Importance of sarcopenia parameter changes after living donor liver transplantation

Abstract

The systemic role of muscle tissue is strengthened by the large system of hormones, chemokines and other mediators that constitute a dense network of communication between the skeletal muscle and the liver (1,2). This, associated with the evidence of a progressive malnutrition and depletion of muscle mass in end-stage liver disease (ESLD) patients, has led many to study the role of sarcopenia and its systemic effects in this setting, and to identify it as critical risk factor for post- liver transplantation (LT) mortality (3-5). Englesbe and colleagues found a direct correlation between central sarcopenia, measured by computerized tomography (CT), the total area of the psoas muscle (psoas area right side + left side), and post-LT mortality in 163 patients (6). CT measurement of the psoas area is a standardized method, but its invasiveness (which does not allow for seriate follow-up at short time intervals), and the analysis limited to a minimum part of the skeletal muscle tissue, affects the reliability of the study. One Japanese study by Kaido et al., in 2012, overcame this limitation by estimating body composition as a whole through the use of bioelectrical impedance analysis (BIA). They showed that a reduction of the values of the body cell mass (BCM), defined as the intracellular water and the sum of the fat free body mass, among which viscera and muscular tissue, excluding bone mineral, is an independent risk factor for sepsis and mortality from infections in patients who underwent living donor liver transplantation (LDLT) (7). The same group, building on its previous results, did a retrospective study of 124 patients who underwent LDLT in order to determine the role of sarcopenia on transplantation outcome. To measure of the degree of sarcopenia they again used segmental BIA, measuring not only the BCM, but also the skeletal muscle mass (SMM). Analysis of the results found that both patients with low BCM and patients with low SMM presented survival rates (up to 60 months post-LDLT) that were significantly lower than patients with normal/high values of BCM or SMM. Sarcopenia, identified as low BCM or SMM, was an independent risk factor for post-LDLT mortality (8). This study also had limitations: it was retrospective, had a low number of patients, and lacked data for patients with acute liver failure and, above all, used only BIA to define the degree of sarcopenia, which seems to be greatest limitation, as underscored by Safer et al. (9). In particular, BIA does not allow us to define sarcopenia, as the European Working Group on Sarcopenia (10) and the Asian Working Group for Sarcopenia (11) have pointed out. Both groups consider not only a reduction in muscle mass as a necessary condition, but also a reduction in muscle strength, and failure of physical performance. In their latest paper, Kaido and colleagues overcame some of the limitations of their previous studies by prospectively analyzing 72 patients who underwent LDLT between January, 2013 and October, 2015 (12). Essential exclusion criteria for the study, also tested as a new criterion of exclusion for LT, was a severe degree of sarcopenia, defined as an inability to walk unaided. Similarly to their previous work, SMM was calculated using BIA, while muscle strength was evaluated by grip strength tests. Of the 72 patients, 10 were defined as pre-LDLT sarcopenia patients. They had an overall survival of 94% at one year, exceeding the 80% reported for similar populations belonging to the same transplant center. This seems to bolster the idea of considering severe sarcopenia as an exclusion criterion for LT. There was a very low survival rate at one year for sarcopenic patients (60%), significantly lower than non-sarcopenic patients. Finally, all the patients had reduced SMM and GS in post-LDLT, with recovery to the pre-LDLT level of about 12 months, and 6 months, respectively. These data are in line with results of a study by Tsien et al. of 53 d