Divya Vohora
Jamia Hamdard, India
Title: Anti-epileptic drugs induced secondary osteoporosis: Multi-factorial mechanisms and current status
Biography
Biography: Divya Vohora
Abstract
Long term association exists between antiepileptic drug (AED) therapy and bone diseases. There is a lattice of the pathophysiological mechanisms of AED-induced bone disease that can be either independent or dependent on each other. Hepatic induction of cytochrome P450 leading to increased metabolism of vitamin D is the principle mechanism reported. Others include secondary hyperparathyroidism, calcitonin or vitamin K deficiency, deprived estrogen levels etc. A better understanding of these mechanisms can aid clinicians in identifying and monitoring vulnerable patients and in defining the optimal therapy for all affected patients. Bisphosphonates, a standard form of treatment for post-menopausal osteoporosis, are potent inhibitors of bone resorption and given the findings of increased bone resorption associated with AEDs, may represent an effective treatment for bone disease in patients receiving AEDs. Similarly, raloxifene, a selective estrogen receptor modulator, may be a potential therapeutic option in view of the fact that AEDs causes estrogen deficiency. Thus, studies were designed to investigate the effect of anti-osteoporotic therapies, in comparison with CVD supplementation, on AEDs-induced bony alterations in mice. Further, the effect of these therapies on seizures and on the antiepileptic efficacy of AEDs was investigated. Our results suggest a potential for bisphosphonates and raloxifene in the management of PHT and/or SVP-induced bone disease and thus merits further investigation to provide an evidenced-based approach for their use. Further, with the newer AEDs gaining importance, our future experiments would focus on comparing them with the conventional AEDs and to examine their impact on multiple aspects of bone health.