Finally, finding an ideal marker to predict mortality or life expectancy is a dream of practicing physicians. All of the reported candidate markers seem to be associated with the existence of NAFLD. It is generally believed that NAFLD is a hepatic manifestation http://www.selleckchem.com/products/iwr-1-endo.html of metabolic syndrome, which contributes to the risk of CVD. According to the chronological sequence of development, NAFLD may be an earlier manifestation of metabolic syndrome compared to CVD. Therefore, NAFLD-related markers including serum GGT, ALT, and hepatic steatosis may predict

CVD risk or even mortality. However, whether liver itself could serve as an alarm bell for mortality or life expectancy deserves further investigations. Chia-Chi Wang M.D.*, Jia-Horng Kao Ph.D.†, * find more Department of Hepatology, Buddhist Tzu Chi General

Hospital, Taipei Branch and School of Medicine, Tzu Chi University, Hualien, Taiwan, † Graduate Institute of Clinical Medicine and Hepatitis Research Center, National Taiwan University College of Medicine and Hospital, Taipei, Taiwan. “
“Kowdley et al.1 recently explored the relationship between demographic, biochemical, clinical factors, and liver fibrosis in patients with nonalcoholic liver disease (NAFLD), and reported the independent association of serum ferritin (SF) with advanced hepatic fibrosis and disease severity. Although this study explored the association of body mass index (BMI) with disease severity by different levels of SF, it did not address the key issues of the relationship between SF and BMI, and the likely interaction effect of BMI and SF on the risk of fibrosis. Furthermore, they only described

the importance of this relationship in NAFLD when increased BMI and elevated SF often coexist with other liver diseases, such as chronic viral hepatitis. We studied 498 patients with chronic hepatitis B (CHB) and explored the effect of BMI on SF, and evaluated the interaction effects of SF and BMI on liver fibrosis as determined by transient elastrography score (TES). The patients were 54% male, of mean age 44 ± 12 years, and BMI of 25 ± 4 kg/m2. The median PAK5 SF (interquartile range [IQR]) was 205 (115, 324) μg/L and 88 (38, 202) μg/L, respectively, for males and females. The median TES (IQR) was 5.4 (4.4, 6.7). The average levels of SF and TES had a significantly increasing trend over higher categories of BMI, defined by the quartiles of observed BMI. To evaluate the association of BMI with SF, multivariate quantile regression models were used. Adjusting for sex and age, the median level of SF would be significantly higher by 20.4 μg/L (95% confidence interval [CI]: 4.5-36.7, P = 0.014) for every 3 kg/m2 increase in BMI. Male patients are likely to have a significantly higher level of SF by 87.3 μg/L (95% CI: 57.5-117.1, P ≤ 0.01).