triiodothyronine--reverse and Epilepsy

Topics: Adult; Anticonvulsants; Epilepsy; Female; Fetal Growth Retardation; Growth Hormone; Humans; Pregnancy; Pregnancy Complications; Thyrotropin; Thyroxine; Triiodothyronine; Triiodothyronine, Reverse

The effects of antiepileptic drugs on thyrotropin (TSH), thyroid hormone, and growth hormone (GH) concentrations in sera of 16 pregnant women with epilepsy were studied. The drugs markedly depressed thyroxine (T4) concentration in maternal and umbilical cord sera, and partly depressed TSH in maternal and umbilical artery sera and GH in umbilical artery sera, but not triiodothyronine (T3) or reverse T3 (r-T3) concentration. The effect of antiepileptic drugs on T4 concentration in maternal serum was not influenced by pregnancy. Ratios of hormone levels in maternal serum compared with those in umbilical cord serum revealed a pattern similar to that seen in normal pregnant women. They suggest that transplacental passage of TSH, thyroid hormone, and GH are not markedly affected by antiepileptic drugs.

Topics: Adult; Anticonvulsants; Epilepsy; Female; Fetal Blood; Growth Hormone; Humans; Infant, Newborn; Pregnancy; Pregnancy Complications; Thyroid Hormones; Thyrotropin; Thyroxine; Triiodothyronine; Triiodothyronine, Reverse

Patients on long-term treatment with either of the stereochemically related antiepileptic drugs phenytoin (DPH) or carbamazepine (CBZ) had similar changes in serum thyroid hormone concentrations. T4, FT4, FT4 index, T3, FT3, FT3 index and rT3 were reduced, whereas T3U and TSH were not significantly different from the reference group levels. Long-term phenobarbitone treatment had no convincing effect on the investigated parameters when used alone, but possibly potentiated the effect of CBZ. In patients starting on CBZ, T4 fell to a stable 70% of the basal level after 1--2 weeks. T3 decreased transitorily to 85% of the basal level. TSH showed a complementary but somewhat delayed transitory increase. T3U and TBG did not change significantly. The effect of CBZ and DPH can be explained by interference with thyroid hormone binding to TBG combined with enzyme-induced increased metabolic clearance rate of thyroid hormones without homeostatic maintenance of premedication levels of FT4 and FT3. We suggest that the regulated factor maintaining euthyroidism in these patients is the total quantity of thyroid hormones being degraded in the tissues per unit time. We conclude that serum concentrations of FT4 and FT3 do not reflect thyroid status adequately under all circumstances.

Topics: Adult; Carbamazepine; Epilepsy; Humans; Phenobarbital; Phenytoin; Radioimmunoassay; Thyroid Hormones; Thyrotropin; Thyroxine; Thyroxine-Binding Proteins; Time Factors; Triiodothyronine; Triiodothyronine, Reverse