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. 2019 Nov;17(9):458-464.
doi: 10.1089/met.2019.0032. Epub 2019 Sep 23.

Protective Effect of Hepatitis B Against Metabolic Syndrome in Patients with Nonalcoholic Fatty Liver Disease But Not in Normal Individuals

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Protective Effect of Hepatitis B Against Metabolic Syndrome in Patients with Nonalcoholic Fatty Liver Disease But Not in Normal Individuals

Chun Pei et al. Metab Syndr Relat Disord. 2019 Nov.

Abstract

Background: Both hepatitis B (HB) and nonalcoholic fatty liver disease (NAFLD) are related to metabolic syndrome (MetS); however, this relationship remains controversial. In this study, we determined the effects of NAFLD and HB infection on the risk of MetS among elderly individuals. Methods: In total, 24,500 individuals aged >65 years were enrolled; they were classified into four groups: normal individuals (N), patients with only HB infection without abnormal echogenicity (HB-alone), patients with only abnormal echogenicity or fatty liver alone (FL-alone), and patients with both HB infection and abnormal echogenicity (HB-FL). Results: After adjustment for age, compared with group N, men and women with NAFLD (FL-alone and HB-FL) had a significantly higher risk of MetS, whereas no significant difference was observed in the incidence of MetS between groups HB-alone and N. However, group HB-FL had a lower risk of MetS than did group FL-alone. HB infection (HB-alone and HB-FL) was associated with a lower risk of high triglycerides (TGs) and fasting plasma glucose (FPG) than HB infection absence (groups N and FL-alone) in men and women. Lower risk of TG derangement was observed in group HB-alone than in group N. In addition, both men and women in group HB-FL had a lower risk of TG and FPG abnormalities than in group FL-alone, whereas a decrease in incidence of high waist circumference and blood pressure was observed only in men. Conclusion: HB infection protects against MetS development, only in patients with HB infection and NAFLD, but not in normal individuals. Additional studies are warranted to clarify the pathogenesis.

Keywords: fasting plasma glucose; hepatitis B; metabolic syndrome; nonalcoholic fatty liver disease; triglyceride.

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