Prior to the introduction of the thioamides in the 1940s, iodides were the major antithyroid agents; today they are rarely used as sole therapy.
Iodides have several actions on the thyroid. They inhibit organifi-cation and hormone release and decrease the size and vascularity of the hyperplastic gland. In susceptible individuals, iodides can induce hyperthyroidism (Jod-Basedow phenomenon) or precipi-tate hypothyroidism.
In pharmacologic doses (> 6 mg/d), the major action of iodides is to inhibit hormone release, possibly through inhibition of thyroglobulin proteolysis. Improvement in thyrotoxic symptoms occurs rapidly—within 2–7 days—hence the value of iodide therapy in thyroid storm. In addition, iodides decrease the vascu-larity, size, and fragility of a hyperplastic gland, making the drugs valuable as preoperative preparation for surgery.
Disadvantages of iodide therapy include an increase in intraglan-dular stores of iodine, which may delay onset of thioamide therapy or prevent use of radioactive iodine therapy for several weeks. Thus, iodides should be initiated after onset of thioamide therapy and avoided if treatment with radioactive iodine seems likely. Iodide should not be used alone, because the gland will escape from the iodide block in 2–8 weeks, and its withdrawal may pro-duce severe exacerbation of thyrotoxicosis in an iodine-enriched gland. Chronic use of iodides in pregnancy should be avoided, since they cross the placenta and can cause fetal goiter. In radiation emergencies involving release of radioactive iodine isotopes, the thyroid-blocking effects of potassium iodide can protect the gland from subsequent damage if administered before radiation exposure.
Adverse reactions to iodine (iodism) are uncommon and in most cases reversible upon discontinuance. They include acneiform rash (similar to that of bromism), swollen salivary glands, mucous membrane ulcerations, conjunctivitis, rhinorrhea, drug fever, metal-lic taste, bleeding disorders, and rarely, anaphylactoid reactions.