Reply to correspondence on “Adverse impact of metabolic dysfunction on fibrosis regression following direct-acting antiviral therapy: A multicenter study for chronic hepatitis C” Chen-Hua Liu, Yu-Ping Chang Clinical and Molecular Hepatology.2025; 31(2): e232. CrossRef
Correspondence to editorial on “Adverse impact of metabolic dysfunction on fibrosis regression following direct-acting antiviral therapy: A multicenter study for chronic hepatitis C” Tom Ryu, Young Chang, Seung Up Kim, Jae Young Jang Clinical and Molecular Hepatology.2025; 31(2): e203. CrossRef
Reply to correspondence on “Adverse impact of metabolic dysfunction on fibrosis regression following direct-acting antiviral therapy: A multicenter study for chronic hepatitis C” Chen-Hua Liu, Yu-Ping Chang Clinical and Molecular Hepatology.2025; 31(2): e232. CrossRef
Viral oncogenesis and immune remodeling: Decoding the therapeutic potential of immune checkpoint inhibitors in virus-associated cancers Lihua Qi, Bai Hu, Canhui Cao, Ting Peng, Miaochun Xu, Shiyi Liu, Yashi Xu, Xiaojie Liu, Wencheng Ding, Li Li, Shitong Lin Biomedicine & Pharmacotherapy.2025; 191: 118515. CrossRef
Background/Aims Direct-acting antivirals (DAAs) effectively eradicate hepatitis C virus. This study investigated whether metabolic dysfunction influences the likelihood of fibrosis regression after DAA treatment in patients with chronic hepatitis C (CHC).
Methods This multicenter, retrospective study included 8,819 patients diagnosed with CHC who were treated with DAAs and achieved a sustained virological response (SVR) between January 2014 and December 2022. Fibrosis regression was defined as a 20% reduction in noninvasive surrogates for liver fibrosis, such as liver stiffness (LS) measured by vibration-controlled transient elastography (VCTE) and the fibrosis-4 (FIB-4) score. Hypercholesterolemia (h-TC) was defined as >200 mg/dL.
Results The median age of the study population was 59.6 years, with a predominance of male patients (n=4,713, 57.3%). Genotypes 1, 2, and others were confirmed in 3,872 (46.2%), 3,487 (41.6%), and 1,024 (12.2%) patients, respectively. Diabetes mellitus (DM) was present in 1,442 (17.2%) patients and the median LS was 7.50 kPa (interquartile range, 5.30–12.50). Multivariate analysis revealed that the presence of DM and pre-DAA h-TC were independently associated with a decreased probability of fibrosis regression by VCTE. Additionally, pre-DAA h-TC was independently associated with a decreased probability of fibrosis regression by the FIB-4.
Conclusions Metabolic dysfunction has an unfavorable influence on fibrosis regression in patients with CHC who achieve SVR after DAA treatment.
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Despite the increasing prevalence of metabolic disorders, the potential effects of metabolic factors on hepatocellular carcinoma (HCC) development in individuals with chronic liver diseases (CLDs) are not well understood. For a metabolic factor to be identified as a risk factor for HCC in patients with CLDs, such as hepatitis B virus (HBV) and hepatitis C virus (HCV) infection, there should be a strong synergistic interaction between the carcinogenic mechanisms of the metabolic factor and the CLD itself. This review aims to comprehensively summarize the published data on the relationship between metabolic factors such as diabetes mellitus (DM), obesity, and blood lipids and the risk of HCC in patients with CLDs. DM consistently increases the risk of HCC in patients with CLD. When associated with DM, the risk of HCC seems to be highest in HCV and non-alcoholic fatty liver disease (NAFLD), followed by alcoholic liver disease (ALD) and HBV. Obesity may increase the risk of HCC. Among CLDs, the evidence is relatively consistent and clear for ALD, while clear evidence is limited in other CLDs including HBV, HCV, and NAFLD. Total cholesterol, potentially low-density lipoprotein cholesterol and triglyceride, seems to have strong inverse associations with HCC in individuals with CLDs. Despite evidence from observational studies, statins had no effect in preventing HCC in randomized controlled trials. Whether statins have a preventive effect against HCC is unclear. A better understanding and management of metabolic factors may be beneficial to reduce the risk of HCC in patients with CLDs.
