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Study of zinc and growth hormone in sickle cell disease
P M Oliveira1, L C Póvoa, M H Oliveira
1Department of Internal Medicine, University of the State of Rio de Janeiro, Brazil. hlpmoliv@amcham.com.br
Insights
Children with sickle cell disease (SCD) often experience growth issues, but low zinc levels alone don't fully explain their statural deficit. Other metabolic disturbances likely contribute to growth deficiencies in pediatric SCD patients.
Area of Science:
- Pediatric Endocrinology
- Hematology
- Nutritional Science
Background:
- Sickle cell disease (SCD) affects approximately 25% of children, leading to growth deficits, delayed skeletal maturation, and pubertal development.
- These growth abnormalities in pediatric SCD patients have been historically linked to low serum zinc concentrations.
Purpose of the Study:
- To investigate the relationship between serum zinc levels and statural deficit in children with SCD.
- To explore potential roles of growth hormone (GH) secretion and thyroid function in growth deficiency among these patients.
Main Methods:
- Serum zinc concentrations were measured in 34 children with SCD (17 with statural deficit - SCS group, 17 without - SCN group) and 20 normal children (N group).
- GH secretion and thyroid function tests were conducted in the SCS group to exclude GH deficiency and hypothyroidism.
Main Results:
- Mean serum zinc levels were significantly lower in normal children (N group) compared to the SCN group (p<0.05).
- No significant difference in mean serum zinc was observed between the SCN and SCS patient groups (N>SCN=SCS).
- Growth hormone secretion and thyroid function were investigated in the SCS group to rule out deficiency and hypothyroidism.
Conclusions:
- While zinc deficiency is recognized in SCD, it may not be the sole cause of statural retardation in affected children.
- Statural deficits in pediatric SCD patients are likely multifactorial, involving other significant metabolic disturbances beyond zinc deficiency.
Abstract:
About 25% of children with sickle cell disease (SCD) have statural deficit and retarded skeletal maturation and pubertal development. These disorders have been attributed to low serum concentrations of zinc. We report the study of serum zinc in 34 patients with SCD, of whom 17 had statural deficit (SCS group) and 17 without growth deficiency (SCN group). They were compared with 20 normal children (N group). GH secretion and thyroid function were investigated in the group with short stature (SCS) in order to rule out GH deficiency and hypothyroidism. The mean serum zinc concentration was 108.45+/-22.888 microg/100 ml in the N group, 87.529+/-30.069 microg/100 ml in the SCN group and 82.765+/-34.766 microg/100 ml in the SCS group. There was a statistically significant difference between the mean of the N group and the mean of the SCN group (p<0.05) but no difference was found between the two groups of patients (N>SCN=SCS). Although there is a well-established zinc deficiency in patients with SCD, the statural retardation found in the SCS group could not be attributed only to zinc deficiency. Many other severe metabolic disturbances are also involved.