HBV and obesity
| Author, year [Ref.] | Method | Findings | Conclusion |
|---|---|---|---|
| Yen et al., 2008 [67] | Cross-sectional study of 8,226 university students | The risk for MetS increases with higher BMI and SUA, while it decreases with vigorous PA and current alcohol consumption. Compared to individuals with seroprotective titers from hepatitis B vaccination [anti-HBs(+) and anti-HBc(–)], those without protective anti-HBs titers after vaccination or without hepatitis B infection [anti-HBs(–) and anti-HBc(–)] had a 34% higher risk for MetS, and those with natural HBV infection [anti-HBc(+)] had a 58% higher risk for MetS. | Hepatitis B vaccination with anti-HBs(+)was associated with a reduced risk of MetS compared to anti-HBs(–). However, HBV infection documented by anti-HBc(+) was associated with a higher risk of MetS. |
| Wang et al.,2010 [68] | Cross-sectional study of 934 patients with HBV infection (25.1% had ALT activity ≥ 40 IU/L). | In a multivariate LRA, BMI and fasting blood glucose levels independently predicted elevated ALT activity, with ORs of 1.73 (95% CI: 1.17 to 2.56) for individuals with a BMI ≥ 25 kg/m2 and 1.88 (95% CI: 1.06 to 3.33) for those with FBG ≥ 126 mg/dL. ALT activity was also associated with BMI among individuals whose ALT activity was within the reference range. | Obesity and fasting hyperglycemia in the diabetic range may worsen liver injury, as assessed by ALT levels. |
| Chung et al., 2012 [69] | Retrospective analysis of 88 treatment-naïve CHB patients treated with ETV | The rate of seroconversion, ALT normalization, and HBV-DNA negativity (< 300 copies/mL) at 3, 6, and 12 months of treatment did not differ significantly between the normal-BMI and high-BMI groups. | Obesity does not impact the outcome of ETV treatment. |
| Chiang et al., 2013 [70] | Cross-sectional analysis of 3,587 HBV-infected participants without liver cirrhosis at study entry | High HBV viral load remained significantly inversely associated with extreme obesity (OR: 0.17; 95% CI: 0.05 to 0.63; P = 0.008) and central obesity (OR: 0.44; 95% CI: 0.25 to 0.78; P = 0.005) in male HBeAg-seropositive participants in sex-stratified analyses. | Extreme obesity and central obesity were linked to a lower prevalence of high HBV viral load in HBeAg seropositive individuals, especially in men. |
| Besharat et al., 2015 [71] | Follow-up study of 304 CHB patients. WC ≥ 102 cm (men) and ≥ 89 cm (women) identified central obesity. LSM ≥ 8 Kpa defined ALS | Nineteen (7.4%) CHB patients developed ALS after 4 years of follow-up. Central obesity and viral load predicted ALS in LRA. | In CHB patients, central obesity is a determinant of ALS. |
| Fan et al., 2016 [72] | Meta-analysis of 16 published studies | Individuals with obesity showed a significant non-response to HBV vaccination (adjusted OR: 2.46; 95% CI: 1.50 to 4.03). | Obesity is significantly associated with a decreased response to HBV vaccines. |
| Sun et al., 2019 [73] | Cross-sectional analysis of 615 CHB patients (287 with abdominal obesity) | In LRA, a high AST value (OR: 2.991; P < 0.001), smoking (OR: 2.002; P = 0.019), and diabetes mellitus (OR: 2.047; P = 0.029) independently predicted liver fibrosis in CHB patients with abdominal obesity. High body weight (OR: 1.113; P < 0.001) and high diastolic blood pressure (OR: 1.079; P = 0.002) were associated with SLD. | Obesity is a significant risk factor for SLD and liver fibrosis among individuals with CHB. |
| Kim et al., 2019 [74] | Study of 13,063 CHB patients, 195 of whom died of liver cancer during a follow-up of 10.6 years | After adjusting for confounders, statin use (HR: 0.17; 95% CI: 0.04 to 0.70) and hypercholesterolemia (HR: 0.46; 95% CI: 0.24 to 0.88 for total cholesterol ≥ 240 mg/dL) were associated with a decreased risk of LCM, while BMI ≥ 30 kg/m2 was associated with an increased risk of LCM (HR: 2.46; 95% CI: 1.20 to 5.06). | Obesity is a risk factor for LCM among patients with CHB. |
| Fan et al., 2021 [75] | Prospective study of 5,754 nucleos(t)ide analogue-treated CHB patients with a 5-year cumulative incidence of HCC of 2.9% | In the overall population, individuals with central obesity (W/H > 0.5) had a significantly higher 5-year incidence of HCC than those without (3.9% vs. 2.1%; HR: 2.06; P = 0.0001). Additionally, in 745 PSM pairs (4.7% vs. 2.3%; HR: 2.04; P = 0.026), central obesity was independently associated with HCC risk (HR: 1.63; P = 0.013). W/H gain within 1 year was associated with a significantly higher HCC risk (AHR: 1.88; 95% CI: 1.12 to 3.13; P = 0.017). | Central obesity is associated with a 2-fold increase in HCC risk among CHB patients receiving antiviral treatment. |
AHR: adjusted hazard ratio; ALS: advanced liver stiffness; ALT: alanine transaminase; anti-HBc: antibody against Hepatis B core antigen; anti-HBs: antibody against hepatitis B surface antigen; AST: aspartate transaminase; BMI: body mass index; CHB: chronic hepatitis B; ETV: entecavir; FBG: fasting plasma glucose; HBV: hepatitis B virus; HCC: hepatocellular carcinoma; HR: hazard ratio; LRA: logistic regression analysis; LCM: liver cancer mortality; MetS: metabolic syndrome; OR: odds ratio; PSM: propensity score matched; SLD: steatotic liver disease; SUA: serum uric acid; W/H: waist-to-height ratio; WC: waist circumference
The supplementary material for this article is available at: https://www.explorationpub.com/uploads/Article/file/1001334_sup_1.pdf.
The graphical abstract was generated using Servier Medical Art, provided by Servier. The authors would like to express their gratitude to Sabine Weiskirchen from the University Hospital Aachen for preparing Figure 2 of this review. Additionally, we would like to extend our sincere thanks to the World Obesity Federation for assisting and granting permission to publish Figure 1B and the Supplementary material.
AI and AI-assisted Technologies: The authors of this article used the Large Language Model RWTHgpt by RWTH Aachen University exclusively for minor translations and grammatical corrections in this work. All sentences revised by RWTHgpt were reviewed and verified by the authors.
AL and RW: Conceptualization, Writing—original draft, Writing—review & editing. Both authors read and approved the submitted version.
Amedeo Lonardo who is the Associate Editor of Exploration of Medicine had no involvement in the decision-making or the review process of this manuscript. Another author declares that there are no conflicts of interest.
Not applicable.
Not applicable.
Not applicable.
Not applicable.
Not applicable.
© The Author(s) 2025.
Open Exploration maintains a neutral stance on jurisdictional claims in published institutional affiliations and maps. All opinions expressed in this article are the personal views of the author(s) and do not represent the stance of the editorial team or the publisher.