UNASSIGNED: Psoas muscle parameters have been proposed as a simple and quick method for sarcopenia assessment. The aim of this study was to assess sarcopenia in cirrhotics by psoas muscle on computed tomography and its impact on mortality.
UNASSIGNED: One hundred and fifty patients (75 cirrhotics, 75 subjects) were assessed for psoas muscle on CT scan. Psoas muscle index (PMI) was calculated as \'total psoas muscle area/(height of subject)2\'. Cut off values for sarcopenia diagnosis were derived from local subjects (n = 75) who did not have cirrhosis/other causes of sarcopenia.
UNASSIGNED: Sarcopenia assessed by PMI was seen in 36% (n = 27) of the cirrhotics. Sarcopenia was significantly higher in patients having Child-Pugh C. Ascites, hepatic encephalopathy (HE) and gastro-intestinal bleed were seen in 48%, 18.7% and 24%, respectively. Sarcopenia was significantly associated with ascites and HE (P < 0.05). Out of the 75 cases, 53 cases completed the follow-up period of 1 year. Among the 20 cases who had sarcopenia, 35% (n = 7) succumbed to liver-related illness during 1 year follow-up, and out of the 33 cases without sarcopenia, only 6% (n = 2) died. The association of sarcopenia and 1 year mortality was statistically significant (P = 0.01).
UNASSIGNED: The PMI, a simple method for sarcopenia assessment detected sarcopenia in 36% of cirrhotics. Patients with sarcopenia had a significantly higher 1 year mortality rate and appropriate prognostication of such patients is needed.

Cirrhosis predisposes to abnormalities in energy, hormonal, and immunological homeostasis. Disturbances in these metabolic processes create susceptibility to sarcopenia or pathological muscle wasting. Sarcopenia is prevalent in cirrhosis and its presence portends significant adverse outcomes including the length of hospital stay, infectious complications, and mortality. This highlights the importance of identification of at-risk individuals with early nutritional, therapeutic and physical therapy intervention. This manuscript summarizes literature relevant to sarcopenia in cirrhosis, describes current knowledge, and elucidates possible future directions.

Alcohol-associated liver disease is one of the main causes of chronic liver disease. It comprises a clinical-histologic spectrum of presentations, from steatosis, steatohepatitis, to different degrees of fibrosis, including cirrhosis and severe necroinflammatory disease, called alcohol-associated hepatitis. In this focused update, we aim to present specific therapeutic interventions and strategies for the management of alcohol-associated liver disease. Current evidence for management in all spectra of manifestations is derived from general chronic liver disease recommendations, but with a higher emphasis on abstinence and nutritional support. Abstinence should comprise the treatment of alcohol use disorder as well as withdrawal syndrome. Nutritional assessment should also consider the presence of sarcopenia and its clinical manifestation, frailty. The degree of compensation of the disease should be evaluated, and complications, actively sought. The most severe acute form of this disease is alcohol-associated hepatitis, which has high mortality and morbidity. Current treatment is based on corticosteroids that act by reducing immune activation and blocking cytotoxicity and inflammation pathways. Other aspects of treatment include preventing and treating hepatorenal syndrome as well as preventing infections although there is no clear evidence as to the benefit of probiotics and antibiotics in prophylaxis. Novel therapies for alcohol-associated hepatitis include metadoxine, interleukin-22 analogs, and interleukin-1-beta antagonists. Finally, granulocyte colony-stimulating factor, microbiota transplantation, and gut-liver axis modulation have shown promising results. We also discuss palliative care in advanced alcohol-associated liver disease.

Anamorelin (ANA) is approved for treating cancer cachexia (CCX) in Japan. We report the case of a 69-year-old man with stage IVB squamous cell lung cancer complicated by CCX, having a 13.6% weight loss in 6 months. After chemotherapy was initiated, his weight was further reduced. Therefore, we started ANA combined with a treatment approach by a multidisciplinary collaboration, including nutritionists and physical therapists. After initiation of ANA, the body weight, appetite, psoas muscle index, and physical functions rapidly improved during chemotherapy. ANA administration combined with a multidisciplinary collaboration approach can be an effective supportive therapy against CCX during chemotherapy.

