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Zinc status of children with sickle cell disease: relationship to poor growth
C K Phebus1, B J Maciak, M F Gloninger
1Division of Hematology/Oncology, University of Pittsburgh School of Medicine, Graduate School of Public Health, University of Pittsburgh, PA.
Insights
Children with sickle cell disease (SCD) have lower serum zinc levels than healthy peers. This deficiency, linked to disease severity and poor growth, is not due to diet but likely other factors.
Area of Science:
- Pediatric Hematology
- Nutritional Biochemistry
- Genetic Blood Disorders
Background:
- Sickle cell disease (SCD) is a genetic blood disorder with significant health implications.
- Zinc is an essential trace element crucial for numerous physiological processes.
- Nutritional status, including zinc levels, can be affected in chronic diseases like SCD.
Purpose of the Study:
- To investigate and compare serum zinc concentrations in children with SCD versus healthy controls.
- To identify factors associated with zinc status in children with SCD, including age, hemoglobinopathy type, and growth.
- To explore potential causes of zinc deficiency in SCD, differentiating from dietary intake.
Main Methods:
- Cross-sectional study comparing 80 children with SCD and 44 healthy sibling controls (ages 3-18).
- Measurement of serum zinc, alkaline phosphatase (AP), and retinol-binding protein (RBP) levels.
- Analysis of variations in zinc status based on age, SCD genotype (Hb SS vs. variant), and growth percentile.
Main Results:
- Children with SCD exhibited significantly lower mean serum zinc levels compared to controls (77.8 vs. 82.2 µg/dl, P < .05).
- Lower levels of zinc-dependent proteins (AP and RBP) were observed in SCD patients (P < .001).
- Zinc levels were lower in older SCD patients (≥12 years), those with Hb SS, and those with poor growth (P < .01).
Conclusions:
- Children with SCD demonstrate significant zinc deficiency compared to healthy controls.
- Zinc deficiency in SCD is associated with disease severity, age, and impaired growth.
- The deficiency is unlikely due to inadequate dietary intake, suggesting other pathophysiological mechanisms in SCD.
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 micrograms/dl, mean +/- 1SD, P less than .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 less than .001; RBP: 1.92 +/- .9 vs. 2.77 +/- .9 mg/dl, P less than .001). Patients greater than or equal to 12 years of age (n = 34) had significantly lower zinc levels than those less than 12 years (74.5 +/- 8.4 vs. 80.3 +/- 10.3 micrograms/dl, P less than .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, micrograms/dl, P less than .05). Patients classified as having "poor" growth (height-for-age less than 5th percentile, n = 24) had a lower serum zinc level than those with "normal" growth (72.8 +/- 8.0 vs. 79.8 +/- 10.0 micrograms/dl, P less than .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.