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Serum amino‐terminal propeptide of type III procollagen and 7S domain of type IV collagen correlate with hepatic iron concentration in patients with chronic hepatitis C following α‐interferon therapy
Author(s) -
Shimizu Ichiro,
Omoya Toshihiro,
Takaoka Tukasa,
Wada Satoshi,
Wada Hisanori,
Taoka Masayo,
Hayashi Hideki,
Hayashi Shigehito,
Honda Hirohito,
Sano Nobuya,
Ito Susumu
Publication year - 2001
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 - 10.1046/j.1440-1746.2001.02402.x
Subject(s) - medicine , procollagen peptidase , alpha interferon , liver biopsy , gastroenterology , alanine transaminase , hepatitis , interferon , alpha (finance) , biopsy , immunology , surgery , construct validity , patient satisfaction
Abstract Background: It has been reported that chronic infection with hepatitis C virus is associated with excess iron deposits in the liver of subjects who are neither alcoholics nor recipients of blood transfusions. However, little is known about the relationship between hepatic iron concentration (HIC) and the serum levels of hepatic fibrogenesis markers, which were caused by interferon therapy for chronic hepatitis C. Therefore, changes in the serum amino‐terminal propeptide of type III procollagen (P‐III‐P) and the 7S domain of type IV collagen (7S‐IV) in 16 patients treated with α‐interferon (IFN‐α) were studied, and their HIC and histological assessment evaluated. Hepatic iron concentrations were measured by using liver biopsy specimens obtained before and 6 months after the cessation of treatment. Methods and Results: Eight subjects (50%) who had normal alanine transaminase levels at 6 months after therapy showed significantly lowered HIC, and attenuated hepatic iron staining with decreased serum levels of P‐III‐P and 7S‐IV compared to the remaining subjects. The HIC was significantly correlated with the serum levels of P‐III‐P and 7S‐IV in all subjects. Conclusions: These findings suggest that IFN‐α treatment may decrease stimuli for fibrogenesis, at least in part, by reducing the hepatic iron deposition in patients with chronic hepatitis C.