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Serum Cystatin C Correlates Negatively With Viral Load in Treatment-naïve Children With Chronic Hepatitis C

Behairy, Behairy E.*; Saber, Magdy A.*; Elhenawy, Ibrahim A.*; Abou-Zeinah, Sahar S.*; El-Sharawy, Ahmed A.; Sira, Mostafa M.*

Journal of Pediatric Gastroenterology & Nutrition: March 2012 - Volume 54 - Issue 3 - p 364–368
doi: 10.1097/MPG.0b013e31823e98c2
Original Articles: Hepatology and Nutrition

Objectives: Hepatitis C virus (HCV) infection is a serious health problem that causes chronic infection in up to 85% of cases. HCV nonstructural (NS) cysteine protease, NS2/3, is required for viral replication in vivo. Cystatin C is a naturally occurring cysteine protease inhibitor in human cells. We aimed to investigate the relation between serum levels of cystatin C and HCV viremia in treatment-naïve children with chronic hepatitis C.

Methods: Serum cystatin C levels were measured in 27 children with chronic hepatitis C and determined their relation with liver functions, histopathological parameters, and hepatitis C viral load. Serum cystatin C was compared with that of 25 age- and sex-matched healthy controls.

Results: Cystatin C was significantly higher in patients than in controls (1.4 ± 0.47 vs 0.99 ± 0.49; P = 0.006), and in those with low viremia than in those with moderate viremia (1.55 ± 0.41 vs 0.99 ± 0.43; P = 0.013). Cystatin C was not correlated with histopathological findings in liver biopsy (P > 0.05 for all). In addition, there was no significant difference of cystatin C levels in patients with normal versus those with elevated transaminases (P > 0.05). Of importance, cystatin C correlated negatively with viral load (P < 0.0001).

Conclusions: Cystatin C levels correlated negatively with HCV viremia. This finding may reflect an inhibitory effect of cystatin C on HCV replication through inhibiting its NS2/3 and tempting for further studies for cystatin C as a possible adjuvant therapy for HCV infection.

*Department of Pediatric Hepatology

Department of Clinical Pathology, National Liver Institute, Menofiya University, Shebin El-koom, Menofiya, Egypt.

Address correspondence and reprint requests to Mostafa M. Sira, Department of Pediatric Hepatology, National Liver Institute, Menofiya University, 32511 Shebin El-koom, Menofiya, Egypt (e-mail:

Received 13 July, 2011

Accepted 24 October, 2011

The present study was funded by the Ministry of Health, Egypt, in collaboration with the National Liver Institute, Menofiya University, Egypt, without any particular role in the study design, recruitment of individuals, data analysis, or the writing of the report.

The authors report no conflicts of interest.

Copyright 2012 by ESPGHAN and NASPGHAN