| |
Treatment of Chronic Hepatitis C in Blacks and Non-Hispanic Whites
|
| |
| |
New England Jnl Medicine August 19, 2004, Volume 351, Number 8
To the Editor: Muir et al. (May 27 issue)1 state that black race is an independent risk factor for a low rate of response to treatment of infection with hepatitis C virus (HCV) infection with peginterferon alfa-2b and ribavirin. There is a further point in their study that merits attention.
Black and non-Hispanic white patients were similar in their baseline characteristics except for a significant difference in weight (89.0 kg vs. 81.6 kg), incidence of hypertension (46 percent vs. 12 percent), and incidence of diabetes mellitus (23 percent vs. 6 percent). Higher body weight has previously been identified as an independent risk factor for a low response to treatment of HCV,2 whereas nonobese patients showed a stronger biologic response on exposure to exogenous interferon alfa.3 An increase in body weight and in the incidence of hypertension and diabetes mellitus are all part of the insulin-resistance syndrome or the metabolic syndrome.
Recently, Shintani et al. showed that HCV infection contributes to the pathogenesis of insulin resistance and diabetes mellitus.4 The data presented suggest that the inverse relation is there as well — namely, that a preexisting insulin-resistance syndrome influences the course of HCV infection by decreasing the rate of response to current standard HCV therapy.
Elmar S. Aigner, M.D.
Paracelsus Medical University Salzburg
5020 Salzburg, Austria
elmar.aigner@gmx.net
References
1.Muir AJ, Bornstein JD, Killenberg PG. Peginterferon alfa-2b and ribavirin for the treatment of chronic hepatitis C in blacks and non-Hispanic whites. N Engl J Med 2004;350:2265-2271. 2.Manns MP, McHutchison JG, Gordon SC, et al. Peginterferon alfa-2b plus ribavirin compared with interferon alfa-2b plus ribavirin for initial treatment of chronic hepatitis C: a randomised trial. Lancet 2001;358:958-965.
3.Lam NP, Pitrak D, Speralakis R, Lau AM, Wiley TE, Layden TJ. Effect of obesity on pharmacokinetics and biologic effect of interferon-alpha in hepatitis C. Dig Dis Sci 1997;42:178-185. 4.Shintani Y, Fujie H, Miyoshi H, et al. Hepatitis C virus infection and diabetes: direct involvement of the virus in the development of insulin resistance. Gastroenterology 2004;126:840-848.
MUIR ET AL
Peginterferon Alfa-2b and Ribavirin for the Treatment of Chronic Hepatitis C in Blacks and Non-Hispanic Whites
Andrew J. Muir, M.D., M.H.S., Jeffrey D. Bornstein, M.D., Paul G. Killenberg, M.D., for the Atlantic Coast Hepatitis Treatment Group
ABSTRACT
Background Several small studies have reported a lower response rate to interferon alfa among black patients with chronic hepatitis C infection than among white patients. The increased prevalence of infection with hepatitis C virus (HCV) genotype 1, which has a lower response rate than other genotypes, has been suggested as the cause.
Methods We treated 100 black patients and 100 non-Hispanic white patients with chronic hepatitis C with peginterferon alfa-2b and ribavirin for 48 weeks. Enrollment was controlled so that the two groups had similar proportions of patients with genotype 1 infection. The primary end point was a sustained virologic response, which was defined as a negative test for serum HCV RNA six months after the completion of therapy.
Results In both cohorts, 98 percent of patients had genotype 1 infection. The rate of sustained virologic response was higher among non-Hispanic white patients than among black patients (52 percent vs.19 percent, P<0.001). The black patients also had significantly lower rates of virologic response at 12 weeks and at the end of treatment. Multivariable analyses examining sociodemographic and clinical characteristics found that black race was the only variable significantly associated with the difference in response rate.
Conclusions Black patients with chronic hepatitis C have a lower rate of response to treatment with peginterferon alfa-2b and ribavirin than non-Hispanic white patients, a difference that is not explained by differences in the viral genotype.
|
|
| |
| |
|
|
|