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Background/Aims Tenofovir alafenamide (TAF) has shown less favorable effect on lipids compared to tenofovir disoproxil fumarate (TDF) in clinical trials. However, data regarding these outcomes in patients with chronic hepatitis B (CHB) are scarce. Therefore, this study aimed to evaluate the effect of TAF on the lipid in patients with CHB.
Methods A total of 237 TAF-treated CHB patients compared with TDF, inactive CHB, and non-hepatitis B virus (HBV)-infected control groups using propensity score matching (PSM).
Results Following PSM, each analysis was conducted on cohorts via the matching of 70:140 (TAF:TDF), 89:89 (TAF:inactive CHB), 140:560 (TAF:non-HBV infected control), and 368:1,472 (TDF:non-HBV-infected control). A significant decrease in the total cholesterol (TC) level was noted at 48 weeks in the TDF group compared to the TAF group (176.3±32.9 vs. 156.7±27.7, P<0.001) and the non-HBV-infected control group (175.0±29.5 vs. 156.2±28.3, P<0.001). However, no significant change in TC was observed in the TAF group and inactive CHB or non-HBV-infected control groups at 48 weeks. For the subgroup analyses of TAF vs. non-HBV-infected control subjects and inactive CHB patients whose detailed lipid profile information were available, no between-group differences in TC, low-density lipoprotein (LDL)-cholesterol, highdensity lipoprotein (HDL)-cholesterol, TC/HDL ratio, and LDL/HDL ratio were observed at 48 weeks.
Conclusions TDF seems to have a lipid-lowering effect compared to the non-HBV-infected control and TAF-treated groups. However, in real practice, TAF might not worsen the lipid profiles of subjects compared to non-HBV-infected controls and patients with inactive CHB.
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Profiling of Peripheral TRBV and CD4+CD25+ Treg in CHB Patients with HBeAg SC during TDF Treatment Jiezuan Yang, Haifeng Lu, Baikun Chen, Lili Jiang, Hua Zhang, Ping Ye, Linfeng Jin, Lele Zhu Journal of Immunology Research.2023; 2023: 1. CrossRef
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Tenofovir Alafenamide for Multiple Drug-Resistant Chronic Hepatitis B: A 3-Year Clinical Trial Jonggi Choi, Young-Suk Lim, Ji-Hoon Kim, Kwan Soo Byun, Byung Chul Yoo Clinical Gastroenterology and Hepatology.2023; 21(12): 3185. CrossRef
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Risk of dyslipidemia in chronic hepatitis B patients taking tenofovir alafenamide: a systematic review and meta-analysis Eui Gwon Hwang, Eun-Ae Jung, Jeong-Ju Yoo, Sang Gyune Kim, Young Seok Kim Hepatology International.2023; 17(4): 860. CrossRef
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Prediction model of hepatitis B virus-related hepatocellular carcinoma in patients receiving antiviral therapy Beom Kyung Kim, Sang Hoon Ahn Journal of the Formosan Medical Association.2023; 122(12): 1238. CrossRef
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Are the New Nucleos(t)ide Analogs Better than the Old Nucleos(t)ide Analogs? Jonggi Choi, Won-Mook Choi, Young-Suk Lim Clinics in Liver Disease.2023; 27(4): 809. CrossRef
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Editorial: switching to tenofovir alafenamide monotherapy is effective and safe for other nucleos(t)ide analogues‐treated patients with chronic hepatitis B Meng‐Lan Wang, En‐Qiang Chen Alimentary Pharmacology & Therapeutics.2022; 56(6): 1090. CrossRef
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