Correct and incorrect use of iodine in the treatment of goiter

Abstract

Iodine has an important relationship to the normal function of the thyroid gland in which it is constantly present and is stored as a normal constituent. Simple colloid goiter, the inactive type of parenchymatous goiter, commonly develops whenever there is a deficient intake or a faulty metabolism of iodine in the body. Simple colloid or endemic goiter may be prevented by the prophylactic administration of minute amounts of iodine. Iodine, in small amounts, together with small amounts of thyroid extract is advised in the treatment of simple goiter. This is the only type of goiter in which the therapeutic administration of iodine is indicated. The prolonged administration of iodine to the simple colloid goiter may however occasionally stimulate the gland with the consequent production of hyperthyroidism. A correct diagnosis as to the type of goiter is therefore of the greatest importance in order to institute correct therapy. A non-toxic goiter may be activated and the symptoms of a toxic goiter may be exacerbated by the indiscriminate administration of iodine. The administration of iodine during pregnancy is indicated only in case inactivity of the thyroid gland is present. The physiologically overactive thyroid gland in pregnancy may be stimulated to further activity resulting in a state of true clinical hyperthyroidism. The administration of iodine does not prevent the growth and development of true adenoma and has no place in the medical treatment of this condition. Non-toxic adenoma is commonly activated by indiscriminate treatment with iodine and the symptoms of toxic adenoma are exacerbated by its use. The preoperative intensive preparation of the majority of patients with toxic adenoma does not produce improvement comparable to that seen in the case of exophthalmic goiter. The acutely toxic adenomatous goiter particularly when the metabolic rate is high, is often favorably influenced by the use of iodine, whereas those cases of adenoma with lesser degrees of hyperthyroidism may show relatively little improvement. An appreciable number in this group may be made acutely worse. The hyperplastic thyroid gland has an extraordinary affinity for iodine which causes the hyperplasia to revert to the colloid or resting state. Accordingly when iodine is intensively administered to the patient with Graves' disease, previously untreated with iodine, a marked clinical remission in the course of the disease is produced. Operation should be and can be safely performed during this period of remission. The mortality of resection operations done during the period of remission has been reduced almost to nil, and stage operations are rarely necessary. If thyroid resection is not done at this favorable time of remission, the patient often relapses into a state of clinical exacerbation in the course of one to two or even three months. A condition of uncontrollable hyperthyroidism may thus result. Similarly, exacerbation may follow upon the administration of iodine even in small doses, over a prolonged period. The hyperplastic thyroid gland in the phase of reactivation following a previous period of treatment with iodine becomes relatively insensitive or refractive to the further administration of iodine. The preoperative treatment with iodine does not protect the iodized patient with toxic adenoma or Graves' disease in any way comparable to the protection afforded the patient not previously so treated. The patient suffering with an acute exacerbation following prolonged use of iodine may be a dangerous operative risk whether iodine is given preoperatively or not. It is particularly in these circumstances that recourse must be had to multiple operations such as preliminary ligation and single lobectomies to eliminate the increased risk involved in a primary double lobectomy. Iodine has little effect in controlling postoperative hyperthyroidism. There is no evidence that the postoperative administration of iodine reduces the incidence of recurrent hyperthyroidism. The spontaneous hyperthyroid crisis occurring occasionally in the course of severe Graves' disease may be effectively controlled by large doses of iodine given either orally or intravenously. When the crisis occurs as a result of the incorrect use of iodine, the further administration of iodine, even in large amounts, is ineffectual and a fatal outcome may ensue.