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Chronic Hepatitis C Virus Infection in a Large Cohort of HIV-infected Spanish Children
Marisa Navarro*1, P Martín Fontelos2, M Mellado2, S Guillen3, P Barreiro2, J Ramos4, J Beceiro5, M de José6, J Bellón1, M Gurbindo1, and Madrid Cohort of HIV-infected Spanish children
1Hosp Gregorio Maranon, Spain; 2Hosp Carlos III, Madrid, Spain; 3Hosp 12 de Octubre, Madrid, Spain; 4Hosp de Getafe; 5Hosp de Alcalá de Henares; and 6Hosp La Paz, Madrid, Spain
Background: Little is known about the
prevalence, natural history, and treatment of hepatitis C virus (HCV) infection
in children vertically infected with HIV.
Methods: Retrospective analysis of all
HIV-infected children followed in a large cohort in 9 public hospitals from
Madrid, Spain, in whom HCV infection was diagnosed by confirmed positive HCV
antibodies (above 18 months) or polymerase chain reaction (PCR). A standarized questionnaire was filled out at the last
clinical visit. Liver stiffness was measured by means of percutaneous
transient elastometry in 12 children; 2 patients
underwent liver biopsy.
Results: Among 265 HIV-1-infected children followed in
the cohort, 97% perinatally infected, 19 were co-infected
with HCV (prevalence 7.2%, CI 95% (3.9% to 10.5%). Vertical transmission was the mode of HCV infection in 18 children. Among HCV-infected children, median age at last visit was 15.3 years (9 to 29.3).
Categorization of 3 children was CDC clinical category C, and of 6 was
immunologic class 3. Current median CD4 count and percentage were 751/mm3
(379 to 1092) and 29.1% (17% to 42%), respectively. Median plasma HIV RNA was <50
copies/mL (<50 to 10,000); 17 patients were on ART
and 2 were untreated (1 naive and 1 interrupted); 2 received specific HCV treatment
because of symptoms (immune reconstitution syndrome and acute retroviral
syndrome). They recieved interferon-α
+ ribavirin and pegylated interferon-α-2a
+ ribavirin, respectively. The treatment was unsuccesful in 1 patient, who is a candidate for liver
transplantation. HCV genotype was determined in 18 children, of whom 12 had
genotype 1, 4 genotype 4, and 2 genotype 3. Hepatomegaly
was observed in 3 children and splenomegaly in 2. No
child had echographic signs of portal hipertensión; 4 children had repeated negative HCV
antibodies and positive PCR despite high CD4 count with HAART. Elastometry showed mild liver fibrosis in all children, but
3, who had grade 4 fibrosis.
Conclusions: While HCV prevalence is low in
HIV-co-infected Spanish patients, it appears to be much higher than in non-HIV-infected
children. Although most vertically HCV-co-infected children are entering
adolescence with apparent low hepatic fibrosis by elastometry,
some patients (15.7% in our series) may have histologic
progression. Despite high CD4 cell count, children vertically co-infected may
have false negative HCV antibodies. Liver disease in HCV/HIV-co-infected
children is of great concern and warrants studies on treatment outcome.
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