Hepatitis C virus infection acquired in childhood

Department of Pediatrics, Hospital Universitario Ramón y Cajal, Universidad de Alcalá de Henares, Carretera de Colmenar, 28034, Madrid, Spain.
European Journal of Pediatrics (Impact Factor: 1.89). 03/2008; 167(2):219-24. DOI: 10.1007/s00431-007-0472-5
Source: PubMed


Hepatitis C virus (HCV) infection occurs less frequently in children than in adult patients, and the natural history, prognosis, and clinical significance of HCV infection in children are poorly defined. We report here a descriptive follow-up of the clinical course, biochemical data, and viral markers observed in 37 children with anti-HCV. Ten patients included in the study tested persistently negative for serum HCV-RNA (group 1) and 27 patients tested persistently positive (group 2). In group 1, serum alanine aminotransferase (ALT) was normal in all patients, while two patients had non-organ-specific autoantibodies. In group 2, serum ALT was elevated in 13 of 27 patients, and five patients had non-organ-specific autoantibodies. HCV genotype 1a and 1b were the most prevalent among HCV-RNA-positive patients. Twenty liver biopsies were carried out on 17 patients in our series (mean evolution time, 11.2 years; range, 3-21 years). The liver specimens showed mild necroinflammatory changes in most patients, and fibrosis was absent or low grade. Two HCV-RNA-positive patients became persistently HCV-RNA negative. Of the 26 children investigated, 7 (one in group 1, six in group 2) had a co-infection with hepatitis G virus. Conclusion Most children chronically infected with HCV were asymptomatic and presented only mild biochemical evidence of hepatic injury. Autoimmunity in the form of non-organ-specific autoantibodies was common. HCV in children induced mild changes in the liver with a low level of fibrosis and at a low rate of progression.

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Available from: Maria Luisa Mateos Lindemann, Feb 07, 2015
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    • "The natural history of chronic hepatitis C in children differs from that in adults since HCV infection is relatively benign, induces mild changes in the liver with a low level of fibrosis and a low rate of progression, and is rarely associated with severe or decompensate liver disease [22]. Bortolotti et al. [23] reported that hepatitis C in children is usually asymptomatic. "
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    ABSTRACT: Liver fibrosis and viremia are determinant factors for the treatment policy and its outcome in chronic hepatitis C virus (HCV) infection. We aimed to investigate serum level of inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4) and its relation to liver fibrosis and viremia in children with chronic HCV. For that, serum ITIH4 was measured by ELISA in 33 treatment-naive children with proved chronic HCV and compared according to different clinical, laboratory and histopathological parameters. Liver histopathological changes were assessed using Ishak score and compared with aspartate transaminase-to-platelet ratio (APRI) and FIB-4 indices as simple noninvasive markers of fibrosis. ITIH4 was measured in a group of 30 age- and sex-matched healthy children serving as controls. ITIH4 was significantly higher in patients than in controls (54.2±30.78 pg/ml vs. 37.21±5.39 pg/ml; P = 0.021). ITIH4, but not APRI or FIB-4, had a significant direct correlation with fibrosis stage (P = 0.015, 0.961 and 0.389 respectively), whereas, the negative correlation of ITIH4 with HCV viremia was of marginal significance (P = 0.071). In conclusion, serum levels of ITIH4 were significantly correlated with higher stages of liver fibrosis indicating a possible relation to liver fibrogenesis. The trend of higher levels of ITIH4 with lower levels of viral load points out a potential antiviral properties and further studies in this regard are worthwhile.
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    ABSTRACT: At least five groups have evaluated treatment for patients with decompensated cirrhosis preliminary to liver transplantation.330–334 In the earliest reported study, 32 patients awaiting liver transplantation were considered for antiviral treatment, but over one-half were found ineligible because of cytopenias.330 Among those treated with standard or low doses of interferon alfa-2b or low doses of both interferon alfa-2b and ribavirin, 33% became HCV RNA negative. Almost all developed adverse effects, most of which was graded as severe. In a second study, 30 patients with HCV-related cirrhosis destined for liver transplantation (half graded as CTP class A) were treated with interferon alfa-2b, 3 mU daily and ribavirin, 800 mg/day if their presumed time to liver transplantion was less than 4 months.331 After a median treatment duration of 12 weeks, 30% responded to treatment and then underwent liver transplantation, 2/3 of whom remained HCV RNA negative over a median follow-up period of 46 weeks. Sixty percent developed neutropenia. Reported in the same year was a study of 20 patients, most with genotype 1 infection, who were treated before transplantation for a mean of 14 months with interferon alfa-2b in a dose of 5 mU daily.332 At transplantation, 60% were HCV RNA negative, but only 20% remained negative after transplantation. A fourth study involved 124 patients with advanced cirrhosis (CTP classes A, B and C) treated mainly with interferon alfa-2b plus ribavirin, and less frequently, with pegylated interferon plus ribavirin.333 Treatment began with half doses that were increased incrementally as tolerated at 2 week intervals (referred to as a low accelerating dose regimen), and growth factors were used as needed. An SVR developed in 13% of patients with genotype 1 and in 50% with non-genotype 1 infections. Adverse events were frequent, requiring dose reductions or treatment termination, but among those who did become HCV RNA negative before transplantation, 80% remained negative 6 or more months after transplantation. The most recent study is the only one to include non-treated controls but these consisted of patients unwilling to participate in the study.334 The treatment administered was peginterferon alfa-2b, 1.0 μg/kg body weight given weekly and ribavirin, 800 to 1000 mg daily for 24 weeks. An SVR developed in 44% of the patients with HCV genotypes 2 or 3, and in 7% of those with genotypes 1 or 4. Treatment had to be discontinued in 20%, was reduced in 39%, and was tolerated in 41%. Over a 30-month follow-up period, decompensated events occurred in 83% of the controls, 62% of the non-responders, and in 23% of the patients who had developed an SVR. The conclusion of this study was that antiviral therapy can be life-saving, improves hepatic function, and that treatment seems appropriate for persons with genotype 2 and 3 infections particularly in those with cirrhosis, CTP classes A and B.
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