The effect of antiepileptic drugs on thyroid hormone homeostasis
Authors:
J. Šimko 1; J. Horáček 2
Authors place of work:
Neurologická klinika LF UK a FN, Hradec Králové, Neurologická ambulance, Rychnov nad Kněžnou
1; II. Interní klinika LF UK a FN, Hradec Králové
2
Published in the journal:
Cesk Slov Neurol N 2007; 70/103(5): 488-493
Category:
Review Article
Summary
The discussion concerning the effect of antiepileptic drugs (AEDs) on thyroid (TH) hormone homeostasis began as early as in the 1960’s. Hormone levels have been shown to decrease only in the case of AEDs – enzymatic inductors (AEDs-IND), namely phenobarbital, primidone, phenytoin, carbamazepine and oxcarbazepine. Patients who are not treated for a thyroid disease remain euthyroid during AEDs-IND medication and do nor require T4(T3) replacement therapy. Patients with TH hypofunction / non-function are exposed to a considerable (approximately 30 %) risk of hypothyreosis decompensation through the mechanism of pharmacokinetic interaction of AED’s-IND with T4 (T3) replacement therapy after the exposure to AED’s-IND. The maximum of this risk can be expected during the initial 2–5 weeks after the start of AED’s-IND medication; specific traits of clinical approach to such patients are mentioned, too. As for the other antiepileptic drugs, the effect on thyroid hormone homeostasis is but of a minor degree, or there are not enough studies on this topic or the existing ones only have the form of case study communications. There are virtually no studies on correlation between the cognitive functions and the thyroid function parameters in patients taking AED’s-IND.
Key words:
antiepileptic drugs – enzymatic induction – hypothyreosis
Zdroje
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Štítky
Paediatric neurology Neurosurgery NeurologyČlánok vyšiel v časopise
Czech and Slovak Neurology and Neurosurgery
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