Zinc status of children with sickle cell disease: Relationship to poor growth

Publisher Website
Google Scholar
Abstract
We examined the zinc status of 80 children with sickle cell disease (SCD) and 44 disease-free sibling controls aged 3 to 18 years. For both patients and controls, variations in serum zinc by age, type of hemoglobinopathy, and growth status were measured. The mean serum zinc concentration of patients was significantly lower than for controls (77.8 ± 9.9 vs. 82.2 ± 9.8 μg/dl, mean ± 1SD, P < .05). Serum levels of alkaline phosphatase (AP) and retinol-binding protein (RBP), two zinc-dependent proteins, were also lower among patients (AP: 171 ± 66 vs. 243 ± 97 IU/L, P < .001; RBP: 1.92 ± .9 vs. 2.77 ± .9 mg/dl, P <.001). Patients ≥ 12 years of age (n = 34) had significantly lower zinc levels than those < 12 years (74.5 ± 8.4 vs. 80.3 ± 10.3 μg/dl, P < .01), and children with homozygous SCD (Hb SS, n = 55) had a more pronounced deficiency than those with a variant hemoglobinopathy (76.3 ± 8.9 vs. 81.5 ± 11.5, μg/dl, P < .05). Patients classified as having “poor” growth (height-for-age < 5th percentile, n = 24) had a lower serum zinc level than those with “normal” growth (72.8 ± 8.0 vs. 79.8 ± 10.0 μg/dl, P < .01). Dietary intake data, body mass index, and serum total protein and albumin levels were similar for patients and controls, suggesting that zinc deficiency in SCD does not relate to inadequate dietary intake. The origin of low serum zinc levels in children with SCD is more likely to relate to factors such as increased urinary zinc excretion, chronic intravascular hemolysis, and/or zinc malabsorption.