UNASSIGNED: Retrospective cross-sectional studies linked sarcopenia and myosteatosis with metabolic dysfunction-associated fatty liver disease (MAFLD). Here, we wanted to clarify the dynamic relationship between sarcopenia, myosteatosis, and MAFLD.
UNASSIGNED: A cohort of 48 obese patients was randomised for a dietary intervention consisting of 16 g/day of inulin (prebiotic) or maltodextrin (placebo) supplementation. Before and after the intervention, we evaluated liver steatosis and stiffness with transient elastography (TE); we assessed skeletal muscle index (SMI) and skeletal muscle fat index (SMFI) (a surrogate for absolute fat content in muscle) using computed tomography (CT) and bioelectrical impedance analysis (BIA).
UNASSIGNED: At baseline, sarcopenia was uncommon in patients with MAFLD (4/48, 8.3%). SMFI was higher in patients with high liver stiffness than in those with low liver stiffness (640.6 ± 114.3 cm2/ Hounsfield unit [HU] vs. 507.9 ± 103.0 cm2/HU, p = 0.001). In multivariate analysis, SMFI was robustly associated with liver stiffness even when adjusted for multiple confounders (binary logistic regression, p <0.05). After intervention, patients with inulin supplementation lost weight, but this was not associated with a decrease in liver stiffness. Remarkably, upon intervention (being inulin or maltodextrin), patients who lowered their SMFI, but not those who increased SMI, had a 12.7% decrease in liver stiffness (before = 6.36 ± 2.15 vs. after = 5.55 ± 1.97 kPa, p = 0.04).
UNASSIGNED: Myosteatosis, but not sarcopenia, is strongly and independently associated with liver stiffness in obese patients with MAFLD. After intervention, patients in which the degree of myosteatosis decreased reduced their liver stiffness, irrespective of body weight loss or prebiotic treatment. The potential contribution of myosteatosis to liver disease progression should be investigated.
UNASSIGNED: NCT03852069.
UNASSIGNED: The fat content in skeletal muscles (or myosteatosis) is strongly associated with liver stiffness in obese patients with MAFLD. After a dietary intervention, patients in which the degree of myosteatosis decreased also reduced their liver stiffness. The potential contribution of myosteatosis to liver disease progression should be investigated.

UNASSIGNED: Liver transplantation (LT) is a game changer in cirrhosis. Poor muscle mass defined as sarcopenia may potentially upset the LT scoreboard.
UNASSIGNED: To assess the prevalence and impact of sarcopenia on the intraoperative and early postoperative outcomes in Indian patients undergoing LT.
UNASSIGNED: Pre LT, single-slice routine computed tomography images at L3 vertebra of 115 LT recipients were analyzed, to obtain cross-sectional area of six skeletal muscles normalized for height in m2 - skeletal muscle index (SMI; cm2/m2). SMI< 52.4 in males and <38.5 in females was called sarcopenia. The intraoperative, postoperative outcome parameters and 90-day mortality were compared between sarcopenics and nonsarcopenics.
UNASSIGNED: Sarcopenia was found in 47.8% of patients [M (90.4%); age, 46.3 ± 10; BMI, 24.5 ± 4.3 kg/m2; child A:B:C = 1%:22%:77%; MELD, 20.6 ± 6.3; etiology alcohol: nonalchohol = 53%:47%; Charlson Comorbidity Index (CCI) > 3:≤3 = 56.5%:43.5%]. Sarcopenics vs. Nonsarcopenics; early postoperative complications: [sepsis, 49(89%) vs. 33(55%), P = 0.001; neurologic complications, 16(29.6%) vs. 5(8.8%), P = 0.040; Clavien-Dindo Classification ≥3-24 (43.6%):15 (25.4%),P = 0.041; ancillary parameters (days), duration of ventilation [median (range)] 1.5(1-3) vs. 1 (1-2), P = 0.021; intensive care unit (ICU) stay 12 (8-16) vs. 10 (8-12), P = 0.024; time to ambulation 9 (7-11) vs. 6 (5-7), P = 0.001; drain removal 18.7 ± 7.3 vs. 14.4 ± 6.2, P = 0.001; need for tracheostomy 5 (9%) vs. 0 (%), P = 0.017; preoperative prevalence of acute kidney injury, comorbidities and requirement for dialysis, intraoperative blood loss & inotropic support were significantly higher in sarcopenics. Ninety-day mortality was comparable between sarcopenics 5 (9.09%) and nonsarcopenics 4 (6.6%) P = 0.63. SMI (OR: 0.83; 95% CI: 0.71-0.97, P = 0.016; Acute on chronic liver failure (ACLF) presentation 12.5 (1.65-95.2), P = 0.015 and intraoperative blood loss 3.74 (0.96-14.6), P = 0.046 were predictors of 90-day mortality.
UNASSIGNED: Almost 50% of LT recipients had sarcopenia, who had a higher incidence of postoperative sepsis, neurological complications, longer ICU stay and ventilatory support. Low SMI, ACLF presentation, and intraoperative blood loss were the independent predictors of early mortality.