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Overexpressed cyclo‐oxygenase‐2 in the background liver is associated with the clinical course of hepatitis C virus‐related cirrhosis patients after curative surgery for hepatocellular carcinoma
Author(s) -
Morinaga Soichiro,
Tarao Kazuo,
Yamamoto Yuji,
Nakamura Yoshiyasu,
Rino Yasushi,
Miyakawa Kaoru,
Ohkawa Shinichi,
Akaike Makoto,
Sugimasa Yukio,
Takemiya Shoji
Publication year - 2007
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2006.04367.x
Subject(s) - medicine , hepatocellular carcinoma , cirrhosis , gastroenterology , hepatitis c virus , proportional hazards model , hepatitis c , hepatectomy , surgery , immunology , virus , resection
Background: The probable role of cyclo‐oxygenase‐2 (COX‐2) in the development of hepatocellular carcinoma (HCC) in patients with chronic liver diseases has been accepted to be relevant. The purpose of the present study was to determine whether overexpressed COX‐2 in the background liver affects the clinical course of hepatitis C virus (HCV)‐related cirrhosis patients after curative surgery for HCC. Methods: Twenty‐nine clinical stage I HCC patients with HCV‐related cirrhosis, who underwent curative surgery, were enrolled in the present study (22 men and seven women, age range 53–73 years; follow‐up period; range 22–159 months, median 61 months). The COX‐2 expression in the cirrhotic liver was examined by immunohistochemistry using the avidin–biotin–peroxidase complex technique on paraffin‐embedded formalin‐fixed tissue. The COX‐2 expression was scored, then correlated with monitored alanine aminotransferase (ALT) levels during the follow‐up period after surgery, response to alternative therapy aiming to improve elevated ALT levels, and recurrence/survival after surgery. Results: The COX‐2 expression scores were significantly higher in the high‐ALT group than in the low‐ALT group (Mann–Whitney, P = 0.010), and were significantly higher in non‐responders to the alternative therapy than in responders (Mann–Whitney, P = 0.028). The higher COX‐2 expression in the cirrhotic liver was the significant independent risk factor for residual liver recurrence (Cox multivariate analysis, P = 0.014), but not for survival. Conclusions: Overexpressed COX‐2 in the background liver may play an important role in prolonged acceleration of necroinflammation, resistance to the alternative therapy, and recurrence/new development of HCC in HCV‐related cirrhosis patients.