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Zinc therapy in children with cystic fibrosis
S Safai-Kutti1, E Selin, S Larsson
1Department of Pediatrics, Ostra Hospital, Gothenburg University, Sweden.
Insights
Oral zinc supplementation normalized low plasma zinc in cystic fibrosis (CF) patients, but this effect was temporary. The study found no improvements in clinical status, growth, or lung function for CF patients receiving zinc.
Area of Science:
- Biochemistry
- Clinical Nutrition
- Pediatric Medicine
Background:
- Cystic Fibrosis (CF) is a genetic disorder affecting multiple organs.
- Patients with CF often exhibit micronutrient deficiencies, including zinc.
- Impaired zinc absorption may contribute to low plasma zinc levels in CF.
Purpose of the Study:
- To investigate the effects of oral zinc supplementation in pediatric patients with cystic fibrosis.
- To assess the impact of zinc therapy on plasma zinc levels, clinical status, growth, and lung function in CF patients.
Main Methods:
- A placebo-controlled, double-blind, crossover study design was employed.
- Twenty-six pediatric patients with cystic fibrosis participated, with treatment periods of 6 months each.
- Plasma zinc and selenium levels, leukocyte counts, clinical status, growth velocity, and lung function were monitored.
Main Results:
- All CF patients presented with low plasma zinc levels before supplementation, which normalized during zinc treatment but was transient.
- Plasma selenium concentrations were also low in CF patients.
- No significant improvements were observed in clinical status, growth velocity, or lung function in response to zinc supplementation.
Conclusions:
- Low plasma zinc in CF patients may result from impaired intestinal absorption, which oral zinc can temporarily correct.
- Zinc supplementation did not demonstrate a beneficial effect on the clinical outcomes, growth, or respiratory function in this cohort of CF patients.
Abstract:
The effect of oral zinc supplementation in patients with cystic fibrosis (CF) was investigated in a placebo-controlled, double-blind, crossover study with each treatment period covering 6 months. CF patients (n = 13, aged 2 years, 3 months to 19 years, 1 month) started with placebo and after 6 months, they received zinc therapy. Another 13 patients (aged 3 years, 5 months to 16 years, 10 months) started in the reverse order. Before zinc supplementation, all CF patients had low plasma levels of zinc which normalized during treatment. This effect was, however, transient. CF patients also had low concentrations of plasma selenium. A small decrease in the number of leukocytes was also noted during zinc therapy. In response to zinc treatment, no changes in the clinical status of the patients were observed either by the investigators or by the patients. Growth velocity was the same during the placebo and zinc treatment periods. No significant changes in lung function occurred in response to either placebo or zinc. It appears that the observed low plasma zinc concentration in CF patients was due to an impaired zinc absorption from the gut which was counteracted by an increased supply of oral zinc. No beneficial effect from zinc supplementation on clinical status, growth velocity, or lung function was found in this study.