activate a number of molecular pathways related to skeletal muscle wasting [16]. These findings suggest a possible link between bacterial translocation from the gut and the development of sarcopenia in cirrhosis

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Summary

Introduction

Sarcopenia, or loss of muscle mass, is a common complication of advanced liver disease, occurring in 40–68% of cirrhotic patients [1,2]. The presence of sarcopenia in this population has been implicated as a risk factor for serious adverse outcomes of liver disease, including an increased incidence of overt and minimal hepatic encephalopathy [3], longer hospital stays [4], and reduced survival, both pre- [5] and post- liver transplantation [6]. Some proposed mechanisms have included an observed reduction in caloric intake and/or nutritional absorption [7], altered substrate metabolism [8], and/or inhibition of skeletal muscle protein synthesis [9]. An increasing body of evidence suggests that chronic inflammation may be an important factor in the development of sarcopenia [10].

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