Effect of alcohol on clinical complications of hepatitis virus-induced liver cirrhosis: a consecutive ten-year study.

BACKGROUND AND AIMS: Although coexisting alcohol-induced liver disease and hepatitis B or C virus-induced liver cirrhosis (ALD + HBV or ALD + HCV) has been the center of recent hepatology researches, numerous controversies still persist. This study aimed to showcase the influence of alcohol on the laboratory values and on the clinical outcomes of patients with hepatitis B and C virus-induced liver cirrhosis. METHODS: Patients diagnosed with liver cirrhosis (n = 22,287) from January 2010 to December 2019 were enrolled, and divided into five groups according to the etiology: alcohol-induced liver disease (ALD, 1652 cases), hepatitis B virus (HBV, 18,079 cases), hepatitis C virus (HCV, 682 cases), ALD + HBV (1594 cases) and ALD + HCV (280 cases). Laboratory results and proportion of different liver cirrhosis complications were contrasted between groups. RESULTS: The proportions of patients with Child Pugh grade C (28.0% vs 18.8%, P < 0.001) or MELD greater than 18 (24.1% vs 18.5%, P < 0.001) in the ALD + HBV group exceeded significantly those in the HBV group. Multivariate logistic regression revealed that the risk of hepatocellular carcinoma (HCC) and that of esophageal gastric variceal bleeding (EGVB) in the ALD + HBV group was respectively 2.01-fold and 1.74-fold that in the HBV group (HCC: OR = 2.01, 95% CI [1.58-2.55]; EGVB: OR = 1.74, 95% CI [1.30-2.33]) after adjusting for potential confounders. Furthermore, a linear-by-linear analysis test showed a decrease in the risk of HCC and EGVB with the duration of alcohol abstinence. Moreover, patients with both antiviral treatment and alcohol abstinence had the lowest risk of HCC and EGVB (HCC: OR = 0.10, 95% CI [0.05-0.20], P < 0.001; EGVB: OR = 0.17, 95% CI [0.06-0.45], P < 0.001) compared to those without any treatment, those with abstinence alone and those with antiviral therapy alone. Similar pattern was noticed while comparing the ALD + HCV group to the HCV group. CONCLUSION: Heavy alcohol use increased the severity of liver function impairment and the prevalence of HCC and EGVB in hepatitis virus-induced liver cirrhosis patients. Remarkably, long-term alcohol abstinence coupled with antiviral treatment effectively decreased the risk of HCC and EGVB in these populations.

FcGBP and VCAM-1 are ponderable biomarkers for differential diagnosis of alcoholic liver cirrhosis.

BACKGROUND/ AIMS: Early diagnosis of alcoholic liver cirrhosis (ALD) and coexisting ALD and hepatitis B virus-induced cirrhosis (ALD+HBV) is primordial for an optimal management of these conditions. However, the lack of specific noninvasive biomarkers coupled with the inaccuracy of self-reported alcohol consumption make the early diagnosis of these pathologies difficult. This study aimed to identify biomarkers to diagnose ALD and differentiate ALD+HBV from HBV. METHODS: Proteomics mass spectrometry technique was used to identify specific proteins of ALD by contrasting serums of ALD to that of healthy subjects. The accuracy of the selected proteins in diagnosing ALD and discriminating ALD+HBV from HBV was assessed in two independent cohorts using the area under the receiver operator characteristic curve (AUROC). RESULTS: 452 cirrhotic and normal subjects were enrolled in this study. The proteomic results revealed that FcGBP and VCAM-1 were the highest overexpressed proteins while comparing ALD samples to the healthy cohort. The combination of these two biomarkers had an AUROC of 0.986 (P < 0.001, sensitivity: 97.2%, specificity: 100%) in identifying ALD from the healthy cohort, and AUROC of 0.781 (P < 0.001, sensitivity: 81.8%, specificity: 77.0%) in differentiating ALD+HBV from HBV. This combination was more accurate than the combination of AST/ALT, MCV and GGT (ALD vs healthy, AUROC = 0.898; ALD+HBV vs HBV, AUROC = 0.599). The discrimination performance of this combination was further validated in another independent cohort. CONCLUSION: FcGBP and VCAM-1 are two promising biomarkers in the diagnosis of ALD and in the differentiating of ALD+HBV from HBV subjects.