We acknowledge the issues raised by Pijak et al. regarding the role of obesity in the low response rates to interferon-based therapies of black patients with hepatitis C. Indeed, the average weight of black patients was higher than that of white patients in our study,1 as well as in the Muir study.2 Although a smaller proportion of black patients with body mass index (BMI) >30 kg/m2 (8 of 35; 23%) achieved sustained virological response (SVR) than did those with BMI <30 kg/m2 (12 of 42; 29%), the rates were not significantly different. Furthermore, the percentages of patients with diabetes (5 of 18; 28%) or hypertension (13 of 43, 30%) who achieved SVR were similar to that of the whole population. Thus, associations with these two common comorbidities also did not provide an explanation for the low response rate in blacks.
When BMI >30 kg/m2 was included in the univariate analysis, it failed to reach statistical significance (odds ratio, 0.74; P = .57) as a predictor for nonresponse. Multivariate analysis that included BMI >30 kg/m2, along with age ≤40 years, male sex, alanine aminotransferase >3 upper limit of normal, hepatitis C virus (HCV) RNA baseline >800,000 IU/mL, and histologic activity index >10, also failed to show a significant association of BMI >30 kg/m2 with nonresponse (odds ratio, 0.66; P = .479). Thus, the key factors associated with the low virologic responses of black Americans are not evident from our analyses and remain to be elucidated. Finally, Muir et al.2 reported that only 19% of black patients achieved SVR, despite the weight-based dosing of pegylated interferon alfa-2b. Therefore, we surmise that increasing the pegylated interferon alfa-2a dose according to weight or BMI is unlikely to override any negative impact of BMI.
With regard to retesting patients with genotype l at week 24, we point out that in our study, serum HCV RNA was assessed by sensitive testing (<50 IU/mL as measured by the AMPLICOR HCV Test, version 2.0 [Roche Diagnostics, Branchburg, NJ]). However, our protocol did not include a 24-week stopping rule because other goals of the study were to determine the differences in viral kinetics over time and to evaluate the histologic benefits of treatment that may be unique to blacks in comparison to whites. Our data show that, of 53 black patients with paired biopsies, 13 (25%) experienced fibrosis improvement, and 36 (68%) showed stabilization. We concluded from our work that although SVR rates were lower, patients with early virological response should continue on treatment. Nevertheless, we concur that if patients demonstrate a positive HCV RNA by a sensitive quantitative assay at 24 weeks, treatment may reasonably be discontinued.