Quantitative measurements of M2BPGi depend on liver fibrosis and inflammation

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 live...

Full description

Saved in:
Bibliographic Details
Published inJournal of gastroenterology Vol. 59; no. 7; pp. 598 - 608
Main Authors Uojima, Haruki, Yamasaki, Kazumi, Sugiyama, Masaya, Kage, Masayoshi, Ishii, Norihiro, Shirabe, Ken, Hidaka, Hisashi, Kusano, Chika, Murakawa, Miyako, Asahina, Yasuhiro, Nishimura, Takashi, Iijima, Hiroko, Sakamoto, Kazumasa, Ito, Kiyoaki, Amano, Keisuke, Kawaguchi, Takumi, Tamaki, Nobuharu, Kurosaki, Masayuki, Suzuki, Takanori, Matsuura, Kentaro, Taketomi, Akinobu, Joshita, Satoru, Umemura, Takeji, Nishina, Sohji, Hino, Keisuke, Toyoda, Hidenori, Yatsuhashi, Hiroshi, Mizokami, Masashi
Format Journal Article
LanguageEnglish
Published Singapore Springer Nature Singapore 01.07.2024
Springer Nature B.V
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary: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.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0944-1174
1435-5922
1435-5922
DOI:10.1007/s00535-024-02100-3