Related Experiment Video
Updated: Aug 12, 2026
Development of an IFN-γ ELISpot Assay to Assess Varicella-Zoster Virus-specific Cell-mediated Immunity Following Umbilical Cord Blood Transplantation
Published on: July 9, 2014
Zinc status and delayed cutaneous hypersensitivity in handicapped children treated with anticonvulsants
Insights
Anticonvulsant therapy in children may lead to zinc deficiency, potentially impairing cellular immunity. This study found lower skin reactions and higher hypozincnemia rates in treated children.
Area of Science:
- Pediatric Medicine
- Clinical Immunology
- Nutritional Science
Background:
- Anticonvulsant medications are widely used in pediatric populations.
- Cellular immunity plays a crucial role in host defense.
- Zinc is an essential trace element vital for immune function.
Purpose of the Study:
- To investigate the relationship between anticonvulsant therapy and zinc status in children.
- To assess the impact of anticonvulsants on delayed cutaneous hypersensitivity (DCH) and zinc levels.
Main Methods:
- A comparative study involving 68 children on anticonvulsants and 14 untreated children.
- Measurement of serum and hair zinc levels in both groups.
- Assessment of delayed cutaneous hypersensitivity (DCH) responses.
Main Results:
- No significant differences in serum or hair zinc levels between treated and untreated children.
- Significantly depressed DCH skin reactions observed in children receiving anticonvulsants (p < 0.05).
- Higher incidence of hypozincnemia (serum zinc < 70 µg/dL) in the anticonvulsant-treated group.
Conclusions:
- Anticonvulsant therapy, particularly phenytoin, may be associated with zinc deficiency.
- Phenytoin-induced zinc deficiency could be a contributing factor to suppressed cellular immunity in children undergoing anticonvulsant treatment.
Abstract:
Delayed cutaneous hypersensitivity and hair zinc contents were investigated in 68 children treated with anticonvulsants and 14 untreated children, and serum zinc contents were also measured in 21 of the treated and 13 of the untreated children. Serum zinc levels in the treated and untreated children were 82.7 +/- 7.1 and 85.1 +/- 18.2 micrograms/dl, respectively. Hair zinc levels in the treated and untreated children were 145.4 +/- 27.0 and 144.3 +/- 20.1 micrograms/g, respectively. These two parameters were not significantly different between the two groups. However, a significantly depressed skin reaction and a higher incidence of hypozincnemia (below 70 micrograms/dl) were found in the treated children (p less than 0.05). The results indicated that phenytoin-induced zinc deficiency might be one of the possible factors or exacerbatory factors in suppressed cellular immunity found with anticonvulsant therapy.
