The lower SVR rate for whites in this study may have been due to the relatively small cohort of patients, the relatively high rate of premature discontinuations, and failure to return for the 72-week follow-up visit, say the authors. In addition, they note, response rates in non-registration trials or clinical practice settings are often lower overall.
The finding of a lower SVR in blacks than in whites is consistent with previous findings that blacks have lower rates of response. For example, in a retrospective analysis, the SVR in response to interferon monotherapy or combination therapy with interferon plus ribavirin was 11% (5/53) in blacks, compared with 27% (432/1600) in whites.
The results presented of the current study also confirm those of 3 previous trials, in which it was shown that the SVR rates to interferon monotherapy were lower in blacks than in whites, even when the 2 groups were otherwise well matched in factors such as HCV genotype, markers of prior hepatitis B infection, and prevalence of diabetes.
Although the reasons for apparent racial differences in the virological response to interferon therapies for chronic HCV are not understood, HCV genotype 1, which has been consistently associated with a poorer response to interferon, is more prevalent among blacks than among whites.
The genotype prevalence cannot explain the difference in this study, say the authors, since all patients in this trial were infected with HCV genotype 1. The presence of higher HCV RNA titers has also been associated with a poorer treatment response. But in this study, the authors note, The number of patients with high viral load is too small to permit interpretation.
The baseline factors identified by multivariate analysis as significant predictors of SVR were age (< 40 years), baseline viral load (<800,000 IU/mL), and ALT (< 3 times ULN), similar to those from a larger clinical trial of peginterferon alfa-2a plus ribavirin in which age of 40 or less, HCV genotype other than 1, and body weight of 75 kg or less were significant predictors of SVR.
Other factors that may lead to racial disparity are socioeconomic or environmental factors, including diet, and genetic factors, including the higher levels of serum testosterone and higher rates of aberrant immune response in blacks.
Of interest in this study is that 13 of 53 black patients, but only 1 of 16 white patients, showed improved fibrosis scores. Five of the black patients also had SVR, 5 were relapsers, and 3 were nonresponders.
In summary, write the authors, we have shown that 48 weeks of therapy with peginterferon alfa-2a plus ribavirin results in an SVR in 26% of blacks chronically infected with HCV genotype 1. To date, this is the highest response rate to treatment observed in a black population.
Our observation of improvement in fibrosis score in the black population requires confirmation in a larger trial.
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