Objective To evaluate the induction of DNA damage in peripheral blood mononuclear cells of patients with sickle cell disease, SS and SC genotypes, treated with hydroxyurea.Methods The study subjects were divided into two groups: one group of 22 patients with sickle cell disease, SS and SC genotypes, treated with hydroxyurea, and a Control Group composed of 24 patients with sickle cell disease who were not treated with hydroxyurea. Peripheral blood samples were submitted to peripheral blood mononuclear cell isolation to assess genotoxicity by the cytokinesis-block micronucleus cytome assay, in which DNA damage biomarkers – micronuclei, nucleoplasmic bridges and nuclear buds - were counted.Results Patients with sickle cell disease treated with hydroxyurea had a mean age of 25.4 years, whereas patients with sickle cell disease not treated with hydroxyurea had a mean age of 17.6 years. The mean dose of hydroxyurea used by the patients was 12.8mg/kg/day, for a mean period of 44 months. The mean micronucleus frequency per 1,000 cells of 8.591±1.568 was observed in the Hydroxyurea Group and 10.040±1.003 in the Control Group. The mean frequency of nucleoplasmic bridges per 1,000 cells and nuclear buds per 1,000 cells for the hydroxyurea and Control Groups were 0.4545±0.1707 versus 0.5833±0.2078, and 0.8182±0.2430 versus 0.9583±0.1853, respectively. There was no statistically significant difference between groups.Conclusion In the study population, patients with sickle cell disease treated with the standard dose of hydroxyurea treatment did not show evidence of DNA damage induction.
Background: Sickle cell anemia is a disease that develops episodes of acute pain and multiple organ dysfunction that can affect the growth hormone/insulin-like growth factor 1 (GH/IGF-1) axis. The severity of sickle cell anemia is influenced by modifying factors, such as levels of fetal hemoglobin (HbF), the co-inheritance of alpha-thalassemia, or treatment with hydroxyurea. Methods: This cross-sectional study in children with sickle cell anemia evaluated bone age (BA), adult height prediction (AHP) using BA, a target height (TH) calculated as the mean SDS of the parents, and laboratory parameters. Children were grouped according to serum levels of HbF, co-inheritance of alpha-thalassemia, and hydroxyurea therapy Results: The mean age of the 39 children was 8.2±2.2 years old. The average height was -0.75±0.30 SDS, and 10.3% (4/39) had short stature. Adjusted levels of IGF-1 or IGFBP-3 were significantly higher in children with sickle cell anemia on hydroxyurea treatment, in children with HbF levels >10%, and in those without alpha-thalassemia. Using SDS, the growth potential of children with sickle cell anemia in relation to their parents, calculated by the difference between AHP and TH, as well as the difference between children’s height and their TH, were lower in children with co-inheritance of alpha-thalassemia. Conclusion: The study showed an association between modifying factors and the GH/IGF-1 axis in children with sickle cell anemia. Additionally, the co-inheritance of alpha-thalassemia was associated with decreased height in these children when adjusted for their parents’ height.
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