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Certain medications can have the unintended side effect of affecting thyroid function. While some medications can lead to significant hypothyroidism or hyperthyroidism and those at risk will need to be carefully monitored, some medications may affect thyroid hormone lab tests without causing any symptoms or clinical changes, and may not require treatment.
Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, or abbreviated TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T 4), and then triiodothyronine (T 3) which stimulates the metabolism of almost every tissue in the body. [1]
Furthermore, reviewing their medications and possible dietary supplements is important, as several medications can affect thyroid hormone levels. [14] Levothyroxine is also used to treat subclinical hypothyroidism, which is defined by an elevated TSH level and a normal-range free T 4 level without symptoms. [14]
Levels may be abnormal in the context of other illnesses, and TSH testing in hospitalized people is discouraged unless thyroid dysfunction is strongly suspected [8] as the cause of the acute illness. [17] An elevated TSH level indicates that the thyroid gland is not producing enough thyroid hormone, and free T 4 levels are then often obtained.
A randomized control trial testing single dose treatment for Graves' found methimazole achieved euthyroidism (normal thyroid function that occurs within normal serum levels of TSH and T4 [23]) more effectively after 12 weeks than did propylthiouracil (77.1% on methimazole 15 mg vs 19.4% in the propylthiouracil 150 mg groups). [24]
Stress suppresses TSH, [5] and alterations in thyroid hormone levels may arise in psychiatric illness. In major depressive disorder, an NTIS-like phenotype may be observed, with reduced T3 and increased rT3. T4 may be elevated, and TSH is usually normal, although TSH's normal circadian rhythm may be disrupted. [2]
Thyroid hormones act on nearly every cell in the body. They act to increase the basal metabolic rate, affect protein synthesis, help regulate long bone growth (synergy with growth hormone) and neural maturation, and increase the body's sensitivity to catecholamines (such as adrenaline) by permissiveness. [12]
[9] [10] The first English-language report, in 1931, originated from Dunlap and Kepler, physicians at the Mayo Clinic; they described the condition in a patient with features of Graves' disease. [ 2 ] [ 10 ] In 1937 periodic paralysis was linked with hypokalemia, as well as precipitation of attacks with glucose and insulin.