Goals: We specifically evaluate the effect of malnutrition on the infection risks of patients admitted with alcoholic hepatitis using a national registry of hospitalized patients in the United States. Background: Malnutrition is a common manifestation of alcoholic hepatitis that affects patient outcomes. Study: 2011 to 2017 National Inpatient Sample was used to isolated patients with alcoholic hepatitis, stratified using malnutrition (protein-calorie malnutrition, sarcopenia, and weight loss/cachexia) and matched using age, gender, and race with 1:1 nearest neighbor matching method. Endpoints included mortality and infectious endpoints. Results: After matching, there were 10,520 with malnutrition and 10,520 malnutrition-absent controls. Mortality was higher in the malnutrition cohort [5.02 vs. 2.29%, P<0.001, odds ratio (OR): 2.25, 95% confidence interval (CI): 1.93-2.63], as were sepsis (14.2 vs. 5.46, P<0.001, OR: 2.87, 95% CI: 2.60-3.18), pneumonia (10.9 vs. 4.63%, P<0.001, OR: 2.51, 95% CI: 2.25-2.81), urinary tract infection (14.8 vs. 9.01%, P<0.001, OR: 1.76, 95% CI: 1.61-1.91), cellulitis (3.17 vs. 2.18%, P<0.001, OR: 1.47, 95% CI: 1.24-1.74), cholangitis (0.52 vs. 0.20%, P<0.001, OR: 2.63, 95% CI: 1.59-4.35), and Clostridium difficile infection (1.67 vs. 0.91%, P<0.001, OR: 1.85, 95% CI: 1.44-2.37). In multivariate models, malnutrition was associated with mortality [P<0.001, adjusted odds ratio (aOR): 1.61, 95% CI: 1.37-1.90] and infectious endpoints: sepsis (P<0.001, aOR: 2.42, 95% CI: 2.18-2.69), pneumonia (P<0.001, aOR: 2.19, 95% CI: 1.96-2.46), urinary tract infection (P<0.001, aOR: 1.68, 95% CI: 1.53-1.84), cellulitis (P<0.001, aOR: 1.46, 95% CI: 1.22-1.74), cholangitis (P=0.002, aOR: 2.27, 95% CI: 1.36-3.80), and C. difficile infection (P<0.001, aOR: 1.89, 95% CI: 1.46-2.44). Conclusion: This study shows the presence of malnutrition is an independent risk factor of mortality and local/systemic infections in patients admitted with alcoholic hepatitis.

BACKGROUND/OBJECTIVES:Patients with cirrhosis have liver-related immune dysfunction that potentially predisposes the patients to increased influenza infection risk. Our study evaluates this cross-sectional relationship using a national registry of hospital patients. METHODS:This study included the 2011-2017 National Inpatient Sample database. From this, respiratory influenza cases were isolated and stratified using the presence of cirrhosis into a cirrhosis-present study cohort and cirrhosis-absent controls; propensity score matching method was used to match the controls to the study cohort (cirrhosis-present) using a 1:1 matching ratio. The endpoints included mortality, length of stay, hospitalization costs, and influenza-related complications. RESULTS:Following the match, there were 2,040 with cirrhosis and matched 2,040 without cirrhosis admitted with respiratory influenza infection. Compared to the controls, cirrhosis patients had higher in-hospital mortality (7.79 vs 3.43% p < 0.001, OR 2.38 95% CI 1.78-3.17), longer length of stay (7.25 vs 6.52 d p < 0.001), higher hospitalization costs ($70,009 vs $65,035 p < 0.001), and were more likely be discharged to a skilled nursing facility and home healthcare (vs routine home discharges). In terms of influenza-related complications, the cirrhosis cohort had higher rates of sepsis (29.8 vs 22% p < 0.001, OR 1.51 95% CI 1.31-1.74). In the multivariate regression analysis, cirrhosis was associated with higher mortality (p < 0.001, aOR 2.31 95% CI 1.59-3.35) and length of stay (p = 0.018, aOR 1.03 95% CI 1.01-1.06). In subgroup analysis of patients with decompensated (n = 597) versus compensated cirrhosis (n = 1443), those with decompensated cirrhosis had higher rates of in-hospital mortality (12.7 vs 5.75% p < 0.001, OR 2.39 95% CI 1.72-3.32), length of stay (8.85 vs 6.59 d p < 0.001), and hospitalization costs ($92,858 vs $60,556 p < 0.001). In the multivariate analysis, decompensated cirrhosis was associated with increased mortality (p < 0.001, aOR 2.86 95% CI 1.90-4.32). CONCLUSION:This study shows the presence of cirrhosis to result in higher hospital mortality and postinfluenza complications in patients with influenza infection.

INTRODUCTION: Obesity-induced hepatic steatosis exerts oxidative stress on the liver. Therefore, obese patients with primary biliary cholangitis (PBC) are at particular risk for exacerbation of hepatic inflammation from hepatic steatosis. In this study, we investigate the effects of obesity on the histopathological findings in PBC. METHODS: This was a retrospective study of patients with biopsy-proven PBC, stratified by the BMI cutoff for obesity (BMI ≥ 30). The endpoints were standard histopathological findings of PBC, including cellular infiltration of the portal tract, florid duct lesions/bile duct loss, parenchymal inflammation, and hepatic necrosis. Univariate and multivariate analysis were performed to identify relationships between obesity and histopathological findings. RESULTS: A total of 107 patients were included in the study, of which 45 patients (42.1%) formed the obese cohort. Between the obese and non-obese cohorts, there was no difference in age (52.1 vs 55y P = 0.1) nor in gender distribution (female/male: 91.1/8.9 vs 88.7/11.3% P = 0.76). The average BMI was 35.9 kg/m2 in the obese cohort and 24.9 kg/m2 in the non-obese cohort (P < 0.01). Of the histopathologic findings, cellular infiltration of the portal tract (combination of lymphocytic, neutrophilic, plasmacytic, and eosinophilic infiltration) was found to be associated with the presence of obesity (P = 0.02, OR 2.5, 95% CI 1.13–5.63). However, no associations were found between obesity and florid duct lesions/bile duct loss (P = 0.89, OR 0.95 95%CI 0.43–2.08), obesity and parenchymal inflammation (P = 0.768, OR 0.88 95%CI 0.39–2.01), or between obesity and hepatic necrosis (P = 0.347, OR 1.45 95%CI 0.67–3.13). The association between obesity and cellular infiltration of the portal tract remained significant (P = 0.04, aOR 2.69 95%CI 1.07–6.76) despite controlling for age (P = 0.94), gender (P = 0.29), race (P = 0.60), diabetes (P = 0.66), alcohol use (P = 0.18), statin use (P = 0.06), advanced fibrosis (P = 0.72) cirrhosis (P = 0.40), parenchymal inflammation (P = 0.09), and liver steatosis (P = 0.54), thus indicating that obesity is independently associated with portal inflammation in patients with PBC. CONCLUSION: Obesity is associated with cellular infiltration and inflammation of the portal tract. Given this finding, weight loss therapies should be introduced early in order to reduce the risks of progression in obese PBC patients.Figure 1.: Multivariate model: cellular infiltration of the portal tract in PBC patients.