Incidence, predictability, and pathogenesis of amiodarone-induced thyrotoxicosis and hypothyroidism

Article Abstract:

Amiodarone is a drug used to treat heart arrhythmias. Over one-third of the drug is iodine, and with normal use, this results in iodine intake that is 20-fold greater than recommended levels. Amiodarone treatment can alter metabolism of thyroxine (thyroid hormone) and of thyrotropin (TSH), the pituitary hormone that stimulates thyroxine production. Amiodarone-induced thyrotoxicosis (high thyroxine levels; AIT) or amiodarone-induced hypothyroidism (low thyroxine levels; AIH) may occur in up to 32 percent of patients. The normal level of a patient's iodine intake may be influential. To better understand the effects of this drug, the incidence and predictability of AIT and AIH in 58 of 69 (16 female) patients were studied in an area where the subjects received a moderate dietary iodine intake. At the start of the study, all patients were euthyroid (had normal thyroxine levels) and had normal TSH responses to stimulation with thyroid releasing hormone (TRH), a hypothalamic hormone that stimulates pituitary production of TSH. During follow-up, which ranged from 6 to 54 months, 27 remained in this first group with normal thyroid function. Of the remainder, 22 developed a decreased TSH response (group II), 6 of whom developed signs of AIT, while 9 patients began to produce more TSH in response to TRH (group III), with 2 patients showing signs of AIH. Eleven of 16 group II patients were studied further, with no new cases of AIT occurring and normalization of TSH in 8 patients. However, of four group III patients who were studied further, two developed AIH and one patient developed AIT and thus switched to Group II. Female patients with antibodies against thyroglobulin (an iodine-containing protein in the thyroid gland) or against microsomes (portions of the cell where proteins are modified) had a 13.5 greater risk of developing AIH than men without thyroid antibodies. Patients who developed hypothyroid TSH responses (group III) had significantly higher initial peak TSH levels and lower levels of a thyroxine-related hormone, rT3. Patients in group III had a higher initial incidence of goiter and thyroid antibodies. The study suggests that amiodarone treatment may unmask pre-existing hypothyroid conditions in patients who are asymptomatic before treatment, while AIT development is unpredictable and of unexplained sudden onset. (Consumer Summary produced by Reliance Medical Information, Inc.)

Risk factors, Hypothyroidism, Amiodarone

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Transient thyrotoxicosis associated with a pheochromocytoma in a patient with multiple endocrine neoplasia type IIa

Article Abstract:

A case is described of a 42-year-old woman with symptoms of thyrotoxicosis, a toxic condition caused by increased activity of the thyroid gland. The signs of thyrotoxicosis include palpitations, agitation, and weight loss. This patient also had a thyroid goiter, or enlarged thyroid gland, and increased levels of thyroid hormones such as thyroxine and triiodothyronine. The symptoms of thyrotoxicosis are similar to those caused by increased activity of the adrenergic nervous system, which may result from pheochromocytoma, a tumor of the sympathetic nervous system and adrenal gland that produces large amounts of norepinephrine and epinephrine. Pheochromocytoma may also be associated with swelling of the thyroid gland. This is the first reported case of biochemical hyperthyroidism, indicated by increased levels of thyroid hormones, caused by pheochromocytoma. It is thought that the excessive levels of norepinephrine resulting from pheochromocytoma stimulated the thyroid gland to produce increased amounts of thyroid hormones. The possibility of a pheochromocytoma should be evaluated in patients with symptoms of thyrotoxicosis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Case studies, Pheochromocytoma, Endocrine gland diseases, Endocrine diseases

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