A randomized trial of pegylated-interferon-alpha2a plus ribavirin with or without amantadine in the re-treatment of patients with chronic hepatitis C not responding to standard interferon and ribavirin.

BACKGROUND: There is yet no established treatment for chronic hepatitis C patients non-responder to standard interferon and ribavirin. AIM: To evaluate efficacy and safety of pegylated-interferon-alpha2a plus ribavirin with or without amantadine in such patients. METHODS: 161 non-responders to standard interferon and ribavirin were randomized into two groups: 81 patients (Group 1) were given weekly Peg-IFN-alpha2a 180 microg plus ribavirin 1,000-1,200 mg/daily for 12 months, 80 patients (Group 2) received weekly Peg-IFN-alpha2a 180 microg plus ribavirin 1,000-1,200 mg/daily and amantadine 200 mg/daily for 12 months. RESULTS: At the end of follow-up, HCV-RNA was negative in 29.6% of Group 1 and in 21.2% of Group 2 patients (P = 0.22). Patients with genotypes 1 and 4 responded better to bi-therapy (21.7%) than to triple therapy (17.3%, P = 0.5) while among patients with genotypes 2 and 3 there was a trend towards a higher sustained virological response rate when retreated with triple treatment (80% vs. 75%, P = 0.82). On multivariate analysis, genotype 1 or 4, high body mass index and >20% reduction of Peg-interferon were associated with the treatment failure. CONCLUSIONS: The addition of amantadine does not improve the overall SVR rate in non-responder patients retreated with Peg-IFN and ribavirin; however, about 30% of non-responders may achieve a sustained response, in particular patients with genotypes 2 and 3 show a high SVR (75%).

Role of Helicobacter pylori infection in peptic ulcer haemorrhage.

AIM: In spite of the diffusion of endoscopic treatment, mortality rate due to peptic ulcer haemorrhage (PUH) remains high. Helicobacter pylori (H. pylori) infection and nonsteroidal anti-inflammatory drugs (NSAIDs) are the 2 main aetiological factors, but their interactive role is controversial. The aim of this study was to determine both the prevalence of H. pylori infection and NSAIDs consumption in PUH and their prognostic importance. METHODS: In a prospective study, 41 consecutive patients (33 males, 8 females) admitted for PUH were recruited. H. pylori status was investigated both by measuring specific antibodies in serum and by histological detection on gastric biopsies obtained after one month from bleeding. In case of doubt, either a 13C urea breath test, or a stool antigen test were associated. All patients were treated with medical therapy associated to endoscopic treatment in most severe cases. RESULTS: Sixteen patients were infected from H. pylori (group A), 12 had a history of NSAIDs consumption (group B), and 13 had both risk factors (group C). The median duration of hospitalisation was 7 days for each group and correlated with age (P<0.04). Severity of PUH (high risk of rebleeding) was higher in group A (13/16; 81%) and group C (9/13; 69%), with respect to group B (6/12; 50%). This difference was not significant. CONCLUSIONS: H. pylori infection has a predominant role in causing PUH as well as in the prognosis and clinical course of this condition. Hence, it is important to determine H. pylori status in every patient with PUH.