Adverse effects of iodides on thyroid function.

The administration of pharmacologic quantities of iodine such as iodides for the 
treatment of pulmonary disease, organic iodine present in medications and x-ray 
contrast dyes, and the ingestion of iodine-rich natural foods, may result 
in goiter, hypothyroidism, or hyperthyroidism, especially in patients with underlying thyroid 
disease. Medications containing iodide may induce hypothroidism in euthyroid patients with 
Hashimoto's thyroiditis, 131I or surgically treated Graves' disease, or following hemithyroidectomy 
for nodules; and they may induce hyperthyroidism in patients with endemic 
iodine- deficient goiter, autonomous nodules or nontoxic nodular goiter, or in 
patients recently treated with antithyroid drugs for Graves' disease. Rarely, hypothyroidism 
or hyperthyroidism may develop in patients with completely normal thyroid function 
during administration of iodide. The etiology of iodide-induced goiter and hypothyroidism 
in patients with cystic fibrosis remains obscure. Iodide-induced myxedema may also 
occur in patients receiving drugs which alter thyroid function, such as 
lithium, phenazone, and sulfisoxazole. Finally, iodides do have a role in 
the treatment of hyperthyroidism but their use should probably be restricted 
to thyroid storm, preoperative preparation of the hyperthyroid patient, and following 
131I treatment. 