TY - JOUR
T1 - Progression of fibrosis in hepatitis C with and without schistosomiasis
T2 - Correlation with serum markers of fibrosis
AU - Kamal, Sanaa M.
AU - Turner, Bradley
AU - He, Qi
AU - Rasenack, Jens
AU - Bianchi, Leonardo
AU - Al Tawil, Ahmed
AU - Nooman, Ahmed
AU - Massoud, Mahmoud
AU - Koziel, Margaret James
AU - Afdhal, Nezam H.
PY - 2006/4
Y1 - 2006/4
N2 - Serial liver biopsies are the gold standard by which the progression of fibrosis is evaluated. This longitudinal cohort study assessed the different rates in the progression of fibrosis using serial liver biopsies and serum fibrosis markers YKL-40 and PIIINP and the cytokines, transforming growth factor beta (TGF-β) and tumor necrosis factor alpha (TNF-α). A 10-year cohort study was performed in patients with hepatitis C virus (HCV) alone or HCV and schistosomiasis. Patients were enrolled at the time of acute HCV infection and prospectively evaluated with two liver biopsies (at entry and end of follow-up), and true rates in the progression of fibrosis were calculated per year. Serum YKL-40, N-terminal propeptide of collagen III (PIIINP), TGF-β, and TNF-α were measured, as well as the expression of TGF-β, TNF-α, and YKL-40 mRNA in liver tissue. A significant increase in the progression rates of fibrosis occurred in the coinfected group (0.61 ± 0.13) compared with the HCV monoinfection group (0.1 ± 0.06; P < .001)). The progression of fibrosis rate/year had a direct linear correlation for YKL-40 (r = 0.892, P < .001) and for PIIINP (r = 0.577, P < .01). YKL-40 showed a linear correlation with TGF-β (r = 0.897, P < .001). Hepatic mRNA levels of YKL-40 and TGF-β correlated with the serum levels, confirming a hepatic source for the elevated serum levels. In conclusion, serial cytokine and fibrosis markers can accurately determine the rate at which fibrosis is progressing, identifying both those with rapid fibrosis and those with stable disease.
AB - Serial liver biopsies are the gold standard by which the progression of fibrosis is evaluated. This longitudinal cohort study assessed the different rates in the progression of fibrosis using serial liver biopsies and serum fibrosis markers YKL-40 and PIIINP and the cytokines, transforming growth factor beta (TGF-β) and tumor necrosis factor alpha (TNF-α). A 10-year cohort study was performed in patients with hepatitis C virus (HCV) alone or HCV and schistosomiasis. Patients were enrolled at the time of acute HCV infection and prospectively evaluated with two liver biopsies (at entry and end of follow-up), and true rates in the progression of fibrosis were calculated per year. Serum YKL-40, N-terminal propeptide of collagen III (PIIINP), TGF-β, and TNF-α were measured, as well as the expression of TGF-β, TNF-α, and YKL-40 mRNA in liver tissue. A significant increase in the progression rates of fibrosis occurred in the coinfected group (0.61 ± 0.13) compared with the HCV monoinfection group (0.1 ± 0.06; P < .001)). The progression of fibrosis rate/year had a direct linear correlation for YKL-40 (r = 0.892, P < .001) and for PIIINP (r = 0.577, P < .01). YKL-40 showed a linear correlation with TGF-β (r = 0.897, P < .001). Hepatic mRNA levels of YKL-40 and TGF-β correlated with the serum levels, confirming a hepatic source for the elevated serum levels. In conclusion, serial cytokine and fibrosis markers can accurately determine the rate at which fibrosis is progressing, identifying both those with rapid fibrosis and those with stable disease.
UR - https://www.scopus.com/pages/publications/33645986652
U2 - 10.1002/hep.21117
DO - 10.1002/hep.21117
M3 - Article
C2 - 16557547
AN - SCOPUS:33645986652
SN - 0270-9139
VL - 43
SP - 771
EP - 779
JO - Hepatology
JF - Hepatology
IS - 4
ER -
