A Case of Osteomalacia with Multiple Fractures and Hypocalcemia Associated with Phenytoin Therapy

Abstract

항경련제는 매우 빈번히 사용되는 약물이나 이와 관련된 합병증인 골대사질환에 대한 인식은 아직 부족한 상태이다. 항경련제 관련 골대사질환은 cytochrome P450 enzyme 유도에 의한 비타민 D의 이화작용 증가 외에도 다양한 요인들이 관여하는 것으로 알려져 있다. 저자들은 장기간 phenytoin을 복용하던 환자에서 저칼슘혈증으로 인한 경련 및 다발성 골절을 동반한 골연화증을 경험하였기에 문헌 고찰과 함께 보고하는 바이다.

Many studies have shown that patients taking antiepileptic drugs are at an increased risk for metabolic bone disease and low bone mineral density. Traditionally, this has been attributed to alterations in vitamin D metabolism by antiepileptic drugs which induce hepatic microsomal cytochrome P450 enzyme. However, there appear to be multiple mechanisms for antiepileptic drug-induced bone loss including lack of physical activity, reduced sunlight exposure, increased propensity for falling, and fractures associated with seizures or loss of consciousness. We experienced a case of antiepileptic drug-induced osteomalacia in a 63-year-old woman who had been on phenytoin for 8 years and was admitted with hypocalcemic seizures and multiple pathological fractures. This patient also had other risk factors for osteomalacia including reduced sunlight exposure, prolonged immobilization, and decreased dietary vitamin D intake. We discontinued phenytoin, and started calcium and vitamin D replacement. The patient’s serum calcium and vitamin D level were normalized after treatment. Metabolic bone disease including osteomalacia should be considered in patients who are taking antiepileptic drugs especially those who are exposed to other risk factors.