AbstractBackgroundThe majority of classic anti‐epileptic drugs can decrease bone mineral density through the acceleration of vitamin D metabolism by cytochrome P450.AimWe tried to investigate the bone metabolism. in adult patients with epilepsy.MethodsBone mineral density was measured in 30 patients (18 men and 12 women, age 24–76 years) treated with classic anti‐epileptic drugs for more than 5 years. Dietary intake of nutrients and laboratory data were assessed in patients, and age‐ and sex‐matched healthy controls.ResultsUsing T‐scores measured at the lumbar spine, seven patients (23%) were diagnosed as osteopenia and two patients (6%) as osteoporosis. Serum 25‐hydroxyvitamin D levels were significantly decreased in patients taking phenytoin, but were unchanged in patients taking valproic acid, compared with those on other prescription anti‐epileptic drugs. Dietary intake of vitamin D, assessed by a nutritionist, did not differ among patients. Bone mineral density score was not correlated with serum 25‐hydroxyvitamin D, but it was significantly correlated with serum under‐carboxylated osteocalcin and serum tartrate‐resistant acid phosphatase isoform 5b. Serum under‐carboxylated osteocalcin levels were significantly higher in patients with decreased bone mineral density compared with age‐ and sex‐matched healthy controls. Dietary intake of vitamin K did not differ between patients and controls.ConclusionThese results suggest that vitamin D plays a pivotal role in the altered bone metabolism in patients taking classic anti‐epileptic drugs. With the use of bone mineral density scores and biomarkers, neurologists in Japan might be able to evaluate bone health in the management of patients with epilepsy.