http://manuscript.elsevier.com/S0168827822000290/pdf/S0168827822000290.pdf

Cigarette Smoking and Liver Diseases.

Baveno VI criteria and spleen stiffness measurement rule out high-risk varices in virally suppressed HBV-related cirrhosis.

Objective We aimed at analyzing the role of smoking in hepatic fibrosis in patients with nonalcoholic fatty liver disease (NAFLD) and at exploring the related risk factors. Methods This was a cross-sectional study that included a total of 225 patients with NAFLD. Among them, 127 were nonsmokers and 98 were smokers. Liver significant fibrosis was diagnosed when the liver stiffness (LS) value was higher than 7.4 kPa. The diagnostic criterion for NAFLD was a controlled attenuation parameter (CAP) value of >238 dB/m. The CAP and LS values were measured using FibroScan. Results FibroScan showed that the LS value in the smokers was significantly higher than that in the nonsmokers (10.12 ± 10.38 kPa vs. 7.26 ± 6.42 kPa, P=0.013). The proportions of patients with liver significant fibrosis and advanced liver fibrosis among the smokers were significantly higher than those among the nonsmokers (P=0.046). Univariate analysis showed that age, weight, high AST level, low PLT level, and smoking were the risk factors associated with liver fibrosis in the smokers with NAFLD while multivariate analysis showed that age (OR = 1.029, P=0.021), high AST level (OR = 1.0121, P=0.025), and smoking (OR = 1.294, P=0.015) were the independent risk factors associated with liver fibrosis in the patients with NAFLD. Moreover, high AST level (OR = 1.040, P=0.029), smoking index (OR = 1.220, P=0.019), and diabetes mellitus (OR = 1.054, P=0.032) were the independent risk factors for liver fibrosis among the smokers with NAFLD. Conclusion This study showed that smoking was closely associated with liver fibrosis among the patients with NAFLD. For patients with NAFLD who smoke, priority screening and timely intervention should be provided if they are at risk of liver fibrosis.

/pdf/association-between-smoking-and-liver-fibrosis-among-238b48ehn4.pdf

Association between Smoking and Liver Fibrosis among Patients with Nonalcoholic Fatty Liver Disease

Introduction The role of reproductive factors in the development of chronic hepatitis B (CHB) remains unknown. We assessed the potential contributions of gender, menopausal status, and menarche age to liver fibrosis in CHB. Methods A cross-sectional prospective study included 716 women and 716 age-matched men with CHB who were not currently receiving antiviral therapy. Liver stiffness measurement using transient elastography was used to stage liver fibrosis as F0-F1 ( Results Of the 716 women, 121 (16.9%) were postmenopausal, and 80 (11.2%) had advanced liver fibrosis. Multivariate logistic regression analysis showed that the postmenopausal status compared with the premenopausal status (odds ratio [OR] = 3.65-8.83; P 14 years compared with 0.05). Longitudinal data analysis showed that postmenopausal women (n = 31) were significantly less likely to undergo regression of liver fibrosis after antiviral treatment vs premenopausal women (n = 19) (26.3% vs 74.2%, respectively; P Discussion Menopause and late menarche aggravated liver fibrosis in untreated CHB, besides menopause delayed fibrosis regression under antiviral therapy. The protective effect of female gender against fibrosis was lost for postmenopausal women. Translational impact It is important to consider menopausal status and age at menarche in establishing surveillance strategies among CHB females. Postmenopausal estrogen therapy may be considered for the prevention or treatment of liver fibrosis.

Influence of Gender and Reproductive Factors on Liver Fibrosis in Patients With Chronic Hepatitis B Infection.

http://manuscript.elsevier.com/S0261561422000255/pdf/S0261561422000255.pdf

Elevated coffee consumption is associated with a lower risk of elevated liver fibrosis biomarkers in patients treated for chronic hepatitis B (ANRS CO22 Hepather cohort).

Background & aims The role of cigarette smoking in the development of chronic hepatitis B (CHB) remains poorly understood. We assessed the potential contributions of cigarette smoking to liver fibrosis and its regression after starting antiviral therapy in CHB patients. Methods In this cohort study, 2144 consecutive male CHB patients under no antiviral therapy were evaluated and 206 patients with significant liver fibrosis (≥F2) initiating antiviral therapy had longitudinal follow-up. Liver fibrosis was measured by liver stiffness measurement using transient elastography. To adjust for imbalances between smoking history and never smoking groups, propensity score (PS) matching model with 1:1 ratios were performed. Cigarette smoking history and intensity (pack-years) were collected and documented using a standardized questionnaire. Results Before PS matching, 432/2144 patients had advanced fibrosis in prevalence cohort. Patients with smoking history (n = 1002) had a greater prevalence of advanced fibrosis than those without (n = 1142) (24.4% vs 16.5%, P = 0.001). Multivariate logistic regression analysis demonstrated that smoking contributed to advanced fibrosis (OR, 1.458; 95% CI, 1.114-1.908). In longitudinal cohort, multivariate logistic regression analysis demonstrated retarded fibrosis regression in patients with history of smoking ≥10 pack-years (OR, 0.288; 95% CI, 0.1-0.825). After PS matching, patients with smoking history had higher prevalence of advanced fibrosis (22.8% vs 18%, P = 0.024) than those non-smokers. In post-PS-matching logistic regression, the effect of smoking on advanced fibrosis persisted (OR, 1.415; 95% CI, 1.047-1.912; P = 0.024). Conclusions Cigarette smoking in male CHB patients aggravated liver fibrosis prior to and delayed fibrosis regression under antiviral therapy.

Impacts of cigarette smoking on liver fibrosis and its regression under therapy in male patients with chronic hepatitis B.

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Influence of Gender and Reproductive Factors on Liver Fibrosis in Patients With Chronic Hepatitis B Infection.

Impacts of cigarette smoking on liver fibrosis and its regression under therapy in male patients with chronic hepatitis B.