Navigating Bone Health in Epilepsy: A Detailed Review of Anticonvulsant-Induced Osteomalacia, Its Mechanisms, and Therapeutic Strategies

Abstract

Anticonvulsants are the drugs given for managing epilepsy and some other types of neurological disorders; however, their long-term use is increasingly suspected of causing adverse skeletal outcomes, including osteomalacia. Osteomalacia is a condition marked by defective mineralization of bone, leading to bone softening, bone pain, muscle weakness, and predisposition to fractures. The disruption of vitamin D metabolism, impaired calcium absorption, and altered bone turnover are mechanisms attributed to several commonly used anticonvulsants, especially enzyme-inducing agents such as phenytoin, carbamazepine, and phenobarbital, in contributing to osteomalacia. Hence, this review aims at providing detailed information about the pathophysiology, clinical manifestations, diagnosis, and treatment of anticonvulsant-induced osteomalacia. The review places further emphasis on the importance of regular monitoring of bone health in individuals receiving long-term antiepileptic treatment, supplementation, lifestyle interventions, and interprofessional care. A proper understanding of this preventable complication will certainly help healthcare providers to minimize the impact in these patients and improve outcomes.

Keywords: Anticonvulsants, Osteomalacia, Vitamin D deficiency, Bone mineralization, Antiepileptic drugs, Enzyme-inducing drugs