Influence of antiepileptic treatment on bone metabolism

Aims: Patients receiving anticonvulsive drugs are considered a high-risk group regarding the development osteoporosis and rachitis. However, pathophysiological pathways and the influence of modifying factors, e.g. comorbities are not finally understood. In this study we investigate the influence of longterm antiepileptic treatment on bone metabolism in otherwise healthy children with epilepsy.

Methods: We performed a multicenter cross sectional study and collected data on calcium, phosphorus, alkaline phosphatase, 25-OH vitamin D and parathormone. Children were treated with a monotherapy of valproic acid, oxcarbazepine, lamotrigine, sulthiame, levetiracetam or topiramate for at least six months. Data on calcium intake were collected by using a standardized questionnaire exploring dietary habits. Data were collected from July 2007 through July 2011. Reference values were obtained from the KIGGS-Study.

Results: 128 probands were included in the study (76 female, mean age 9 years, 11 months). Most probands were treated either with valproic acid (67), oxcarbazepine (26) or lamotrigine (11). We found 31 patients with hypocalcaemia, 30 patients with hypophosphataemia and 17 patients with 25-OH-vitamin D deficiency. All patients were clinically asymptomatic. There were no significant correlations between laboratory values and type, duration or dose of medication or calcium intake.

Conclusion: The results suggest that anticonvulsive monotherapy may have effects on bone mineral metabolism. From a clinical perspective it seems appropriate to determine parameters of bone metabolism at least once a year in patients under long term antiepileptic treatment.