B-Vitamin deficiency in patients treated with antiepileptic drugs

Enzyme-inducing antiepileptic drugs (AEDs) produce many alterations in metabolism, including vitamin levels. Whether they produce clinically relevant deficiency of B vitamins has rarely been assessed. We obtained B‐vitamin levels in patients who were being converted from an inducing AED (phenytoin or carbamazepine) to a non-inducing AED (levetiracetam, lamotrigine, or topiramate), with measurements both before and ≥ 6 weeks after the switch. A group of normal subjects underwent the same studies. Neither folate nor B12 deficiency was seen in any patient. Vitamin B6 deficiency was found in 16/33 patients (48%) taking inducers, compared to 1/11 controls (9%; p = 0.031). After switch to non-inducers, only 7 patients (21%) were B6 deficient (p = 0.027). The incidence of deficiency was similar regardless of which inducing or non-inducing AED was being taken. Our findings demonstrate that treatment with inducing AEDs commonly causes pyridoxine deficiency, often severe. This could conceivably contribute to the polyneuropathy sometimes attributed to older AEDs, as well as other chronic heath difficulties.

► We examined the incidence of B-vitamin deficiency in AED-treated patients.
► Neither folate nor vitamin B12 deficiency was seen amongst the drug-treated patients.
► B6 deficiency was seen in 48% of inducer-treated patients.
► Deficiency resolved in most of these patients after switch to a non-inducing AED.