Changes in Serum Fibrogenesis Markers During Interferon Therapy for Chronic Hepatitis Type C

Abstract

KAZUNOBU ISHIBASHI, TORU KASHIWAGI, AKIHIKO ITO, YOSHIO TANAKA, MASAFUMI NAGASAWA, TAKASHI TOYAMA, SHINITI OZAKI, MASAFUMI NAITO, AND MASAYOSHI AZUMA the changes in serum levels of hepatic fibrogenesis markers We serially measured the levels of serum N-terminal caused by interferon therapy for chronic hepatitis. 9,10peptide of type III procollagen (PIIINP), the 7S domain In this study, the serum levels of PIIINP, IV-7S, and HA of type IV collagen (IV-7S), and hyaluronate (HA) before were determined before, during, and after interferon therapy (0 month), at the end (6 months), and 24 weeks after the in chronic hepatitis type C, and the relationship between the end of interferon therapy (12 months) in patients with levels of these markers and the effectiveness of interferon chronic hepatitis type C to estimate the effects of intertherapy was investigated. feron alfa (IFN-a) divided into three groups: sustained complete response 21-67 years) who had persistently elevated ALT levels (more than (CR-S), complete response with rebound (CR-R), and 1.5 times the normal upper limit; the normal levels of ALT range nonresponse (NR). Serum PIIINP, IV-7S, and HA levels between 8 and 35 IU/L) for at least 6 months. The mean ALT level were significantly decreased and reached normal levels at initiation of IFN-a therapy was 115.2 { 77.6 IU/L (mean { SD). at 12 months in CR-S; only IV-7S levels were significantly All patients were positive for HCV RNA (assayed by RT-PCR using primers derived from the 5-untranslated region) and anti-HCV (asdecreased at 12 months in CR-R, whereas these levels sayed by Abbott HCV-EIA second-generation kit, Abbott Laboraremained abnormally high in the NR. These results sugtories, North Chicago, IL) in serum. The route of HCV infection in-

Evaluation of serum biomarkers of fibrosis and injury in Egyptian patients with chronic hepatitis C

“…Most previous studies reported HA levels could not predict grade of hepatic inflammation. However, Ishibashi et al reported HA levels correlated with inflammatory changes in their patients' biopsies [10]. Our initial analysis also showed that HA and YKL-40 levels could predict hepatic inflammation, but after adjusting for fibrosis, these associations were not statistically significant.…”

“…Noninvasive reliable biomarkers for diagnosing and grading hepatic fibrosis and to monitor outcome of treatment and the course of HCV infection are an active area of clinical interest [3,4,[8][9][10][11][12][13][14][15][16][17][18][19][20][21][22]. This study's objective was to evaluate individually and in combination the ability of routine laboratory tests and two serum biomarkers of extracellular matrix to predict hepatic fibrosis, inflammation and steatosis and compare them with liver biopsy findings in Egyptian patients being evaluated for a clinical trial comparing antiviral therapy for genotype-4 HCV.…”

Early decrease in serum IV-7S levels during IFN treatment predicts anti-fibrogenic effect in nonresponders with chronic hepatitis C

“…9,11 On the other hand, the effect of IFN on the long-term outcome of patients, including the suppression of progression to cirrhosis or the prevention of HCC, has recently been reported. 9,11,[17][18][19][20][21][22][25][26][27] These reports suggest that IFN treatment has a suppressive effect on disease progress, irrespective of whether or not HCV is eradicated.…”

“…[12][13][14][15][16] Although IFN is known to lower the levels of these serum markers of fibrogenesis by improving hepatic fibrosis, [17][18][19][20][21][22] there has, as yet, been no report which has concerned itself with the clinical significance of an early decrease in serum levels of these markers during IFN treatment.…”

An independent and prospective comparison of two commercial fibrosis marker panels (HCV FibroSURE and FIBROSpect II) during albinterferon alfa‐2b combination therapy for chronic hepatitis C

“…Retrospective studies of patients with CHC who received combination therapy have demonstrated that the FT-AT index decreased in patients who achieved a sustained virological response (SVR), and that there was significant concordance between FT-AT and fibrosis stage [19,20]. Changes in other serum markers have also been demonstrated following interferon (IFN)-based therapy, but results have been variable and have not been validated prospectively [21][22][23][24]. Although none of the currently available marker panel algorithms were designed to detect subtle changes in matrix turnover with treatment, early changes in marker indices may be important for predicting eventual antifibrotic responses to therapy.…”