We read with great interest the article by Petta et al.1 The compound 25-hydroxyvitamin D3 (25[OH]D3) was reported as an independent predictor of cardiovascular disease (by a decreased expression of profibrotic markers, and an increased expression of antifibrotic markers) despite the fact that its real pathological pathway is still not clear.2 Incubation of the multipotent mesenchymal cell with 25(OH)D3 also resulted in antiproliferative and antiapoptotic processes.2 Therefore, the lower levels of 25(OH)D3 in liver with greater fibrosis is understandable. Lower cholesterol and lower 25(OH)D3 levels, along with greater steatosis, were found to be risk factors affecting sustained virological response (SVR) as seen in recent studies. The stage of fibrosis was found to be a risk factor for SVR not only in hepatitis C virus (HCV) alone, but also in patients coinfected with human immunodeficiency virus and HCV, in contrast to the results of the current article.3, 4 Moreover, age, sex, and body mass index were also described as predictors for SVR in patients infected with HCV,5 in contrast to the current study. These challenging results could be related in the methodologic differences between the present study and recent studies, or mistakes could have happened during the sampling and/or analyzing periods. For example, SVR was reached in the half the male patients, whereas it was reached in just one-third of the females, results which are also different from the recent data. The patients in the study may also be infected with an unknown subgroup of HCV, which could explain these patients' characteristics.
To the Editor:
Akif Altınbaş M.D.*, Şahin Coban M.D.*, Osman Yüksel M.D.*, * Department of Gastroenterology, Dışkapı Yıldırım Beyazit Education and Research Hospital, Ankara, Turkey.