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Sci Rep. 2016 Oct 14;6:35282. doi: 10.1038/srep35282.

Serum YKL-40 as a marker of liver fibrosis in patients with non-alcoholic fatty liver disease.

Author information

1
The Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Ichikawa, Japan.
2
Department of Gastroenterology, Juntendo University School of Medicine, Hongo, Bunkyo, Tokyo, Japan.
3
Department of Pathology and Laboratory Medicine, Kohnodai Hospital, National Center for Global Health and Medicine, Ichikawa, Japan.
4
Division of Gastroenterology, Department of Internal Medicine, Nippon Medical School Chiba Hokusoh Hospital, Inzai, Japan.
5
Department of Gastroenterology and Metabolism, Hiroshima University, Hiroshima, Japan.
6
Department of Gastroenterology and Hepatology, JA Hiroshima General Hospital, Hiroshima, Japan.
7
Division of Gastroenterology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
8
Division of Gastroenterology, Department of Medicine, Kurume University School of Medicine, Kurume, Japan.
9
Department of Gastroenterology, National Center for Global Health and Medicine, Central Hospital, Tokyo, Japan.

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a common cause of chronic non-viral liver disease. YKL-40, chitinase-like protein expressed in multiple tissues including liver, is involved in cell proliferation, inflammation and remodeling of the extracellular matrix. The aim of this study was to assess whether serum YKL-40 levels are associated with liver fibrosis in NAFLD patients. Serum YKL-40 levels were quantified in 111 NAFLD patients and 23 HCC patients with NAFLD. To identify the source of YKL-40, immunofluorescence staining of liver specimens from NAFLD patients was performed. Serum YKL-40 levels in NAFLD patients increased in accordance with the progression of liver fibrosis. Multivariate analysis revealed that YKL-40 was one of the independent factors significantly associated with severe fibrosis (F3-4). We established a new predictive model for fibrosis of NAFLD, using logistic regression analysis: YKL-40 based fibrosis score = -0.0545 + type IV collagen 7s * 0.3456 + YKL-40 * 0.0024. Serum YKL-40 levels of HCC patients with non-cirrhotic NAFLD were significantly higher than those without HCC. Immunofluorescence staining showed that YKL-40 was expressed by macrophages in liver tissue of NAFLD patients. In conclusion, macrophage-derived YKL-40 is a feasible biomarker of liver fibrosis in NAFLD patients.

PMID:
27739482
PMCID:
PMC5064386
DOI:
10.1038/srep35282
[Indexed for MEDLINE]
Free PMC Article

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