Abstract
This study aimed to investigate the relationship between serum zinc level and hepatic fibrosis in patients with nonalcoholic fatty liver disease (NAFLD). A cross-sectional study was conducted using nationally representative samples from the Korea National Health and Nutrition Examination Survey 2010. Significant hepatic fibrosis was defined as Fibrosis-4 (FIB-4) index>1.3. Zinc level was measured using inductively coupled plasma mass spectrometry. Univariable and multivariable logistic regression analyses were performed to assess risk factors for significant hepatic fibrosis in patients with NAFLD. A total of 300 patients with NAFLD were analyzed in this study. The mean serum zinc level was 139.8±29.9 μg/dL. FIB-4 index was significantly increased as the serum zinc level decreased (Adjusted correlation coefficient = -0.177, p = 0.003). Significant liver fibrosis was observed in 62 patients (21%). The multivariable analysis showed that significant liver fibrosis in NAFLD was associated with diabetes mellitus (odds ratio [OR], 3.25; 95% confidence interval [CI], 1.71-6.19; p<0.001), male (OR, 2.59; 95% CI, 1.31-5.12; p = 0.006), and zinc level <140 μg/dL (OR, 2.14; 95% CI, 1.16-3.94; p = 0.015). There was an inverse relationship between serum zinc level and FIB-4 index in NAFLD. Low levels of serum zinc were an independent risk factor for significant hepatic fibrosis in NAFLD.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease, which is defined as intrahepatic triglyceride content of >5%
We investigated the effect of serum Zn level on hepatic fibrosis represented by simple and noninvasive blood-based biomarker in patients with NAFLD
The present study demonstrates that there is a significant inverse relationship between serum Zn level and liver fibrosis represented by FIB-4 index in patients with NAFLD
Summary
Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease, which is defined as intrahepatic triglyceride content of >5%. It has become widespread with the increasing prevalence of obesity and metabolic syndrome. The spectrum of NAFLD includes simple steatosis, nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. It results in liver cancer [1]. NAFLD is a multifactorial disease with complex pathophysiology such as obesity, insulin resistance (IR), dyslipidemia, and metabolic syndrome [2]. In many cases, the progression of NASH to cirrhosis remained indolent without specific symptoms until advanced liver disease
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