Perhaps the most common of all the disorders of the thyroid gland is multinodular goiter. Even in nonedemic regions it is clinically detected in about 4% of all adults beyond the age of 30. Pathologically it is much more frequent, the percentage of incidence being roughly the same as the age of the group examined. The disease is much more common in women than in men.
Multinodular goiter is thought to be the result of primarily two factors. The first factor is genetic heterogeneity of follicular cells with regard to function (i.e. thyroid hormone synthesis) and growth. The second factor is the acquisition of new qualities that were not present in mother cells and become inheritable during further replication. Mutations may occur in follicular cells leading to constitutively activated adenomas and to thyrotoxicosis. These factors may lead to loss of anatomical and functional integrity of the follicles and of the gland as a whole. These processes ultimately lead to goiter formation and are accelerated by stimulatory factors. These stimulatory factors may be TSH, brought about by events such as iodine deficiency, inborn errors of thyroid hormone synthesis, goitrogens or local tissue growth-regulating factors. These basic and secondary factors may cause the thyroid to grow and gradually evolve into an organ containing hyperplastic islands of normal glandular elements, together with nodules and cysts of varied histologic pattern.
Nodular goiter is most often detected simply as a mass in the neck, but at times an enlarging gland produces pressure symptoms on the trachea or esophagus. Occasionally tenderness and a sudden increase in size herald hemorrhage into a cyst. Thyrotoxicosis develops in a large proportion of these goiters after a few decades. Rare complications are paralysis of the recurrent laryngeal nerve, and pressure on the superior sympathetic ganglion causes a Horner's syndrome.
The diagnosis is based on the physical examination. Thyroid function test results are normal or disclose subclinical or overt hyperthyroidism. Thyroid autoantibodies are usually absent or low, excluding Hashimoto's thyroiditis. Imaging procedures may reveal distortion of the trachea, calcified cysts, or impingement of the goiter on the esophagus.
From 4 to 17% of multinodular thyroids removed at operation contain foci that on microscopic examination fulfill the criteria of malignant change. The infrequency of thyroid cancer as a cause of death clearly proves that the vast majority of these lesions are not lethal or even clinically active. One of the reasons for the high incidence of cancer in surgical specimens is that patients with multinodular goiters were often selected for surgery because of a concern for carcinoma.
If a clinically and biochemically euthyroid multinodular goiter is small and produces no symptoms , treatment is not necessary. T4 given in an effort to shrink the gland or to prevent further growth may be unsuccessful and may cause thyrotoxic symptoms. This therapy is more likely to be effective if begun at an early age while the goiter is still diffuse than in older patients in whom certain nodules may have already become autonomous. If the clinically euthyroid goiter is unsightly, shows subclinical hyperthyroidism or is causing pressure symptoms, treatment with 131I is successful in virtually all cases but causes hypothyroidism at varying degree. Surgery is an acceptable alternative. The efficacy of T4 treatment after surgery, to prevent regrowth, is uncertain.
Overt toxic nodular goiter is usually treated with RAI. A gratifying reduction in the size of the goiter and control of the thyrotoxicosis may be expected. Hypothyroidism often ensues. Surgery is an alternative but usually not necessary treatment.
The term colloid goiter is applied to glands composed of uniformly distended follicles appearing as a diffuse enlargement of the thyroid gland. The condition is found almost exclusively in young women. With time and due to a number of primary and secondary factors it may gradually develop into a multinodular goiter which becomes increasingly prominent as the decades pass. Appropriate therapy, if required, is the timely administration of thyroid hormone, that may be continued for several years.
An intrathoracic goiter is usually an acquired rather than a developmental abnormality. It may come about in embryonic life by a carrying downward into the thorax of the developing thyroid anlage, or in adult life by protrusion of an enlarging thyroid through the superior thoracic inlet into the yielding mediastinal spaces. These lesions may produce pressure symptoms and may also be associated with hyperthyroidism. If too large for treatment with 131I, the appropriate therapy is resection of the goiter through the neck, if possible. Attachment of the intrathoracic goiter to the gland in the neck ordinarily proves the site of origin and provides a method for its easy surgical removal.