Hepatitis B virus (HBV) infection in the US is the most common among Asians followed by non-Hispanic blacks. However, there have been few studies that describe HBV infection and immunity by racial group. Our study aims to assess racial/ethnic disparities in the prevalence and awareness of HBV infection and immunity using nationally representative data. In the National Health and Nutrition Examination Survey 2011–2014, 14,722 persons had HBV serology testing. We estimated the prevalence of HBV infection, past exposure, and immunity by selected characteristics and calculated adjusted odds ratios using survey-weighted generalized logistic regression. Awareness of infection and vaccination history was also investigated. The overall prevalence of chronic HBV infection, past exposure, and vaccine-induced immunity was 0.34% [95%CI 0.24–0.43], 4.30% [95%CI 3.80–4.81], and 24.4% [95%CI 23.4–25.4], respectively. The prevalence of chronic infection was 2.74% [95% CI 1.72–3.76] in Asians, 0.64% [95% CI 0.35–0.92] in non-Hispanic blacks, and 0.15% [95% CI 0.06–0.24] in non-Asian, non-blacks. Only 26.2% of those with chronic infection were aware of their infection. The prevalence of the past exposure was 21.5% [95%CI 19.3–23.7] in Asians, 8.92% [95%CI 7.84–9.99] in non-Hispanic blacks, 2.05% [95%CI 1.49–2.63] in non-Hispanic whites, and 4.47% [95%CI 3.25–5.70] in Hispanics. Prevalence of vaccine-induced immunity by each race was 34.1% [95%CI: 32.0–36.2] in Asians, 25.5% [95%CI: 24.0–27.0] in non-Hispanic blacks, 24.0% [95%CI: 22.6–25.4] in non-Hispanic whites, and 22.2% [95%CI: 21.3–23.3] in Hispanics. There are considerable racial/ethnic disparities in HBV infection, exposure, and immunity. More active and sophisticated healthcare policies on HBV management may be warranted.
Drug induced liver injury (DILI) is a common cause of acute liver injury. Paracetamol, also known as acetaminophen, is a widely used anti-pyretic that has long been established to cause liver toxicity once above therapeutic levels. Hepatotoxicity from paracetamol overdose, whether intentional or non-intentional, is the most common cause of DILI in the United States and remains a global issue. Given the increased prevalence of combination medications in the form of pain relievers and antihistamines, paracetamol can be difficult to identify and remains a significant cause of acute hepatotoxicity, as evidenced by its contribution to over half of all acute liver failure cases in the United States. This is especially concerning given that, when co-ingested with other medications, the rise in serum paracetamol levels may be delayed past the 4-hour post-ingestion mark that is currently used to determine patients that require medical therapy. This review serves to describe the clinical and pathophysiologic features of hepatotoxicity secondary to paracetamol and provide an update on current available knowledge and treatment options.
Background and Aims: There has been increasing evidence that vitamin D deficiency may increase the risk of metabolic syndrome. Since metabolic syndrome is a major risk factor for non-alcoholic fatty liver disease (NAFLD), we aimed to investigate the association between vitamin D and the severity and mortality of NAFLD.Methods: Data was obtained from the United States Third National Health and Nutrition Examination Survey conducted in 1988–1994, with follow-up mortality data through 2011. NAFLD was defined by ultrasonographic detection of hepatic steatosis in the absence of other liver diseases and categorized as normal, mild, moderate or severe. The severity of hepatic fibrosis was determined by NAFLD fibrosis score (NFS). ANOVA (F-test) was used to evaluate the association between vitamin D level and degree of NAFLD, and Cox proportional hazards regression analysis was used for survival analyses.Results: Vitamin D levels for normal, mild, moderate and severe steatosis were 25.1 ± 0.29 ng/mL, 24.7 ± 0.42 ng/mL, 23.7 ± 0.37 ng/mL and 23.6 ± 0.60 ng/mL, respectively (trend p < 0.001). Likewise, vitamin D levels for low, intermediate and high NFS categories were 24.7 ± 0.38 ng/mL, 23.4 ± 0.42 ng/mL and 21.5 ± 0.57 ng/mL, respectively (trend p < 0.001). After median-follow up over 19 years, vitamin D deficiency was significantly associated with diabetes- and Alzheimer’s disease-related mortality (hazard ratio (HR): 3.64, 95%CI: 1.51–8.82 and HR: 4.80, 95%CI: 1.53–15.1, respectively), with a borderline significance in overall mortality (HR: 1.16, 95%CI: 0.99–1.36, p = 0.06).Conclusions: Vitamin D level was inversely related to the degree of liver steatosis and fibrosis. Moreover, vitamin D deficiency was associated with diabetes- and Alzheimer’s disease-related mortality in NAFLD patients.
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