sodium-perchlorate and Thyroiditis

Iodine is essential for thyroid hormone synthesis and is an important regulator of thyroid function. Chronic iodine deficiency leads to hypothyroidism, but iodine excess also impairs thyroid function causing hyperthyroidism, hypothyroidism, and/or thyroiditis. This study aimed to investigate the underlying mechanisms by which exposure to chronic iodine excess impairs pituitary-thyroid axis function.. Male Wistar rats were treated for two months with NaI (0.05% and 0.005%) or NaI+NaClO. NaI-treated rats presented high levels of iodine in urine, increased serum thyrotropin levels, slightly decreased serum thyroxine/triiodothyronine levels, and a decreased expression of the sodium-iodide symporter, thyrotropin receptor, and thyroperoxidase mRNA and protein, suggesting a primary thyroid dysfunction. In contrast, thyroglobulin and pendrin mRNA and protein content were increased. Kidney and liver deiodinase type 1 mRNA expression was decreased in iodine-treated rats. Morphological studies showed larger thyroid follicles with higher amounts of colloid and increased amounts of connective tissue in the thyroid of iodine-treated animals. All these effects were prevented when perchlorate treatment was combined with iodine excess.. The present data reinforce and add novel findings about the disruption of thyroid gland function and the compensatory action of increased thyrotropin levels in iodine-exposed animals. Moreover, they draw attention to the fact that iodine intake should be carefully monitored, since both deficient and excessive ingestion of this trace element may induce pituitary-thyroid axis dysfunction.

Topics: Animals; Antidotes; Gene Expression Regulation; Iodide Peroxidase; Iodine; Male; Perchlorates; Pituitary Gland; Poisoning; Rats, Wistar; Receptors, Thyrotropin; Renal Elimination; RNA, Messenger; Sodium Compounds; Sodium Iodide; Symporters; Thyroid Gland; Thyroiditis; Thyrotropin; Thyroxine; Toxicity Tests, Chronic; Toxicokinetics; Triiodothyronine

We report a case of amiodarone-induced thyrotoxicosis of protracted duration, unresponsive to conventional thionamide therapy, with therapy limited by severe adverse drug reactions. Other treatment modalities included high dose corticosteroids, plasmapheresis, lithium and perchlorate. Temporary amelioration was achieved following plasmapheresis; however, this and other measures were unsuccessful in controlling the thyrotoxicosis, which deteriorated to thyroid storm. Histopathologically, a degenerative, inflammatory thyroiditis was evident. We discuss the limitations of conventional drug therapy and the lack of a sustained response to plasmapheresis. The failure of high doses steroids to alter the course of illness and to completely suppress the thyroidal inflammatory process is highlighted. A potential role for renal and hepatic impairment in the observed protracted course of amiodarone-induced thyrotoxicosis is suggested.

Topics: Amiodarone; Anti-Arrhythmia Agents; Anti-Inflammatory Agents; Antithyroid Agents; Fatal Outcome; Humans; Lithium; Male; Middle Aged; Perchlorates; Plasmapheresis; Prednisolone; Sodium Compounds; Thyroid Crisis; Thyroiditis