Elevated serum CK18 levels in chronic hepatitis C patients are associated with advanced fibrosis but not steatosis

Jazwinski, A. B., Thompson, A. J., Clark, P. J., Naggie, S., Tillmann, H. L. and Patel, K. (2012) Elevated serum CK18 levels in chronic hepatitis C patients are associated with advanced fibrosis but not steatosis. Journal of Viral Hepatitis, 19 4: 278-282. doi:10.1111/j.1365-2893.2011.01546.x

Author Jazwinski, A. B.
Thompson, A. J.
Clark, P. J.
Naggie, S.
Tillmann, H. L.
Patel, K.
Title Elevated serum CK18 levels in chronic hepatitis C patients are associated with advanced fibrosis but not steatosis
Journal name Journal of Viral Hepatitis   Check publisher's open access policy
ISSN 1352-0504
Publication date 2012-04
Sub-type Article (original research)
DOI 10.1111/j.1365-2893.2011.01546.x
Open Access Status
Volume 19
Issue 4
Start page 278
End page 282
Total pages 5
Place of publication West Sussex United Kingdom
Publisher Wiley-Blackwell Publishing
Language eng
Subject 2721 Hepatology
2725 Infectious Diseases
2406 Virology
Formatted abstract
Cytokeratin-18 (CK-18) is a major intermediate filament protein in liver cells. The M30 fragment of CK-18 has been identified as a useful marker of apoptosis associated with fibrosis and steatosis in nonalcoholic steatohepatitis (NASH). We sought to assess the relationship of this marker and steatosis in a cohort of adult patients with chronic hepatitis C. The study cohort included sera from 267 treatment-naîve chronic hepatitis C (CHC) patients and 100 healthy controls with normal alanine aminotransferase (ALT). Biopsies from CHC patients were assessed for METAVIR fibrosis stage, Histology Activity Index (HAI) inflammation score and steatosis grade by expert histopathologists. The M30 fragment of CK-18 was quantified by ELISA. Wilcoxon Rank Sum, Spearman Correlation and Linear Regression tests were performed for statistical analysis. Median CK-18 levels were higher in CHC patients compared to controls (411 vs 196 U/L, P < 0.0001). Fibrosis stage was associated with increasing serum CK-18 levels (P = 0.015) and CK-18 levels were higher for F2-F4 vs F0-F1 (500 vs 344 U/L; P = 0.001). There was no association between CK-18 and increasing steatosis grade 1, 2 or 3 (460.7 vs 416.8 vs 508.3 U/L; P = 0.35) and presence or absence of steatosis (445.3 vs 365.8 U/L; P = 0.075). Fibrosis stage was independently associated with serum M30 in a multivariable linear regression model (P = 0.03). CK-18 levels were higher in CHC compared to healthy controls and associated with hepatic fibrosis. There was no difference in CK-18 M30 levels between CHC patients with and without steatosis. Although apoptosis may still contribute to hepatitis C virus (HCV)-mediated steatosis, our results suggest that serum CK-18 will not be a clinically useful test for identifying significant steatosis in CHC.
Keyword Apoptosis
Chronic hepatitis C
Cytokeratin 18
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Medicine Publications
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