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Hepatol Commun. 2019 Feb 8;3(4):493-503. doi: 10.1002/hep4.1321. eCollection 2019 Apr.

Mac-2 Binding Protein Glycosylation Isomer as a Hepatocellular Carcinoma Marker in Patients With Chronic Hepatitis B or C Infection.

Author information

1
Department of Medicine Stanford University Medical Center Palo Alto CA.
2
Division of Gastroenterology and Hepatology Fu Jen Catholic University Hospital New Taipei Taiwan.
3
School of Medicine Fu Jen Catholic University New Taipei Taiwan.
4
Division of Gastroenterology and Hepatology E-Da Hospital Kaohsiung Taiwan.
5
Graduate Institute of Clinical Medical Science China Medical University Taichung Taiwan.
6
Department of Virology and Liver Unit Nagoya City University Graduate School of Medical Sciences Nagoya Japan.
7
Institute of Statistical Science Academia Sinica Taipei Taiwan.
8
Hepatobiliary Division, Department of Internal Medicine Kaohsiung Medical University Hospital, Kaohsiung Medical University Kaohsiung Taiwan.
9
Division of Gastroenterology and Hepatology Stanford University Medical Center Palo Alto CA.

Abstract

Mac-2 binding protein glycosylation isomer (M2BPGi) is a novel glycoprotein biomarker that correlates with liver fibrosis. It has been investigated in East Asian populations as a hepatocellular carcinoma (HCC) biomarker. We assessed M2BPGi as an HCC biomarker in an ethnically diverse cohort of patients with chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infection. We enrolled 947 treatment-naive patients mono-infected with HBV or HCV without HCC at baseline. Biomarker levels were measured from baseline sera and correlated with longitudinal clinical data. The primary outcome was HCC occurrence during long-term follow-up. Median M2BPGi was significantly higher among patients with cirrhosis (2.67 versus 0.80; P < 0.001) and patients who developed HCC (3.22 versus 1.16; P < 0.001). The area under the receiver operating characteristic (AUROC) for M2BPGi and alpha-fetoprotein (AFP) was similar overall (0.77 versus 0.72; P = 0.15), but M2BPGi outperformed AFP among patients with HBV (0.84 versus 0.75; P = 0.02). M2BPGi performed poorly among patients with HCV (AUROC, 0.51). M2BPGi was an independent predictor of HCC among patients with HBV but not among patients with HCV. M2BPGi performed better in patient subgroups with a lower prevalence of cirrhosis. Conclusion: In our HBV cohort, M2BPGi was more effective than AFP in predicting HCC and was an independent predictor of HCC. However, M2BPGi had limited predictive value in our HCV cohort, likely due to a high cirrhosis burden in this cohort. Further studies are needed to evaluate M2BPGi as an HCC biomarker in broader patient populations with more diverse disease etiology, non-Asian ethnicity, and more advanced fibrosis.

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