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• W1991036625 abstract "According to 2005 data from the Organ Procurement and Transplantation Network, hepatitis C is the leading indication for liver transplantation, accounting for more than 40% of cases. Among adults, 95% of transplanted livers are reinfected after surgery.1, 2 Reinfection and progression of fibrosis in the new liver are associated with genotype, viral load, immune state, and age of the donor.3, 4 In teasing out the factors that lead to reinfection, rarely is the age of the recipient mentioned. Yet as we have come to know hepatitis C, we have found that it is clearly an immune-mediated disease, with many disease features influenced by age, and thus facts stated for adults do not necessarily hold for children. Whereas transplantation for hepatitis C has been the center of many adult-focused studies, there is a paucity of equivalent information in the pediatric population. The NHANES III study estimates that 250,000 children in the United States are suspected of having hepatitis C. Because the disease often goes undetected, the number may be larger. The majority of children with hepatitis C have a relatively benign course before reaching adulthood. Liver enzymes are often normal, and rarely is there progression to cirrhosis. Autoimmune features such as cryoglobulinemia, vasculitis, and porphyria cutanea tarda are exceedingly rare.5 However, sometimes the disease is more aggressive, as in the case of the children presented by Barshes et al. in this issue.6 Certain aspects of hepatitis C are distinctly different in children compared with adults; for that reason, it is important to present and analyze pediatric data separately. The mode of acquisition, the ability to spontaneously clear the virus, and the response to antiviral therapy all differ. The most common modes of acquisition for children are maternal-fetal transfer or exposure to blood products, usually related to a comorbid process such as hemoglobinopathy or cancer.5, 7 Maternal-fetal transfer depends on maternal immune state and the mother's viral titers at the time of delivery. Transfer in healthy women ranges 1-7%, but it increases to 20% in the presence of coinfection with human immunodeficiency virus.7 However, unlike adults, and unlike children with hepatitis B, children who acquire this disease early in life have a good chance of clearing this virus. Ceci et al.8, 9 report that up to 75% clear the virus by 2 years. Furthermore, the course in neonatal-acquired hepatitis C virus is slowly progressive, with little, if any, marked liver damage.5, 7 Despite this optimistic data, hepatitis C is such a common disease that many children in the United States become chronically infected. As such, a number of patients will present with a more virulent course before adulthood. Children who acquire the disease through blood products have a different course. For these children, progression of fibrosis is tied to the underlying comorbidity. We suspect this by comparing data published regarding transfusion-acquired hepatitis C among different diseases. Transfusion-acquired hepatitis C after cardiac repair in infants tends to have a benign course, as shown by both Vogt et al.10 and Matsuoka et al.,11, 12 whereas transfusion-acquired hepatitis C for thalassemia and childhood cancers can have a much more aggressive course.13, 14 Among the hemoglobinopathies, the accelerated rate of fibrosis parallels the degree of iron overload. In cancer, it is probably related to chemotherapy, radiation, and immune state.14 Response to treatment in children is surprisingly different than in adults. A meta-analysis of pediatric studies published between 1990 and 2000, before any multicenter large studies had been conducted, showed a sustained viral response (SVR) of 36% for monotherapy with interferon.15 Adults treated comparably only have 7-15% SVR.16, 17 A more recent study in children aged 5-17 years who were treated with interferon and ribavirin exhibited a SVR of 46%, and for treated children younger than 12, SVR was 57%.18 Large-scale trials with pegylated interferon and ribavirin are likely to have even better response rates. These studies are currently in progress for both pegylated interferon-alfa 2a and pegylated interferon-alfa 2b. In the field of pediatric hepatology, clinicians have been influenced by these data and the adult data, which show that shorter duration of infection and less fibrosis correspond to increased likelihood of response to antiviral therapy. The current trend has been to offer more children early therapy. The choices of therapies have limits, but such treatments have the best chance at efficacy early in the disease process and in younger patients. The information presented by Barshes et al. is very important. It shows that transplantation in children is effective—perhaps even better than it is in adults. Patient and graft survival in this small data set exceeded typical adult data. However, there are some major limitations of this research—aspects of the data that could not be overcome because of circumstances. The group of children is small, and the data collection spans 17 years. It is unclear whether some children acquired hepatitis C at the time of liver transplantation for a primary disease such as biliary atresia or alpha-1 antitrypsin deficiency. A number of these reported transplantations occurred before 1992, when transfusions were considered highly tainted. Acquisition of hepatitis C in a newly transplanted liver would influence the rate of progression. In other words, their transplant for hepatitis C is actually the second liver given to that child. During the decades covered by this group of children, preservation solutions and immunosuppression regimens changed, and these variables are likely to influence the data. As such, the data need to be incorporated into our armamentarium of therapies cautiously. From these 70 patients, we will not know the exact chance of recurrence or the exact percentage that will have aggressive hepatitis C in the graft. Yet it is clear that both complications can occur in the pediatric setting—a striking feature because it is expected that a child should have decades of future life. These data reveal that children can benefit from liver transplantation, but more importantly, it reminds us of the shortcomings of our treatment for this disease. Many of the reported patients date to an era when treatment for hepatitis C was not initiated unless there was progression of disease. The data also highlight our difficulties in controlling the posttransplantation damage and reinfection, even in children. The current antiviral therapies are poorly tolerated after transplantation and have diminished benefit.4 The children described in this paper underwent treatment that predates our current treatment strategies, and the data strongly indicate that treatment in the pediatric population should be pursued. Yet if necessary, transplantation remains a therapeutic option. Hepatitis C cannot be assumed to be a benign disease in children. It behooves us to approach pediatric hepatitis C aggressively. We should advocate therapy early in the disease course when possible, and we should develop new therapies. Finally, we should develop different strategies for hepatitis C, considering that the liver graft has a limited life span and posttransplant therapies are suboptimal." @default.
• W1991036625 created "2016-06-24" @default.
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• W1991036625 date "2006-01-01" @default.
• W1991036625 modified "2023-10-18" @default.
• W1991036625 title "Hepatitis C, liver transplantation, and why we should consider children separately" @default.
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• W1991036625 doi "https://doi.org/10.1002/lt.20789" @default.
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