Hepatitis Monthly
Year:2020 | Volume:20 | Issue:10|Papers Count:5

Context: Hepatitis B serology is very important for both diagnosis and treatment of the diseases. However, evidence regarding the association between income and hepatitis B seroprevalence are not sufficient to make a definitive conclusion. Objectives: This meta-analysis aimed to investigate the association between income inequality and hepatitis B seroprevalence. Methods: We searchedPubMedandWeb of Science databases to identify all relevant epidemiological studies published up to February 10, 2020. A categorical meta-analysis was applied to pool risk effects of income on hepatitis B seroprevalence. Results: A total of 1525 pieces of literature related to income level and hepatitis B seroprevalence were retrieved, of which 10 articles were finally included. The results revealed a borderline risk (OR: 1. 14, 95%CI: 1. 00-1. 30) for hepatitis B seroprevalence (positive for one or more seromarkers) among low-income groups. A significant income effect was observed for HBsAg seroprevalence with a 28% higher risk for low income versus high cases (OR: 1. 28, 95%CI: 1. 16-1. 41). However, no statistically significant associations were found between seroprevalence of Anti-HBs, Anti-HBc, and income. Conclusions: This study demonstrated that low income may increase the risk of hepatitis B seroprevalence, especially for HBsAg seroprevalence. Programs on hepatitis B prevention should focus on those with low income. Further studies are warranted to establish causality.

Hepatitis C virus (HCV) is a major cause of chronic hepatitis, which carries high mortality and morbidity (1). It’ s several decades that interferon-based regimens and direct-acting antiviral (DAAs) have improved the treatment of HCV (2). Although theWorld Health Organization (WHO) proposed a framework for eliminating HCV, several multiple-layered barriers may delay this goal (3). The barriersmaybe related to the patients (e. g. poor knowledge and asymptomatic infection), providers (e. g. treatment misconception), and health-care systems (e. g. high price and lack of strategies) (3). . . .

Objectives: The current study aimed to investigate the characteristics of HBV serum markers (HBsAg, HBeAg), biochemical indicators, HBV DNA, and the age to distinguish minimal from non-minimal liver histological inflammation group in HBeAg-positive chronic HBV-infected patients with ALT 1ULN (40U/L). Methods: The HBeAg-positive patients with treatment-naï ve hospitalized at Ditan hospital from January 2008 to January 2017 are investigated. Patients were separated into two groups of minimal and non-minimal (mild and moderate) histological inflammation group by liver biopsy specimens. Data were analyzed using the SPSS package. Results: There were both positive (age, ALT, and AST) and negative correlation factors (serum HBsAg, HBeAg, or HBV DNA quantitation) to the liver inflammation grades. Multivariate regression analysis indicated that HBeAg (P < 0. 001, b =-0. 554, Exp (B) = 0. 575) and AST (P = 0. 003, b = 0. 074, Exp (B) = 1. 077) were independent influential factors. The cutoff values of HBeAg and AST were separately 2. 85 Log10S/CO (AUC0. 724, Sensitivity64%, Specificity79%), 28U/L (AUC0. 726, Sensitivity68%, Specificity 78%) to distinguish Minimal from Non-minimal liver histological inflammation in chronic HBV-infected patients with ALT 1 ULN (40U/L). Conclusions: In total, 31. 34% (115/367) of patients with chronic HBV infectionwhohad non-minimal (mild and moderate) liver histological inflammation reached the required inflammation levels for antiviral treatment in HBeAg-positive patients with persistently normal ALT. HBeAg (cutoff < 2. 85 Log10S/CO) and AST (cutoff > 28 U/L) were the independent influential factors of predicting nonminimal liver inflammation with ALT 1 ULN (40U/L).

Background: HBsAg is synthesized in the endoplasmic reticulum and is necessary for the formation of complete HBV particles. A decreased synthesis of this antigen leads to an intracellular inhibition of virus production. Methods: The study aimed to assess the incidence of HBsAg elimination among 1, 290 patients who suffered from chronic HBV infection undergoing an antiviral treatment with nucleoside or nucleotide analogs (NAs). Furthermore, possible predictive factors for this elimination were analyzed. Results: A permanent HBsAg loss was confirmed in 3% of the patients, which was more frequent in men than in women (4. 4% vs. 1. 9%; P = 0. 009). The HBsAg elimination occurred in 5% of HBeAg (+) patients and 2. 8% of HBeAg (-) patients. The age of patients whose HBsAg was eliminated was higher than the age of the remaining patients (60 vs. 51 y/o). The effect of initially used pegylated interferon alfa (PEG-IFN) therapy on the HBsAg elimination was not observed. It occurred with the use of entecavir (ETV) and tenofovir (TDF); however, among patients treated with ETV, HBsAg was significantly more often eliminated in HBeAg (+) patients. Conclusions: The HBsAg elimination in patients undergoing antiviral treatment occurs more often in men, patients with positive HBeAg before treatment, individuals above 60 years, and patients treated with ETV.

Background: Insulin resistance can be a predictor of adverse fatty liver disease and health problems. Objectives: The present study aimed to investigate the effect of insulin resistance on fatty liver disease. Methods: This study used the data of 2, 160 individuals registered in a cross-sectional studywhowererandomlyselectedfromamong clients of a nutrition clinic in Tehran from April to December 2019. Insulin resistance and beta-cell activity were calculated by the homeostasis model assessment formula. The study outcome was defined as having fatty liver disease. The odds ratio (95% CI) was calculated using logistic regression models. Results: The mean age was 35 ( 9) in healthy subjects and 49 ( 8) in fatty liver disease patients (age range: 16 to 42 years). Nearly 34. 5% of the individuals had fatty liver disease. According to the adjusted results of the logistic regression model, the risk of NAFLD was 1. 05 (P < 0. 001) for one unit increase in fasting insulin and 1. 01 (P < 0. 001) for one unit increase in 2-h insulin, which indicated the statistically significant relationship of NAFLD with fasting insulin and 2-h insulin. Also, the risk of NAFLD was 1. 01 P < 0. 001) for one unit increase in FPG, which was statistically significant. Moreover, the adjusted risk of NAFLD was 1. 00 (P < 0. 001) for one unit increase in 2-h glucose, which was not statistically significant. Finally, the adjusted risk of NAFLD was 1. 29 (P < 0. 001) for one unit increase in HOMA-IR, which was statistically significant. Conclusions: The findings of the present study demonstrated that insulin resistance could increase the risk of fatty liver disease. Also, each one-unit increase in fasting blood sugar, fasting insulin, and 2-h insulin increased the risk of fatty liver disease. Therefore, the results of this study may be useful for health policymakers to design suitable preventive and therapeutic interventions for those with NAFLD to prevent and control this disease.