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Long-Term suppression of hepatitis B e antigen-negative chronic hepatitis B by 24-month interferon therapy

2003; Lippincott Williams & Wilkins; Volume: 37; Issue: 4 Linguagem: Inglês

10.1053/jhep.2003.50148

1527-3350

Pietro Lampertico, E. Del Ninno, M. Viganò, R. Romeo, Maria Francesca Donato, Erwin Sablon, Alberto Morabito, Massimo Colombo,

Liver Disease Diagnosis and Treatment

To assess whether extended treatment with interferon improves the outcome of hepatitis B e antigen (HBeAg)–negative chronic hepatitis B, 101 consecutive patients were treated with 6 MU of interferon alfa 2b 3 times weekly for 24 months. During the 68–month study, 30 patients (30%) had a sustained response ( i.e. , normal serum transaminase levels and undetectable hepatitis B virus DNA by non–polymerase chain reaction [PCR] assays), and 15 cleared serum surface antigen. Twenty–five nonresponders, 16 relapsers, and 30 who discontinued treatment were considered treatment failures. Multivariate analysis predicted a sustained response for young age (odds ratio, 0.94; 95% confidence interval, 0.89–0.99; P = .041) and high pretreatment serum levels of immunoglobulin M (IgM) anti–hepatitis B core antigen (HBc) (odds ratio, 4.52; 95% confidence interval, 1.63–12.5; P = .004). Liver disease progressed in none of the sustained responders but in 16 with treatment failure (0% vs. 22%, P = .002); hepatocellular carcinoma (HCC) developed with similar frequency in both groups (7%). Overall, estimated 8–year complication–free survival was longer for the 30 sustained responders than the 71 patients with treatment failure (90% vs. 60%, P < .001), but 8–year patient survival was similar in the 2 groups (100% and 90%). Short complication–free survival was predicted by failure to respond to interferon (hazard ratio, 7.8; 95% confidence interval, 1.8–34.0; P = .006) and high scores for liver fibrosis (hazard ratio, 1.71; 95% confidence interval, 1.17–2.50; P = .005). In conclusion, 24 months of treatment with interferon alfa 2b led to sustained disease suppression in a significant proportion of patients with HBeAg–negative chronic hepatitis B. (Hepatology 2003;37:756–763.)