Abstract
We aimed to analyze the serum level of a novel fibrosis marker, Mac-2-binding protein glycosylation isomer (M2BPGi), and its predictive value for hepatocellular carcinoma (HCC) development in chronic hepatitis B (CHB) under nucleot(s)ide analogue (NA) therapy. Serum M2BPGi levels were quantified in 147 CHB patients at baseline, 48 weeks after starting NA therapy, and at the patients’ last visit. The serum M2BPGi level serially decreased at each time point. During the median follow-up time of 6.6 years, 14 of 147 patients developed HCC. Multivariate Cox proportional hazard analysis demonstrated that high serum M2BPGi at 48 weeks was an independent risk factor for HCC development. A cutoff value of M2BPGi at 48 weeks > 1.5 showed an adjusted hazard ratio = 34.9 (95% confidence interval, 4.3–284.9). The 3- and 5-year cumulative incidence of HCC in patients with low M2BPGi were 0.9% and 4.2%, respectively, whereas those in patients with high M2BPGi were 10.1% and 25.6%, respectively (p < 0.001). In conclusion, Serum M2BPGi level at 48 weeks is a useful predictor for HCC development in patients with CHB who receive NA therapy.
Highlights
Persistent hepatitis B virus (HBV) infection is a major global health problem and an estimated 400 million individuals worldwide are HBV carriers
nucleot(s)ide analogue (NA) therapy has been reported to reduce the risk of hepatocellular carcinoma (HCC) development in patients with chronic hepatitis B (CHB)
The aim of this study was to evaluate factors that affect the occurrence of HCC in patients with CHB during NA therapy, with a special focus on the change and its predictive value of baseline and on-treatment serum Mac-2-binding protein glycosylation isomer (M2BPGi) levels
Summary
Persistent hepatitis B virus (HBV) infection is a major global health problem and an estimated 400 million individuals worldwide are HBV carriers. Oral administration of nucleot(s)ide analogues (NAs) are the most popular treatment strategy for patients with chronic hepatitis B (CHB) because of their excellent virologic efficacy and safety profile. Long-term administration of NAs suppresses HBV replication in most patients, resulting in biochemical remission and histological improvement, including the regression of fibrosis and cirrhosis [3,4]. NA therapy has been reported to reduce the risk of HCC development in patients with CHB. The long-term effect of lamivudine (LAM), the first generation of NAs, was demonstrated in a prospective placebo-controlled trial in 2004. The risk of HCC development was reduced by 55% in the LAM group, compared to a placebo group [5]
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