Effects of deferoxamine versus deferasirox on hematology and liver parameters in children with beta-thalassemia major: A cross-sectional study from a single center

Iron chelating agents (ICAs) may induce changes in the blood and the liver indices. This study aimed to compare the effects of deferasirox (oral) and deferoxamine (parenteral) on the hematological and liver indices.

A cross -sectional study was conducted on patients at the Thalassemia Center in Sulaymaniyah, Iraq. The study included 76 β -thalassemia major children (37 females and 39 males, with a median age of 6 years). The patients were divided into Group I (n = 51, treated with deferasirox) and Group II (n = 25, treated with deferoxamine). Complete blood count and liver enzymes (alanine [ALT] and aspartate [AST] aminotransferase) were determined; the hemoglobin densities were calculated to differentiate absolute from restrictive iron deficiency; and the fibrosis-4 score (FIB-4, aspartate-to-platelet ratio index (APRI), and (AST/ALT ratio) were calculated.

Hemoglobin density indices showed restricted iron deficiency in both treated groups . However, serum ferritin level was higher in Group II than in Group I (1.9 times higher, p=0.037). Also, the median value of MCV in Group II was significantly higher than in Group I (79.8 fL vs. 77.0 fL, respectively). In contrast, liver fibrosis indices defined with the mean values of AST -to -ALT ratio and FIB -4 score were higher in Group I compared to Group II. A positive and significant correlation was observed between APRI level and serum ferritin in Group I (r = 0.518, df = 49, p<0.001).

Based on the data, it can be concluded that both deferasirox and deferoxamine affect red blood cells parameters , which may be related to their function as ICAs, leaing to temporary iron deficiency in treated patients. Both drugs may induce inconsistent changes in the liver which are highly associated with circulating ferritin level. However, the destructive effect of deferasirox on the liver is more evident, leading to the induction of fibrosis.