Correlation of serum Mac-2-binding protein glycosylation isomer (M2BPGi) and liver stiffness in chronic hepatitis B infection

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.