D.* † ‡, Sayak Ohno B.S.*, Haruna Yamamoto M.S.*, Keiko Fujiwara B.S.*, Toshihiko Yoshida B.S.*, Yuji Sawabe B.S.*, Kazuyuki VX-809 Sogawa Ph.D.‡, Kazuyuki Matsushita M.D., Ph.D* † ‡, Osamu Yokosuka M.D., Ph.D§, Fumio Nomura M.D., Ph.D.* † ‡, * Division of Laboratory

Medicine, Chiba University Hospital, Chiba, Japan, Chiba University Chiba City, Chiba, Japan, † Clinical Proteomics Research Center, Chiba University Hospital, Chiba, Japan, Chiba University Chiba City, Chiba, Japan, Chiba, Japan, ‡ Department of Molecular Diagnosis, Graduate School of Medicine, Chiba University, Chiba, Japan, § Department of Medicine and Clinical Oncology, Graduate School of Medicine, Chiba University, Chiba, ABT 888 Japan. “
“We read with interest the article by Feuerstadt et al.1 published in a recent issue of HEPATOLOGY. The authors reported the results of the treatment of chronic hepatitis C virus patients in two centers in New York under the conditions of everyday clinical practice. They showed overall sustained virological response (SVR) rates of 14% in 173 genotype 1 patients and 37% in 82 genotype 2/3 patients. These very low SVR rates were

related to poor adherence to treatment: only 51% of the patients completed their treatment and follow-up, 26% of the patients were lost to follow-up, and 23% discontinued therapy prematurely because of side effects. The majority of the study patients were Hispanic (58%); they were followed by African Americans (20%), others (12%), and Caucasians (20%). The authors suggested that ethnic origin might be related to SVR. The SVR rate in their population was lower than the SVR rates in other populations previously reported.2, 3 We reported the results in our population of Hispanic patients treated in routine clinical practice: 7.6% of the patients discontinued therapy because of adverse events, and 1.2% of the patients dropped out of treatment. The overall SVR rate was 60.8%: 51.8% in genotype 上海皓元 1 patients, 80.3% in genotype 2 patients, and 69% in genotype 3 patients.4 These results are similar

to those reported by European and North American studies of daily clinical practice5-8 and to those reported in registered randomized clinical trials and are higher than those in other Hispanic populations.2, 3 Ethnic origin clearly has a role in SVR rates. This might be related to ancestral origin and genetics. A genetic polymorphism near the interleukin 28B gene has been related to SVR and can explain differences in response rates between African Americans and patients of European ancestry.9, 10 This genetic polymorphism (or another genetic variation) might also explain the difference between Hispanics of American and European ancestry. Besides genetic variations, which cannot be modified, improving adherence must be a key issue in the treatment of chronic hepatitis C virus in routine clinical practice. Feuerstadt et al.