Zinc level and its impact on the phenotype of sickle cell disease.

Zinc is an important antioxidant, and its deficiency contributes to oxidative damage in sickle cell disease (SCD). Emerging evidence supports zinc’s beneficial effects on SCD phenotype. This study aimed to determine the prevalence of zinc deficiency and assess the impact of zinc supplementation on clinical, hematological, and oxidative parameters in SCD children. Sixty SCD children were enrolled in this single-arm prospective study. All participants received daily oral zinc sulfate for 12 months [10 mg for ages 4–8, 20 mg for ages 9–13, and 30 mg for ages 14–18]. Clinical assessments and laboratory evaluations, including serum zinc, copper, nitric oxide, and total antioxidant activity, were conducted at baseline and after 12 months. The patients’ mean age was 9.2 ± 4.1 years; 80% had HbSS and 20% had sickle β-thalassemia. All patients were zinc-deficient at baseline (mean zinc: 42.8 ± 14.1 µg/dl). Post-supplementation, there were significant improvements in weight and height Z-scores (p-values < 0.001), and reductions in the frequency of vaso-occlusive crises, infections, hospitalizations, and transfusions (p-values < 0.001). Significant increases were observed in hemoglobin, hematocrit, fetal hemoglobin, zinc, nitric oxide, and total antioxidant activity (p-values < 0.001, < 0.001, 0.001, < 0.001, < 0.001, and < 0.001 respectively), while serum bilirubin, ferritin, and copper levels decreased significantly (p-values = 0.029, < 0.001, and 0.009, respectively). Zinc deficiency appears highly prevalent among SCD children, and supplementation may offer clinical, hematological, and antioxidant benefits. This study highlights the potential beneficial effects of zinc in this high-risk population.