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Nutrition Interventions for Children with Special Health Care Needs

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Chapter 5 - Medication-Nutrient Interactions<br />

Vitamin D<br />

Long-term use of anticonvulsants has been associated <strong>with</strong> vitamin D deficiency,<br />

resulting in rickets or osteomalacia (1). The effects of anticonvulsant therapy on<br />

vitamin D status are multiplied by the following factors (1,4):<br />

• multiple medication regimens<br />

• inactivity<br />

• little exposure to sunlight<br />

• dark skin<br />

• poor dietary intake of vitamin D<br />

The anticonvulsants most frequently implicated in vitamin D deficiency are phenytoin<br />

(Dilantin), phenobarbital, and carbamazepine (Tegretol). Primidone (Mysoline) and<br />

valproic acid (Depakene/Depakote) have also been shown to be associated <strong>with</strong><br />

vitamin D deficiency and decreased bone mineral density (1,3,4).<br />

Recent research on vitamin D has shown that optimal levels are much higher than<br />

previously thought (>30ng/mL versus >20 ng/mL). Vitamin D deficiency has been<br />

found to be widespread in the normal population, especially <strong>for</strong> those living at<br />

greater than 45 degrees latitude (north or south) (5,6). It is imperative that vitamin<br />

D levels are evaluated and deficiencies treated at time of initiation of anticonvulsant<br />

therapy, and regularly thereafter. <strong>Children</strong> on anticonvulsant therapy who have<br />

normal vitamin D levels should be given a prophylactic dose of up to 2000 IU<br />

vitamin D daily. Those <strong>with</strong> documented deficiencies will need pharmacologic doses<br />

prescribed by their physicians (7).<br />

Folic Acid<br />

Longterm use of anticonvulsants has also been strongly associated <strong>with</strong> folic acid<br />

deficiency and possibly <strong>with</strong> deficiencies of other B vitamins and vitamin C. Folic acid<br />

deficiency has been observed <strong>with</strong> phenytoin alone and in combination <strong>with</strong> other<br />

medications; the strongest effects have been observed <strong>with</strong> multiple medication<br />

regimens. There is some indication that folic acid supplementation may result in<br />

more frequent seizures. However, supplementation <strong>with</strong> Dietary Reference Intake<br />

(DRI) levels of folic acid and close monitoring of seizure activity is appropriate to<br />

prevent folic acid deficiency (1). Folic acid deficiency is associated <strong>with</strong> hyperhomocysteinemia<br />

which in turn increases risk <strong>for</strong> heart disease. Supplementation <strong>with</strong> folic<br />

acid has been shown to both replete folic acid levels and decrease homocysteinema<br />

levels in individuals on anticonvulsants (8,9).<br />

60 <strong>Nutrition</strong> <strong>Interventions</strong> <strong>for</strong> <strong>Children</strong> With <strong>Special</strong> <strong>Health</strong> <strong>Care</strong> <strong>Needs</strong>

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