Notably, epilepsy is a neurological disorder which is characterized by periodic seizures. It is an illness that must be managed to enhance the health of the patients and reduce the negative impacts on their well-being. This treatment can be done by admission of antiepileptic drugs (AEDs). Additionally sometimes one type of AEDs will not adequately control seizures. As such, an epileptic patient may need to use a combination of several drugs. Epileptic patients may also use AEDs while taking other drugs (non-AEDs) for treatment of different illnesses. Importantly, most of these AEDs interact with both non antiepileptic and other antiepileptic drugs. Hence, it is vital to identify these interactions and their consequences in order to determine the best way to maintain the well-being of the epileptic patients. This paper will, therefore, discuss the consequences drug interactions in the use of AEDs with other AEDs, as well as, with non- antiepileptic drugs (1).
Most interactions from AEDs are caused by inhibition or induction of enzymes involved in the metabolism of drugs. Other mechanisms such as pharmacodynamics may also cause these interactions. What is more, when different AEDs interact, the consequences to the patients could be varied. For instance, while some interactions cause a fall in the concentration of the affected drug, others cause a rise in the concentration of the influenced drug. Notably, many older AEDs such as phenytoin, carbamazepine, primidone and phenobarbital tend to act as enzyme inducers while others like valproic acid act as inhibitors. The reaction between such AEDs has potentially serious consequences which fall under level 1 or 2 interactions. In level 1 interactions, since the clinical implications are very serious, the AEDs combination should be stopped while Level 2 interactions call for more caution in administering particular AEDs combinations with a possibility of modifying the dosage. It is also vital to understand that some enzyme inducing AEDs influence biochemical pathways such as bone metabolism, hemostasis of vitamin D, cholesterol synthesis and sex hormones metabolism. When this AEDs interact, most enzyme inducers increase the metabolism rate of co-administered AEDs. However, the clinical importance of this interactions is insignificant since lowering of the serum concentration is compensated by the pharmacological impact of the added medication. In some cases however, the control of seizures becomes unfavorably affected. For newer AEDs, there is lower susceptibility to interactions with other AEDs or other drugs. For example Lacosamide has no known interaction. However, other drugs such as stripentol and rufinamide have their use limited to particular pediatric populations due to their interaction potential (1).
There is also a rather important need to determine the consequences of interactions of AEDs with non-AEDs. These drugs may interact resulting to lower AED concentrations while others cause a rise in the concentration of AEDs. In other cases, the interactions result in a decline or rise in the concentration of non-antiepileptic drugs. In addition, AEDs interact with some oral anticoagulants used to treat thromboembolic disorders resulting in serious complications. For instance, carbamazepine enhances metabolism of coumarin drugs hence leading to a need for incremental dosage requirements (3).
Notably, while contraception is a vital consideration for women who have attained the reproductive age, women with epilepsy (WWE) face great challenges in the use of these contraception with their AEDs. This can be attributed to the interactions between AEDs and contraceptives since reproductive steroids contain neuroactive properties which can potentially affect the mechanism in which AEDs work. Some AEDs also affect the working mechanism of contraceptives. Further, there is a possibility that hormonal contraception will influence co-morbidities of epilepsy. For instance, headaches and depression will tend to be more pronounced in WWEs. Therefore, AEDs which do not interact with oral contraceptives are best suited for use by WWEs (2).
- Johannessen, S., & Johannessen Landmark, C. (2010). Antiepileptic Drug Interactions Principles and Clinical Implications. Current Neuropharmacology, 8(3), 254-267. http://dx.doi.org/10.2174/157015910792246254
- Herzog, A. (2015). Differential impact of antiepileptic drugs on the effects of contraceptive methods on seizures: Interim findings of the epilepsy birth control registry. Science
- Direct. Retrieved 22 April 2018, from https://www.sciencedirect.com/science/article/pii/S1059131115000394
- Perucca, E. (2006). “Clinically relevant drug interactions with antiepileptic drugs.” British Journal of Clinical Pharmacology, 61(3), 246-255. http://dx.doi.org/10.1111/j.13652125.2005.02529.x