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Goitre associated with autoimmunity |
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Autoimmune thyroid disease commonly leads to goitre. Most patients with Graves' disease (about 80%) have a diffuse goitre. This is presumably due to thyroid cell proliferation induced by activation of the TSH-receptor by TSH-receptor autoantibodies. The larger the size of the thyroid in hyperthyroid Graves' disease, the less favorable the response to medication (fig. 2) The follicular cells of Graves' disease react to the chronic stimulation by an increase in T3 synthesis in thyroglobulin and by a high rate of T4 deiodination to T3. This high T3 state (fig. 3) is a normal and reversible reaction.
Figure 2:
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Outcome of 2 years of therapy of hyperthyroidism with a combination of thionamide and thyroxine. Per cent of patients remaining euthyroid after cessation of medication. Note the rapid relaps of hyperthyroidism in nearly all patients with multinodular toxic goitre. Data from 8. |
Figure 3:
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Thyroglobulin obtained by standardized fine needle aspiration from patients with euthyroid multinodular goitre (MNG, n = 10), untreated Graves' disease (GD, n = 8), untreated primary autoimmune hypothyroidism (MY, n = 9), and control subjects (C, n = 7). Thyroglobulin was measured by RIA, iodine by Ce/As method after alkaline inceneration, and T4 and T3 by RIA after pronase digestion. Data from 4 and 5. |
Approximately 15% of patients with autoimmune hypothyroidism have goitre (Hashimoto's disease), but the majority have atrophic thyroiditis. The main cause for the goitre in Hashimoto's disease is excessive accumulation in the thyroid gland of lymfocytes. This type of goitre may occur with normal or only slightly impaired thyroid function. The follicular cells in autoimmune hypothyroidism are more or less stimulated by TSH. They react similarly to stimulation as the follicular cells in Graves' disease (fig. 3). Hence, the functional defect in autoimmune hypothyroidism seems to be caused by a reduction in the number of functioning cells, and not by inadequate function of the single cell.
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