Serum YKL-40 is increased in patients with hepatic fibrosis

Background/Aims: YKL-40, a mammalian member of the chitinase family, is a lectin that binds heparin and chitin. The function of YKL-40 is unknown, but it may function in tissue remodelling. The aims of this study were to assess the level of circulating YKL-40 in patients with various kinds and degree of chronic liver disease and its possible relation to liver fibrosis. Methods: Serum YKL-40 levels were determined byradioimmunoassay in 129 patients with suspected liver disease and related to histological findings and immunohistochemical staining of YKL-40 in a liver biopsy taken simultaneously with the blood sample. Results: The median serum YKL-40 was highest in patients with alcoholic cirrhosis (532 μg/l), in particular in patients with additional alcoholic hepatitis (740 μg/l). Patients with alcoholic cirrhosis, post-hepatitic cirrhosis (425 μg/l) and non-cirrhotic fibrosis (330 μg/l) had significantly higher serum YKL-40 than normal subjects (102 μg/l), patients with fatty liver (195 μg/l) or patients with viral hepatitis without fibrosis (174 μg/l). Serum YKL-40 was significantly (p<0.001) related to the degree of liver fibrosis with the highest levels in patients with moderate (466 μg/l) to severe (676 μg/l) fibrosis. Serum YKL-40 was also increased (p=0.018) in patients with slight fibrosis (270 μg/l) compared to patients without fibrosis. Immunohistochemical analysis demonstrated positive staining for YKL-40 antigen in areas with fibrosis, particularly areas with active fibrogenesis. YKL-40 staining was never found in hepatocytes. Conclusions: Our study indicates that the increased serum YKL-40 in patients with liver disease of various degree and aetiology seems to reflect fibrosis and fibrogenesis.