Serum Mac-2 binding protein glycosylation isomer predicts the activation of hepatic stellate cells after liver transplantation.


Journal

Journal of gastroenterology and hepatology
ISSN: 1440-1746
Titre abrégé: J Gastroenterol Hepatol
Pays: Australia
ID NLM: 8607909

Informations de publication

Date de publication:
Feb 2019
Historique:
received: 02 01 2018
revised: 11 07 2018
accepted: 30 07 2018
pubmed: 14 8 2018
medline: 31 7 2019
entrez: 14 8 2018
Statut: ppublish

Résumé

Serum Mac-2 binding protein glycosylation isomer (M2BPGi) is a novel fibrosis marker for various chronic liver diseases. We investigated the ability of M2BPGi to predict liver fibrosis in liver transplant (LT) recipients. A total of 116 liver biopsies were performed in 113 LT recipients. The serum level of M2BPGi was also measured on the same day. The median age at LT and liver biopsy was 1.1 and 11.8 years, respectively. Serum M2BPGi levels and liver fibrosis status using METAVIR fibrosis score were compared. Immunohistological evaluation by anti-α-smooth-muscle actin (αSMA) was performed, and the relationship between αSMA positive rate and serum M2BPGi levels was investigated. The median M2BPGi level was 0.78 (range, 0.22-9.50), and 65, 29, 16, 5, and 1 patient(s) had METAVIR fibrosis scores of F0, F1, F2, F3, and F4, respectively. In patients with F0 fibrosis, median M2BPGi level was 0.69 and was significantly lower than in patients with F1 (median 0.99, P < 0.01), F2 (median 1.00, P = 0.01), and F3 fibrosis (median 1.53, P < 0.01). Area-under-the-curve analysis of the ability of M2BPGi level to predict liver fibrosis grade were > F1: 0.716, > F2: 0.720, and > F3: 0.900. Three patients with acute cellular rejection showed high levels of M2BPGi, which decreased after the treatment. A positive correlation existed between M2BPGi levels and αSMA positive rate (r Mac-2 binding protein glycosylation isomer is a novel liver fibrosis marker in LT recipients and is also increased in patients with acute liver injuries, especially acute cellular rejection, even when fibrosis is absent.

Sections du résumé

BACKGROUND AND AIM OBJECTIVE
Serum Mac-2 binding protein glycosylation isomer (M2BPGi) is a novel fibrosis marker for various chronic liver diseases. We investigated the ability of M2BPGi to predict liver fibrosis in liver transplant (LT) recipients.
METHODS METHODS
A total of 116 liver biopsies were performed in 113 LT recipients. The serum level of M2BPGi was also measured on the same day. The median age at LT and liver biopsy was 1.1 and 11.8 years, respectively. Serum M2BPGi levels and liver fibrosis status using METAVIR fibrosis score were compared. Immunohistological evaluation by anti-α-smooth-muscle actin (αSMA) was performed, and the relationship between αSMA positive rate and serum M2BPGi levels was investigated.
RESULTS RESULTS
The median M2BPGi level was 0.78 (range, 0.22-9.50), and 65, 29, 16, 5, and 1 patient(s) had METAVIR fibrosis scores of F0, F1, F2, F3, and F4, respectively. In patients with F0 fibrosis, median M2BPGi level was 0.69 and was significantly lower than in patients with F1 (median 0.99, P < 0.01), F2 (median 1.00, P = 0.01), and F3 fibrosis (median 1.53, P < 0.01). Area-under-the-curve analysis of the ability of M2BPGi level to predict liver fibrosis grade were > F1: 0.716, > F2: 0.720, and > F3: 0.900. Three patients with acute cellular rejection showed high levels of M2BPGi, which decreased after the treatment. A positive correlation existed between M2BPGi levels and αSMA positive rate (r
CONCLUSION CONCLUSIONS
Mac-2 binding protein glycosylation isomer is a novel liver fibrosis marker in LT recipients and is also increased in patients with acute liver injuries, especially acute cellular rejection, even when fibrosis is absent.

Identifiants

pubmed: 30101431
doi: 10.1111/jgh.14438
doi:

Substances chimiques

Antigens, Neoplasm 0
Biomarkers 0
Membrane Glycoproteins 0
TAA90K protein, human 0

Types de publication

Journal Article

Langues

eng

Pagination

418-424

Informations de copyright

© 2018 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.

Auteurs

Naoya Yamada (N)

Department of Transplant Surgery, Jichi Medical University, Tochigi, Japan.
Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan.

Takumi Katano (T)

Department of Transplant Surgery, Jichi Medical University, Tochigi, Japan.

Yuta Hirata (Y)

Department of Transplant Surgery, Jichi Medical University, Tochigi, Japan.

Noriki Okada (N)

Department of Transplant Surgery, Jichi Medical University, Tochigi, Japan.

Yukihiro Sanada (Y)

Department of Transplant Surgery, Jichi Medical University, Tochigi, Japan.

Yoshiyuki Ihara (Y)

Department of Transplant Surgery, Jichi Medical University, Tochigi, Japan.

Taizen Urahashi (T)

Department of Transplant Surgery, Jichi Medical University, Tochigi, Japan.

Kentaro Ushijima (K)

Division of Clinical Pharmacology, Department of Pharmacology, Jichi Medical University, Tochigi, Japan.

Tadayoshi Karasawa (T)

Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan.

Masafumi Takahashi (M)

Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan.

Koichi Mizuta (K)

Department of Transplant Surgery, Jichi Medical University, Tochigi, Japan.

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