Antiepileptic Drugs and Thyroid Hormone Homeostasis: Literature Review and Practical Guideline

Abstract Thyroid hormones play an essential role in central nervous system development, normal physiological brain function and repairing mechanisms. On one hand, thyroid hormone alterations influence cortical excitability and on the other hand anti-epileptic drugs (AEDs) are associated with alterations in thyroid hormone metabolism. Although this interaction has long been described, and epilepsy is a common and chronic neurological disease, studies describing the interplay are often small and retrospective. We performed a systematic review of the current literature on epilepsy, AED therapy and thyroid hormone metabolism. Forty-seven studies were included. Most studies were retrospective cross-sectional studies (n=25) and investigated thyroid function alterations in patients on older AEDs such as phenobarbital, phenytoin, carbamazepine and valproic acid. Overall, almost one third of patients with epilepsy had subclinical hypothyroidism, especially patients on valproate and carbamazepine. Studies with patients receiving polytherapy are scarce, but reported a higher risk for hypothyroidism in patients with older age, female sex, longer duration of epilepsy, intractable epilepsy and polytherapy. Studies on newer AEDs are also scarce and further studies essential to improve the care for epilepsy patients. AEDs are associated with alterations in thyroid hormone metabolism. Thyroid function monitoring is indicated in patients on AEDs, especially those with refractory chronic epilepsy and those on polytherapy. We provide a practical guideline for thyroid function monitoring for the clinician taking care of patients on AEDs.

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Thyroid function and thyroid hormone metabolism in elderly people low T3-syndrome in old age?

Klinische Wochenschrift ◽

10.1007/bf01525000 ◽

1981 ◽

Vol 59 (7) ◽

pp. 315-323 ◽

Cited By ~ 50

Author(s):

J. Herrmann ◽

E. Heinen ◽

H. J. Kr�ll ◽

K. H. Rudorff ◽

H. L. Kr�skemper

Keyword(s):

Thyroid Hormone ◽

Elderly People ◽

Old Age ◽

Thyroid Function ◽

Hormone Metabolism ◽

Low T3 Syndrome ◽

Thyroid Hormone Metabolism ◽

Low T3

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Euthyroid sick syndrome in older people

Reviews in Clinical Gerontology ◽

10.1017/s095925980101111x ◽

2001 ◽

Vol 11 (1) ◽

pp. 1-4

Author(s):

Nadya Kagansky ◽

Sari Tal ◽

Shmuel Levy

Keyword(s):

Thyroid Hormone ◽

Older People ◽

Thyroid Function ◽

Clinical Evidence ◽

Thyroid Function Tests ◽

Hormone Metabolism ◽

Euthyroid Sick Syndrome ◽

Thyroid Hormone Metabolism ◽

Function Tests ◽

Altered Thyroid

The term euthyroid sick syndrome (ESS) is used to describe abnormalities in thyroid function tests that are observed in patients with systemic non-thyroid illness. Despite these abnormalities, there is usually little clinical evidence of hypothyroidism. Patients with ESS are generally considered to have altered thyroid hormone metabolism and to be euthyroid.

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Effects of tyrosine kinase inhibitors on thyroid function and thyroid hormone metabolism

Seminars in Cancer Biology ◽

10.1016/j.semcancer.2020.12.008 ◽

2021 ◽

Author(s):

Alessio Basolo ◽

Antonio Matrone ◽

Rossella Elisei ◽

Ferruccio Santini

Keyword(s):

Thyroid Hormone ◽

Tyrosine Kinase ◽

Tyrosine Kinase Inhibitors ◽

Thyroid Function ◽

Kinase Inhibitors ◽

Hormone Metabolism ◽

Thyroid Hormone Metabolism

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Thyroid function in rats with iodine deficiency is not further impaired by concurrent, marginal zinc deficiency

British Journal Of Nutrition ◽

10.1079/bjn19930150 ◽

1993 ◽

Vol 70 (2) ◽

pp. 585-592 ◽

Cited By ~ 6

Author(s):

John G. G. Smit ◽

Daan Van Der Heide ◽

Gerrit Van Tintelen ◽

Anton C. Beynen

Keyword(s):

Body Weight ◽

Thyroid Hormone ◽

Thyroid Function ◽

Body Weight Gain ◽

Male Rats ◽

Zn Deficiency ◽

Hormone Metabolism ◽

Thyroid Hormone Metabolism ◽

Marginal Zinc Deficiency ◽

Thyroid Hormone Levels

The hypothesis tested was that Zn deficiency aggravates impaired thyroid function as induced by I deficiency. In two separate experiments male rats were fed on diets either deficient in Zn or in I, or deficient in both. An identical, restricted amount of food was given to each rat so that body-weight gain of the experimental groups was comparable. Zn deficiency was evidenced by reduced tibial Zn concentrations. I deficiency was evidenced by goitre, reduced urinary I excretion, reduced plasma thyroxine concentrations and reduced absolute amounts and concentrations of thyroxine in the thyroid. Zn deficiency had no effect on the raised thyroid weight as induced by I deficiency. Zn restriction from 184 μmol Zn/kg diet to 31 μmol Zn/kg diet, hut not to 92 μmol Zn/kg diet, significantly lowered plasma thyroxine concentration. There were no interrelated effects of Zn and I deficiencies on thyroid hormone levels. These results indicate that marginal Zn deficiency does not influence thyroid hormone metabolism in I deficiency.

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Interference of dimethyl α-(dimethoxyphosphinyl) p-chlorobenzyl phosphate (SR-202) in thyroid hormone. metabolism: evidence of inhibition of monodeiodination

Journal of Endocrinology ◽

10.1677/joe.0.1120171 ◽

1987 ◽

Vol 112 (1) ◽

pp. 171-175 ◽

Cited By ~ 1

Author(s):

C. Liniger ◽

D. Pometta ◽

A. G. Burger

Keyword(s):

Thyroid Hormone ◽

Thyroid Hormones ◽

Thyroid Function ◽

Clinical Investigation ◽

Compelling Evidence ◽

Hormone Metabolism ◽

Thyroid Hormone Metabolism ◽

Peripheral Conversion

ABSTRACT SR-202 is a non-iodinated potential lipid-altering agent. When administered (100 mg) three times per day for 3 days to six euthyroid subjects it was associated with a 30 ± 3% (mean ± s.e.m.) fall in 3,3′,5-tri-iodothyronine(T3)(P < 0·001), a reciprocal 104 ± 14% rise in 3,3′,5′-tri-iodothyronine (reverse T3, rT3) (P < 0·01), and a 37 ± 7% rise in thyroxine (T4) (P < 0·001). Basal and TRH-stimulated TSH did not change. These results suggested that SR-202 was acting as an inhibitor of the peripheral monodeiodination of T4 to T3. During a second study the same subjects received the same dose of SR-202 for a further 3 days following 15 days of progressive substitutive treatment with l-T4, which they continued to take at 200 μg/day until the end of the study. Despite higher levels of thyroid hormones in the substituted subjects, similar results were observed, serum T3 falling by 40 ± 2% (P < 0·001), serum rT3 and T4 rising by 168 ± 24% (P < 0·01) and 37 ± 9% (P < 0·01) respectively. These changes provide compelling evidence that SR-202 is an inhibitor of the peripheral conversion of T4 to T3 that acts on thyroid hormone metabolism without provoking a counter-regulatory pituitary response. It might prove to be a useful tool for the clinical investigation of thyroid function. J. Endocr. (1987) 112, 171–175

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