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Retreatment of chronic hepatitis C (CHC) with sequential interferon-ribavirin combination (IFN-RIBA) therapy

1998; Elsevier BV; Volume: 28; Linguagem: Inglês

10.1016/s0168-8278(98)80628-4

1600-0641

L. Chemello, Luisa Cavalletto, E. Bernardinello, Carlo Donada, F. Belussi, Pietro Casarin, F Urbán, Patrizia Pontisso, M.G. Ruvoletto, A. Albertí,

Liver Disease Diagnosis and Treatment

Most patients with CHC have transient response (Relapsers-R) or no response (NR) when treated with IFN. To assess efficacy of IFN-RIBA in these patients, 50 R and 50 NR after IFN therapy were randomized to be retreated with IFN alone or with IFN-RIBA. IFN was given to all cases at 6MU tiw and at 2 mo patients were randomized to continue with IFN alone or to add RIBA 1800-1200 mglday) for 6 mo. ALT and HCV-RNA (PCR) End Theraov Resoonse and Sustained (12 mo) Resoonse are shown in the table. Previous NR (ALT) ETR(RNA) (ALT) SR (RNA) IFN monotherapy (24) 5(21 %I 3(12%) 0 0 IFN-RIBA (241 12(50%) 4(16%) 1(4%1 0 Previnus R IFN monotherapy (26) 1 16(61X) 10(38%) 1 6(23%) 4(15%) IFN.RIBA (28) 1 22(85%1 18(69%) 1 14(54%) 12(46%) IFN-RIBA significantly improved rate of SR in R (P=O.O3) but not in NR, in which only ALT ETR was improved. IFN-RIBA vs IFN improved SR by 27% with HCV-1 and by 4% with HCV-213. SR rates were 27% and 40% respectively with IFN alone and IFN.RIBA in R after 3MU x 6 mo IFN while the corresponding figures for R after higher/longer IFN therapy were 7% and 57%. Addition of RIBA to IFN improved SR only in patients with normal ALT at randomization. In conclusion, IFN-RIBA combination therapy was superior to IFN monotherapy in retreating previous IFN relapsers, particularly those with HCV-1 and those who had already being treated with high dose IFN during the I” cycle. Our schedule of IFN.RIBA was not effective in previous IFN non responders. A NOVEL HEPATITIS E (HEY) ISOLATED FROM A PATIENT WITH ACUTE nA-C HEPATITIS IN ITALY L. Roman& E. Tanzi. A. Zanetti. G. Sl *Viral Discovery Group, Abbott Laboratories, USA Objective: To assess the aetiological role of HEV in acute nA-C hepatitis and to characterize a viral isolate from a patient with no history of travel to areas where HEV is endemic. P&t&s and methods: We studied 216 patients with nA-C hepatitis (negativity for IgM anti-HAV, HBsAg, IgM anti-HBc, anti-HCV, HCV-RNA and exclusion of autoimmunity, alcohol or hepatotoxic drugs). All sera were tested by EIA for both IgG (Abbott Labs) and IgM (in house assay) anti-HEV. Sera and stools (when available) collected during the acute phase were examined by nested RT-PCR using primers derived from the ORFl region. Oligonucleotide primers based on the 5’-end of the ORFl of HEV-US1 were used to identified an isolate from a patient with no known risk factors. Results: 22/216 (10.2%) patients were found HEV-RNA and IgM positive during acute phase (ALT mean peak 2768 IUil, range 396-12290). The acute disease had a benign course with ALT normalization in 3-5 weeks in 20 (91%) patients. One patient with a history of chronic hepatitis C died from fulminant hepatitis and 1 patient (co-infected with HAV) had a clinically severe course (ALT 12290 IU/l, AST 17870 IUil) with ALT normalization within 8 weeks. 17 (77.3%) acute hepatitis E infections occurred in patients who travelled in endemic areas and 5 (22.7%) in patients with no history of travel. Pairwaise alignments of the nucleotide sequence from a HEV F’CR positive patient with no history of travel indicate that the isolate is significantly divergent from the two original isolates of HEV Burma and Mexico (79.9 and 80.7% respectively) and also significantly divergent from the new US isolates (85.8-88.6%). Phylogenetic analysis indicates that the Italian isolate represents a fourth branch distinct from those represented by the Burmese, Mexican and US isolates. Conclusions: HEV is responsible of about 10% of acute nA-C hepatitis in Italy. The identification of a new HEV variant may be important in understanding the epidemiology of HEV infection in our country.