In chronic hepatitis B, treatment with interferon alfa-2b (5 million units per day for 16 weeks) was effective in inducing a sustained loss of viral replication and achieving remission, assessed biochemically and histologically, in over a third of patients. Moreover, in about 10 percent of the patients treated with interferon, hepatitis B surface antigen disappeared from serum.
AND THE HEPATITIS INTERVENTIONAL THERAPY GROUP* with continued therapy at that dose; however, a propor-To evaluate response rates to 3, 5, or 10 million units tion of patients who do not respond to 12 weeks of treat-(MU) of interferon alfa-2b, given thrice weekly, and to ment with 3 or 5 MU may respond to higher doses. Aldetermine whether higher doses of interferon increase though the long-term sustained response rates are the likelihood or durability of the response, a multicenmarginally increased with interferon doses above 3 MU ter, randomized trial was performed at nine academic three times per week, the side effects are difficult to medical centers in the United States. Two hundred forty tolerate. The analysis of baseline factors in relation to eight patients with chronic hepatitis C were randomized response identified no single baseline factor associated to receive 3, 5, or 10 MU of interferon alfa-2b thrice with a low-enough response rate to warrant withholding weekly for 12 weeks. Based on the alanine aminotransinterferon therapy from patients with chronic hepatitis ferase (ALT) response at treatment-week 12, the patients C. (HEPATOLOGY 1996;24:1034-1040.) were rerandomized to additional therapy at the same or at increased doses for an additional 12 to 36 weeks; in the case of no response to the highest dose, the patients Recombinant interferon (IFN) has been shown to be effecwere discontinued from the study. Serum ALT concentive in decreasing serum alanine aminotransferase (ALT) levtrations and liver histology were measured. The overall els, 1-6 in eliminating detectable hepatitis C virus ribonucleic complete response rates to 3, 5, or 10 MU were not differacid (HCV RNA), 7 and in reducing histologic evidence of heent at treatment-week 12 (31% vs. 42% vs. 40%, not signifipatic inflammation in patients with chronic hepatitis C. 1,6 cant). The majority of week-12 responders continued to After nearly a decade of research, however, two major probrespond during additional treatment. When the treatlems with treatment remain. First, a response by the end of ment was discontinued, 15.4% to 19.0% of patients maintreatment occurs in fewer than half of patients. In our previtained their response. Of the nonresponders to 3 MU at ous study, the normalization of the serum ALT levels was week 12, who were continued on 3 MU for an additional seen in 38% of patients treated with a dose of 3 million units 12 weeks, none responded. However, response to addi-(MU) of interferon alfa-2b three times per week for 24 weeks, 1 tional therapy occurred in 12% of week-12 nonrespondand all responding patients achieved their response by treaters, whose dose was escalated from 3 or 5 MU to 10 MU. ment weeks 8 to 12 of treatment. 8 Similar response rates have The only baseline features associated with the treatment now been obtained from several other randomized controlled response were the absence of fibrosis or cirrhosis on studies. 2-6 Second, a response to IFN is usually not mainthe pretreatment liver biopsy and viral genotype. We t...
Chronic non-A, non-B hepatitis (NANBH) is a common and often progressive liver disease. Based on current serological tests, hepatitis C virus (HCV) infection is responsible for most cases. Interferon-alpha (IFN) treatment at a dose of 3 x 10(6) units given three times per week for 24 weeks has been shown to be effective in normalizing serum alanine aminotransferase (ALT) levels and reducing hepatic inflammation in approximately 40% of these patients. The purpose of this study was to identify pretreatment characteristics in patients with chronic hepatitis C(CH-C) which would best predict a favourable response to IFN treatment (normalization of serum ALT). One hundred and sixty-three adult patients who had participated in a large multicentre treatment trial were included in the study group; 84 had been treated with 3 x 10(6) units of recombinant IFN-alpha-2b (rIFN) subcutaneously three times per week for 24 weeks and 79 patients had been treated with 1 x 10(6) units rIFN in the same dosage schedule. Forty-one pretreatment historical, clinical, laboratory and histological variables were evaluated. In addition, early biochemical improvement during treatment was evaluated as a predictor of ultimate response. Univariate analysis identified six variables (dose, dose m-2, weight, body surface area, ongoing ethanol use, white blood cell count and the presence of symptoms) as potential predictors of response (two-tailed, P < 0.15). By multivariate analysis, however, only the 3 x 10(6) dose of rIFN was independently predictive of response (P < 0.01). When the analysis of response was confined to those patients who received treatment with 3 x 10(6) units of rIFN, seven variables [body weight, surface area, dose m-2, current ethanol use, serum albumin and the presence of chronic persistent hepatitis (CPH) on entry liver biopsy] were more frequent in patients who responded to therapy. In a multivariate model, only CPH and body weight predicted an increased likelihood of response (P < 0.01). However, the model was not a sensitive predictor of response as only 18% of the study group had CPH on liver biopsy. A decrease in serum ALT levels within the first 12-16 weeks of rIFN treatment was found to be the strongest indicator of an ultimate response to treatment. Thus, assessment of early response to IFN treatment is the only practical means of predicting complete response and avoiding prolonged and unnecessary therapy in those with little chance of response.
Nelfinavir-containing therapy is associated with enhanced increases in CD4 T-cell number compared to RTI therapy alone with equivalent antiviral effect. These data suggest that PIs influence CD4 T-cell number through a nonvirologic effect.
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