A study to compare the effects of three AEDs on female mice

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Huanyu Kong , Pushparajan Perianna Pillai, Haryati Binti Ahmad Hairi


Epilepsy is a common neurological condition that often necessitates the use of antiepileptic medications for the rest of one's life (AEDs). The use of prolonged AED treatment has been consistently established over the last four decades to be related with decreased bone density and a greater risk of fracture. "Recent clinical data has also confirmed prior research showing long-term use of AEDs affects bone mineral density (BMD), increases the frequency of fractures, and causes overt osteomalacia (decreased bone density). It has been observed that AED-induced effects on bone occur at rates of 50 percent or more in some cases. Not only do AEDs, but also the illness itself, has an intricate effect on bone microarchitecture and bone mineral density (BMD), increasing the likelihood of fractures. Because a variety of variables may be involved, gross bone alterations and higher risk of fractures are not simply attributed to AEDs, but also to seizure activity-associated falls, trauma, and" an inactive lifestyle.

Despite the fact that the mechanisms responsible for AED-related bone fragility are likely to be numerous and still poorly understood, the AEDs most commonly reported to cause disorders of bone "metabolism are potent inducers of the cytochrome P450 (CYP 450) monoxygenase system (phenytoin; carbamazepine; phenobarbitone) that influence the calcium-vitamin D axis by reducing bio-available vitamin D resulting in hypocalcemia and compens. Despite the fact that this has been considered to be the primary and most common mechanism for AED-induced bone loss, this is not always the case for a variety of reasons, including the fact that not all patients who develop bony deficits have deficient vitamin D levels, and the fact that AEDs that are enzyme inhibitors have also been associated with bony adverse effects. Another mechanism that has been described during AED medication includes hypovitaminosis K, calcitonin insufficiency, decreased" intestinal absorption of calcium, hyperhomocysteinemia, and low levels of oestrogen. These and other processes might all play a role in the detrimental effects on bone.

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