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Quantitative measurements of M2BPGi depend on liver fibrosis and inflammation

  • Original Article―Liver, Pancreas, and Biliary Tract
  • Published:
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Abstract

Background

The relationship between liver fibrosis and inflammation and Mac-2-binding protein glycosylation isomer (M2BPGi) in patients with chronic liver disease (CLD) other than hepatitis C remains uncertain, owing to the limitations of qualitative methods. Here, we evaluated the influence of liver fibrosis and inflammation on quantitative M2BPGi (M2BPGi-Qt) in CLD, considering each etiology.

Methods

We recruited 1373 patients with CLD. To evaluate the influence of liver fibrosis and inflammation on M2BPGi-Qt levels, we assessed M2BPGi-Qt levels at each fibrosis and activity stage within different etiologies of CLD based on pathological findings. Subsequently, we evaluated if the accuracy of fibrosis staging based on M2BPGi-Qt could be improved by considering the influence of liver inflammation.

Results

In patients with viral hepatitis, non-alcoholic fatty liver disease, and primary biliary cholangitis, the median M2BPGi-Qt levels increased liver fibrosis progression. Median M2BPGi-Qt levels were not associated with the degree of fibrosis in patients with autoimmune hepatitis (AIH). Median M2BPGi-Qt levels increased with the progression of liver activity in all etiologies. A significant difference was found at each stage in AIH. Considering the liver inflammation, we established an algorithm, M2BPGi-Qt, to determine the alanine aminotransferase-to-platelet ratio (MAP-R) in liver cirrhosis (LC). The area under the receiver operating characteristic curve (AUC) of MAP-R was higher than that of the M2BPGi-Qt for detecting LC (AUC MAP-R = 0.759 and M2BPGi-Qt = 0.700, p < 0.001).

Conclusions

The quantitative measurement system for M2BPGi depends on liver fibrosis and inflammation, regardless of etiology. Liver inflammation complicates the interpretation of M2BPGi-Qt results when assessing the fibrosis stage.

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Acknowledgements

We thank STATISTA Corporation for assisting with the statistical analyses in this study.

This study was supported by Sysmex Corporation.

Funding

This study was supported by Sysmex Corporation.

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Authors and Affiliations

Authors

Contributions

HU, KY, NI, MM, TK, TS, SJ, and HT collected and analyzed the data; HU and MM drafted the manuscript; KS designed and supervised the study; KY, TK, and HY offered technical or material support. All authors have read and approved the final version of the manuscript.

Corresponding author

Correspondence to Haruki Uojima.

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Conflict of interest

Takeji Umemura received lecture fees from AbbVie GK and Gilead Sciences and research grants from AbbVie GK, Eisai Co., Otsuka Pharmaceutical Co., and Tosoh Co. Masayuki Kurosaki received lecture fees from AbbVie, Eisai, Chugai, AstraZeneca, Lilly, and Takeda Co. Masashi Mizokami received lecture fees from Sysmec Co. Yasuhiro Asahina received lecture fees from Fujirebi Inc. and Abbott Japan LLC. Takumi Kawaguchi received lecture fees from Taisho Pharmaceutical Co., Kowa Company, Otsuka Pharmaceutical Co., Eisai Co., Janssen Pharmaceutical K.K., AbbVie GK., ASKA Pharmaceutical Co., and EA Pharma Co., and a research grant from Eisai Co., Ltd.

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Uojima, H., Yamasaki, K., Sugiyama, M. et al. Quantitative measurements of M2BPGi depend on liver fibrosis and inflammation. J Gastroenterol (2024). https://doi.org/10.1007/s00535-024-02100-3

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  • DOI: https://doi.org/10.1007/s00535-024-02100-3

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