Pegylated interferon-alpha 2b-ribavirin combination in Egyptian patients with genotype 4 chronic hepatitis

被引:51
|
作者
Derbala, M
Amer, A
Bener, A
Lopez, AC
Omar, M
El Ghannam, M
机构
[1] Hamad Med Corp, Dept Gastroenterol, Doha, Qatar
[2] Hamad Med Corp, Dept Hematol, Doha, Qatar
[3] Hamad Med Corp, Dept Med Stat & Epidemiol, Doha, Qatar
[4] Hamad Med Corp, Dept Histopathol, Doha, Qatar
[5] Theodore Bilharz Res Inst, Giza, Egypt
关键词
Chronic HCV; genotype; 4; pegylated interferon;
D O I
10.1111/j.1365-2893.2005.00604.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Egypt has a high prevalence rate of hepatitis C (HCV) infection and as much as 90% is genotype 4. Response to interferon (IFN) varies with viral genotype and degree of fibrosis. Genotype 4 is poorly sensitive to standard IFN and IFN-ribavirin combination. We evaluated pegylated interferon (PEG-IFN)-alpha 2b in our patients. Sixty-one patients with compensated chronic HCV genotype 4 were enrolled in two groups: group A (31 patients) received IFN-alpha 2b 3 MU three times per week and group B (30 patients) received 1.5 mu g/kg PEG-IFN-alpha 2b once weekly. Ribavirin was added to each regimen in a dose of 800-1200 mg based on body weight. Patients were followed up for 24 weeks to assess the sustained response (SR). End-of-treatment response (ETR) was achieved in 11 of 31 patients (35.48%) in group A, and 13 of 30 patients (43.33%) in group B (P < 0.05). Only eight patients in group A and 10 in group (B) achieved a sustained virological response (25.8 and 33.3%, respectively) (P < 0.05). By computing ETR, SR or relapse and pretreatment baseline data (pretreatment, viral load, alanine transaminases, necroinflammatory and hepatic fibrosis), both inter- and intragroup, no significant correlations could be detected. In terms of safety and tolerability, PEG-IFN-alpha 2b and IFN-alpha 2b were comparable. In spite of mild insignificant increase in ETR and SR with the pegylated form, the poor response of genotype 4 in Egypt (genotype 4a) to different forms of IFNs may be related to an intrinsic resistance to the direct antiviral effect of IFN.
引用
收藏
页码:380 / 385
页数:6
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