The aim of this study was to investigate whether rapid depletions of fat mass and skeletal muscle mass predict mortality in hepatocellular carcinoma (HCC) patients treated with sorafenib. This retrospective study evaluated 61 HCC patients. The cross-sectional areas of visceral and subcutaneous fat mass and skeletal muscle mass were measured by computed tomography, from which the visceral fat mass index (VFMI), subcutaneous fat mass index (SFMI), and skeletal muscle index (L3SMI) were obtained. The relative changes in these indices per 120 days (ΔVFMI, ΔSFMI, and ΔL3SMI) before and after sorafenib treatment were calculated in each patient. Patients within the 20th percentile cutoffs for these indices were classified into the rapid depletion (RD) group. Kaplan–Meier analysis revealed that with respect to ΔL3SMI (p = 0.0101) and ΔSFMI (p = 0.0027), the RD group had a significantly poorer survival. Multivariate analysis using the Cox proportional-hazards model also demonstrated that ΔL3SMI (≤−5.73 vs. >−5.73; hazard ratio [HR]: 4.010, 95% confidence interval [CI]: 1.799–8.938, p = < 0.001) and ΔSFMI (≤−5.33 vs. >−5.33; HR: 4.109, 95% CI: 1.967–8.584, p = < 0.001) were independent predictors. Rapid depletions of subcutaneous fat mass and skeletal muscle mass after the introduction of sorafenib indicate a poor prognosis.
A higher dose of loop diuretic use was associated with more rapid skeletal muscle depletion and poor survival in patients with liver cirrhosis, independent of the severity of liver disease.
Background: Handgrip strength (HGS) is a simple and convenient method to assess nutrition status in patients with cirrhosis. This retrospective study aimed to investigate the utility of HGS for predicting patients with covert hepatic encephalopathy (CHE) and patients at high risk of overt hepatic encephalopathy (OHE). Methods:We reviewed 963 patients with cirrhosis and consequently enrolled eligible 270 patients. HGS was measured using a digital grip dynamometer. CHE was diagnosed using a computer-aided neuropsychiatric test. Factors associated with CHE were estimated using the logistic regression model. Predictors associated with OHE occurrence were analyzed using the Fine-Gray competing risk regression model. Results:Of the 270 eligible patients, reduced HGS was observed in 102 (38%), reduced muscle mass in 107 (40%), and CHE in 53 (20%). Multivariate analysis showed that serum ammonia levels (odds ratio [OR], 2.23; 95% CI, 1.14-4.36; P = 0.014) and reduced HGS (OR, 3.68; 95% CI, 1.93-7.03; P < 0.001) were independently associated with CHE. During the median follow-up period of 24.5 months, 43 (16%) patients experienced OHE. After adjusting for possible confounding factors, multivariate analysis showed that reduced HGS (subdistribution hazard ratio, 2.36; 95% CI, 1.27-4.38; P = 0.007) was a significant predictor in the development of OHE. Conclusion:Patients with reduced HGS had a higher prevalence of CHE and a higher risk for OHE occurrence than those with normal HGS. The measurement of HGS could be a simple bedside modality to stratify the patients' risk for CHE and OHE.
Aim: Minimal hepatic encephalopathy (MHE) is associated with poor outcomes and the development of overt hepatic encephalopathy (OHE) in patients with liver cirrhosis (LC). Zinc plays a key role in the detoxification of ammonia, a risk factor of hepatic encephalopathy. This study aimed to investigate whether zinc deficiency predicts OHE occurrence and mortality in LC patients with MHE. Method: This retrospective study included 100 LC patients with MHE. MHE was diagnosed using a computer-aided neuropsychiatric test. Predictors associated with the development of OHE were analyzed using the Fine-Gray competing risk regression model. Cox proportional hazards regression analysis was carried out to evaluate the risk factors of mortality. Survival rates were analyzed using the Kaplan-Meier method and log-rank test.Results: Of the 100 LC patients with MHE, 41% had zinc deficiency (<60 μg/dl). Zinc deficiency was observed more frequently in the patients with reduced liver function reserve. During the median follow-up period of 9.9 months, 16% of the patients with MHE developed OHE. The patients with zinc deficiency had a higher risk of OHE than those without zinc deficiency (p = 0.03). Zinc deficiency was also associated with poor survival (p = 0.004). Multivariate analyses showed that zinc predicts the development of OHE (subdistribution hazard ratio [HR], 0.95; 95% confidence interval [CI], 0.92-0.99; p = 0.008) and mortality (HR, 0.96; 95% CI, 0.93-0.99; p = 0.02), independently of liver function reserves. Conclusion:Zinc deficiency is likely to be a predictor of both OHE development and mortality in LC patients with MHE.
Aim The Global Leadership Initiative on Malnutrition (GLIM) criteria, a newly developed global consensus around core diagnostic criteria for malnutrition, needs validation studies for use in daily clinical settings. This study aimed to determine whether the GLIM criteria could predict sarcopenia and mortality in patients with chronic liver disease (CLD). Methods We retrospectively reviewed 858 patients with CLD who were treated at our hospital between March 2013 and December 2019. Sarcopenia was diagnosed based on the criteria proposed by the Japan Society of Hepatology. Malnutrition was assessed using the GLIM criteria, subjective global assessment (SGA), and Royal Free Hospital‐global assessment (RFH‐GA) and their predictive ability for sarcopenia and mortality were assessed using the logistic regression analysis and the Cox proportional hazards regression model, respectively. Results Among the eligible 406 patients, 67% were men, the median age was 74 years, and 26% had sarcopenia. The prevalence of malnutrition according to the GLIM criteria, SGA, and RFH‐GA was 21%, 35%, and 26%, respectively. Comparing malnourished with well‐nourished patients, the odds ratio for complicating sarcopenia was 2.54 (95% confidence interval [CI], 1.44–4.49) for the GLIM criteria, 2.13 (95% CI, 1.09–4.15) for the SGA, and 2.78 (95% CI, 1.56–4.95) for the RFH‐GA. During a median follow‐up period of 2.0 years, 176 (43%) patients died. After adjusting for confounding factors, the GLIM criteria could independently predict mortality (hazard ratio, 1.95; 95% CI, 1.37–2.81). Conclusions The GLIM criteria are useful in identifying sarcopenia and predicting mortality in patients with CLD.
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