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CHILDHOOD HEPATITIS C VIRUS INFECTION
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Journal of Gastroenterology and Hepatology
Volume 20 Page 1948 - December 2005
LETTERS TO THE EDITOR
Donatella Comparcola*, Valerio Nobili*, Maria Rita Sartorelli*, Matilde Marcellini*, Francesca Cainelli andSandro Vento
*Department of Liver Diseases, Bambino Gesu Children's Hospital, Rome and Department of Pathology, University of Verona, Verona, Italy
To the Editor,
Rerksuppaphol et al. have recently reported their retrospective analysis of 31 children with hepatitis C virus (HCV) infection.1 We have carried out a similar analysis of our own cases, reviewing retrospectively the medical records of the much higher number (54) of children followed at Bambino Gesu Children's Hospital for chronic HCV over a 10-year period. The analysis included epidemiology (source of infection), virological data (genotype), histology (when available), ultrasound examinations, eventual antiviral treatments and their outcomes.
Of the children in the present study, there were 28 males and 26 females. Their ages, at the time of data analysis, ranged between 6 and 26 years (mean 14.5). The patients whose ages were above 18 years were first seen at our unit several years earlier, during their childhood, and continued their follow up with us.
Vertical transmission was responsible for HCV acquisition in 19 cases, transfusions were likely to be responsible in 17 cases and surgical procedures in seven cases, whereas in 11 cases no factors were identified. Vertical transmission was deemed responsible if either the mother was anti-HCV antibody positive and the child was persistently antibody-positive for over 2 years after birth or (once tests for HCV-RNA became available) the mother was HCV-RNA positive in the last 3 months of pregnancy and the child was HCV-RNA positive at birth and thereafter, and mother and child had the same HCV genotype. All the mothers of the transfused children were anti-HCV antibody negative. The mean age of the children at the time of transfusion was 6.3 months (range 15 days-1 year).
All the children were HBsAg-negative. The prevailing HCV genotype was 1b (25 cases, 46.2%). Autoantibodies were detected in 13 patients: antinuclear antibodies in 11 cases, antiliver-kidney microsomes type 1 in two.
Ultrasound examination showed steatosis in 11/54 cases (20.3%).
Liver biopsy was carried out at least once in 40 patients. The results indicated the presence of cirrhosis in only one case, whereas mild chronic active hepatitis (CAH) was detected in 29 patients and moderate CAH in five. Steatosis was found in five cases. In the four cases where histology was available twice, no progression of liver disease was found 6-9 years apart. Autoantibody-positive cases did not differ histologically in respect of negative cases. The only patient with cirrhosis was alive 8 years after the histological diagnosis.
Of the untreated patients, 4/28 spontaneously became persistently HCV-RNA negative during follow up.
Interferon alpha-2a was given to 26 patients (with ribavirin in three cases). Sustained response (normal aminotransferases and negative HCV-RNA maintained for over 6 months after the end of treatment) was obtained in 4/23 cases treated with interferon alone and 1/3 cases treated with interferon and ribavirin.
The histological findings of the present study are in agreement with those of numerous others. Vogt et al. found that among 29 HCV-infected children followed for at least 4 years, 50% had chronic hepatitis,2 Jara et al. reported that as few as 2% of their biopsied children had severe activity with cirrhosis,3 and Kage4 and Matsuoka5 found no cases of cirrhosis among their pediatric patients.
Hence, chronic HCV infection is an illness with a slow rate of progression during the first two decades of life in almost all patients. Indeed, 4/28 untreated cases spontaneously cleared HCV, a percentage similar to the success rate of interferon therapy in our patient population. It is difficult, on this basis, to justify an indiscriminate use of antiviral treatment and we think that an understanding of the factors underlying progression in exceptional cases is urgently needed in order to treat only those few individuals at risk.
REFERENCES
1 Rerksuppaphol S, Hardikar W, Dore GJ. Long-term outcome of vertically acquired and post-transfusion hepatitis C infection in children. J. Gastroenterol. Hepatol. 2004; 19: 1357-62.
2 Vogt M, Lang T, Frosner G et al. Prevalence and clinical outcome of hepatitis C infection in children who underwent cardiac surgery before the implementation of blood-donor screening. N. Engl. J. Med. 1999; 341: 866-70.
3 Jara P, Resti M, Hierro L. Chronic hepatitis C virus infection in childhood: clinical patterns and evolution in 224 white children. Clin. Infect. Dis. 2003; 36: 275-80.
4 Kage M, Fujisawa T, Shiraki K et al. Pathology of chronic hepatitis C in children. Child Liver Study Group of Japan. Hepatology 1997; 26: 771-5.
5 Matsuoka S, Tatara K, Hayabuchi Y et al. Serologic, virologic, and histologic characteristics of chronic phase hepatitis C virus disease in children infected by transfusion. Pediatrics 1994; 94: 919-22.
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