Interferon treatment of chronic hepatitis C in patients cured of pediatric malignancies.
OBJECTIVE
Chronic hepatitis C was a frequent complication in patients treated for malignancy until the introduction of anti-HCV screening tests for blood donors. The association between chronic hepatitis C and progression to cirrhosis and hepatocellular carcinoma has been reported in about 20% and 5% of patients, respectively, within 20-30 years of infection. In adult patients, interferon has proved to be effective in decreasing the abnormal values of transaminases and the level of HCV viremia. Our purpose was to assess efficacy of and tolerance to interferon in a group of young patients who had acquired HCV infection during a period of chemotherapy.


METHODS
Interferon-a (IFN) was administered to 26 adolescents and young adults (13 males, age range 17-36 years; median age 24) with chronic hepatitis C, including 4 with hepatitis B virus co-infection, who had been treated for leukemia or solid tumor 5 to 19 years before joining this trial. Patients were treated with natural IFN alpha at a dose of 4 MU/m(2) thrice weekly for 12 months and followed up for another 6 months thereafter.


RESULTS
Nine patients stopped treatment during the first 6 months because of side effects (2 cases) or lack of response. At the end of the trial, 8 (31%) cases had responded, with alanine amino-transferase normalization and clearance of hepatitis C virus (HCV) RNA. A sustained response was only documented in 15% of cases, however, irrespective of any hepatitis B virus co-infection. The 2 patients with HCV genotype 2 were both responders, whereas only 8% of those with genotype 1 responded.


CONCLUSIONS
These data show that the efficacy of IFN in this series of young patients is similar to that reported for otherwise healthy adults with hepatitis C. Patients with genotype 2 are strong candidates for IFN treatment while other therapeutic strategies should be designed for patients with HCV genotype 1.
Cesaro
S
S
Clinica Oncoematologica Pediatrica, Dipartimento di Pediatria, Università di Padova, via Giustiniani 3, 35128 Padua, Italy. seguno@child.pedi.unipd.it.
Bortolotti
F
F
Petris
M G
MG
Brugiolo
A
A
Cusinato
R
R
Guido
M
M
Rossetti
F
F
Masiero
L
L
Zanesco
L
L
D000082:Acetaminophen / Q000008:administration & dosage; D000293:Adolescent; D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000505:Alopecia / Q000139:chemically induced; D001247:Asthenia / Q000139:chemically induced; D002744:Chlorpheniramine / Q000008:administration & dosage; D004279:DNA, Viral / Q000097:blood; D005260:Female; D005334:Fever / Q000139:chemically induced; D006509:Hepatitis B / Q000097:blood; D006514:Hepatitis B Surface Antigens / Q000097:blood; D006513:Hepatitis B e Antigens / Q000097:blood; D019698:Hepatitis C, Chronic / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D006801:Humans; D016898:Interferon-alpha / Q000008:administration & dosage* / Q000633:toxicity*; D008297:Male; D009369:Neoplasms / Q000150:complications; D009503:Neutropenia / Q000139:chemically induced; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000139:chemically induced; D012367:RNA, Viral / Q000097:blood; D012307:Risk Factors; D065227:Transfusion Reaction
D004279:DNA, Viral; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; D016898:Interferon-alpha; D012367:RNA, Viral; D000082:Acetaminophen; D002744:Chlorpheniramine; D000410:Alanine Transaminase