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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 remain-ing
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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Figure 3 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 inade-quate
function of the single cell.
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