Hepatol Int. 2019 Jan 22. doi: 10.1007/s12072-019-09928-5. [Epub ahead of print]
Correlation of serum Mac-2-binding protein glycosylation isomer (M2BPGi) and liver stiffness in chronic hepatitis B infection.
Mak LY1, Wong DK2,3, Seto WK4,5, Ning Q6, Cheung KS2, Fung J2,3, Lai CL2,3, Yuen MF7,8.
Author information
1
Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road 102, Hong Kong, China. [email protected].
2
Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road 102, Hong Kong, China.
3
State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong, China.
4
Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road 102, Hong Kong, China. [email protected].
5
State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong, China. [email protected].
6
Institute of Infectious Disease, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
7
Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road 102, Hong Kong, China. [email protected].
8
State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong, China. [email protected].
Abstract
BACKGROUND AND AIM:
Mac-2-binding protein glycosylation isomer (M2BPGi) is a novel serum diagnostic marker for liver fibrosis in various liver diseases. We aimed to evaluate its role in assessment of liver fibrosis in chronic hepatitis B infection (CHB) with reference to liver stiffness measurement (LSM).
METHODS:
CHB patients with LSM by transient elastography technology and retrievable serum samples were recruited. Ten-year re-assessments of LSM and M2BPGi were repeated in a patient subgroup.
RESULTS:
240 CHB patients (M:F = 116:124; median age 47.5 years) were recruited. The median M2BPGi values for F0/F1/F2, F3 and F4 progressively increased with more advanced stages of liver fibrosis: 0.39, 0.46 and 0.82 COI, respectively (p < 0.01). M2BPGi levels correlated well with liver stiffness (r = 0.611), FIB-4 (r = 0.616), and strongly with APRI (r = 0.825) (all p < 0.001). Using cut-off values of 0.605 and 0.615 COI, the AUROCs were 0.754 and 0.799 for ≥ F3 and F4, respectively. M2BPGi identified one-quarter patients at risk of advanced fibrosis/cirrhosis otherwise classified into 'grey area' by LSM. In 86 patients with reassessment LSM, 21 (24.4%) showed significant fibrosis regression with corresponding decline in median M2BPGi level (- 0.11 COI) compared with the increase of +0.03 COI in patients without significant fibrosis regression (p = 0.011). Male gender, older age, use of potent antiviral therapy and change in serum M2BPGi were independently associated with significant fibrosis regression.
CONCLUSIONS:
Serum M2BPGi can risk-stratify CHB patients whose liver stiffness fell into the 'grey area'. Significant fibrosis regression occurring in one-quarter patients was reflected by a reduction in M2BPGi levels at 10-year interval.
KEYWORDS: