Abstract
Olivieri et al. (Aug. 13 issue)1 retrospectively evaluated liver-biopsy specimens from patients with thalassemia who were treated with deferiprone and concluded that progression of fibrosis in 5 of 14 patients was due to the drug. The authors minimized the potential role of known factors that could, on their own, explain the progression of fibrosis in the five patients and the fact that many had received inadequate chelation therapy before they started taking deferiprone. Fibrosis and even cirrhosis are prominent in patients with thalassemia, as illustrated by the fact that 3 of 18 patients had cirrhosis before treatment with deferiprone was begun. Most important, four of the five patients with progression had antibodies to hepatitis C virus (HCV), one of the major causes of hepatic fibrosis in patients with thalassemia. Moreover, the authors did not acknowledge studies that reported no deferiprone-induced progression of fibrosis.2-4