IODIDES
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.
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