Auto-immune thyroiditis

Abstract

The study of thyroid auto-immunity is still in its early stages and much work remains to be done. Thus, it is still uncertain whether the thyroid auto-antibodies arise because of some subtle alteration in the chemical constitution of the thyroid auto-antigens, because of failure to acquire tolerance or because of some derangement of the antibody-forming mechanism which renders it incapable of recognizing self; or whether the thyroid auto-antibodies merely reflect the pathologic changes brought about by other immunity mechanisms such as “cell-bound” or “delayed” hypersensitivity. Nevertheless, the auto-immune concept has had important repercussions in the diagnosis and treatment of thyroid disease. Auto-immune thyroiditis can readily be differentiated from other forms of thyroid disease on the basis of a combination of clinical and laboratory findings including serologic, biochemical and radioiodine tests. The precipitin test is the most reliable laboratory test, but the occasional occurrence of a positive test in thyroid neoplasm makes it necessary to carry out thyroid biopsy when the clinical findings are equivocal. The Hyland Laboratories T-A test provides a rapid screening procedure for auto-immune thyroiditis, but false positives may occur in patients with rheumatoid arthritis. On the other hand, the tanned red cell hemagglutination and complement fixation tests are too sensitive for routine diagnostic purposes. Increases in gamma globulin, abnormal flocculation tests, and an accelerated erythrocyte sedimentation rate are of diagnostic value in auto-immune thyroiditis and the results of routine radioiodine tests may be helpful, although occasionally misleading in the euthyroid patient who manifests symptoms of thyrotoxicosis. In the difficult case additional radioiodine tests, such as the perchlorate discharge, thyroxin or triiodothyronine suppression, and thyrotropin stimulation, or stable iodine studies may be necessary to establish the diagnosis without recourse to thyroid biopsy. The treatment of choice in auto-immune thyroiditis is thyroxin in a daily dose of between 0.2 and 0.3 mg. by mouth. This results in a variable but significant shrinkage of the goiter and a return toward normal of the biochemical abnormalities. Thyroxin should be prescribed to all patients irrespective of their clinical status and should be continued indefinitely. In rare instances surgical intervention will be necessary to relieve pressure symptoms or when a thyroid neoplasm is suspected. There is now good evidence that hypothyroidism without goiter, i.e., “primary” hypothyroidism, and auto-immune thyroiditis are variants of the same pathologic process, and that the chronic thyroiditis present in the thyrotoxic gland is a focal lesion of the same type. Patients with thyrotoxicosis who have positive precipitin tests have severe and extensive thyroiditis present in the gland and should be treated with long-term antithyroid drug therapy. Thyrotoxic patients with positive tanned red cell and complement-fixation tests are also best treated with antithyroid drugs, unless there is a definite indication for surgery or radioiodine therapy.