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Pyridoxine deficiency in children treated with isoniazid
Insights
Isoniazid therapy can cause vitamin B6 deficiency in children, even without symptoms. Higher doses increase deficiency risk, suggesting pyridoxine supplementation should be reconsidered for pediatric patients.
Area of Science:
- Pediatric Medicine
- Nutritional Science
- Pharmacology
Background:
- Isoniazid is a common antitubercular drug.
- Pyridoxine (vitamin B6) deficiency is a known side effect of isoniazid in adults, but considered rare in children.
- Clinical manifestations of pyridoxine deficiency in children are not well-documented.
Purpose of the Study:
- To investigate the incidence of pyridoxine deficiency in children undergoing isoniazid therapy.
- To assess the relationship between isoniazid dosage and pyridoxine status in pediatric patients.
- To evaluate the need for pyridoxine supplementation in children receiving isoniazid.
Main Methods:
- Serum pyridoxine levels were measured in 38 children receiving isoniazid.
- Pyridoxine status was determined using a biologic assay with Tetrahymena thermophila.
- Children were monitored for 2 to 18 months of isoniazid therapy.
Main Results:
- 13% (5 out of 38) of children exhibited pyridoxine deficiency.
- No children presented with definitive clinical symptoms or signs of deficiency.
- Higher isoniazid dosages (>10 mg/kg/day) were associated with a greater incidence of deficiency.
- Nerve conduction velocity was normal in three tested children.
Conclusions:
- Isoniazid-induced pyridoxine deficiency occurs in children, contrary to previous assumptions of rarity.
- Current recommendations to withhold pyridoxine prophylaxis in children on isoniazid may need reevaluation.
- Pyridoxine supplementation should be strongly considered for pediatric patients, especially those who are debilitated, malnourished, or have pre-existing vitamin B6 deficits.
Abstract:
Isoniazid-induced deficiency of pyridoxine (vitamin B6) is reportedly not uncommon in adults but rare in children. In the present study, 38 children had serum levels of pyridoxine tested while receiving therapy with isoniazid. A biologic assay using the protozoan Tetrahymena thermophila determined pyridoxine status after 2 to 18 months of therapy with isoniazid. Five children (13 percent) were deficient. None had definitive clinical symptoms or signs consistent with pyridoxine deficiency. Three had normal nerve conduction velocity. Children receiving isoniazid in dosages greater than 10 mg/kg/day had a higher incidence of deficiency. Present recommendations for withholding pyridoxine prophylaxis from children receiving isoniazid therapy must be reconsidered in light of these findings, particularly in those children who are debilitated or have a poor nutritional history with a known pyridoxine deficit prior to therapy with isoniazid.