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Abstract
Epilepsy is a chronic disease and its treatment is lifelong in one-third of patients. Data from cross-sectional and prospective studies have reviewed the influence of antiepileptic drugs (AEDs) on thyroid hormones. Thyroid abnormalities were reported in one-third of the patients on AEDs. Subclinical hypothyroidism, reduced thyroxine, triiodothyronine, free thyroxine, free triiodothyronine and thyroid binding globulin concentrations were reported with phenobarbital, phenytoin, carbamazepine, valproate and oxcarbazepine, but not with lamotrigine, levitracetam, tiagabine and vigabatrine. All reported patients were clinically euthyroid and hormonal changes were reversible after AED withdrawal. The mechanisms for thyroid dysfunction with AEDs include enhanced metabolism and/or altered protein binding or interference of hypothalamic–pituitary–thyroid axis function. This review focuses on the evidence, mechanisms of thyroid abnormalities with AEDs and their clinical implications. The associations between subclinical hypothyroidism and metabolic risks due to AEDs are also discussed.
Financial & competing interests disclosure
The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.
Epilepsy is a chronic medical disease and its treatment may be lifelong.
The majority of patients with epilepsy have common metabolic comorbidities including subclinical hypothyroidism (SCH), which are associated with the use of antiepileptic drugs.
SCH (high thyroid stimulating hormone levels) and reduced thyroxine, free triiodothyronine, free thyroxine and thyroid binding globulin concentrations were reported with phenobarbital, phenytoin, carbamazepine, valproate and oxcarbazepine, but not with lamotrigine, levitracetam, tiagabine and vigabatrine.
The proposed mechanisms for SCH with antiepileptic drugs include enhanced metabolism and/or altered protein binding or interference of the function of the hypothalamic–pituitary–thyroid axis.
Physicians should be aware of the possible cumulative adverse effect of SCH on the metabolic states of patients with epilepsy and fetal brain development for children of mothers with epilepsy.