We’ve been discussing thyroiditis lately (see posts from 4/27/09 and 4/28/09). There are four kinds of thyroiditis: Hashimoto, subacute granulomatous, lymphocytic, and fibrosing. The most common of these, by far, is Hashimoto thyroiditis.
Hashimoto is an autoimmune disease in which the patient’s own immune system attacks and slowly destroys the thyroid gland. It’s much more common in women (as is typical of autoimmune diseases), and it is the most common cause of hypothyroidism in parts of the world where there is enough iodine. It typically presents with an enlarged, non-tender thyroid gland. Patients gradually lose thyroid function and eventually become hypothyroid.
The main problem in this disorder is that the T cells (for some unknown reason) recognize the patient’s own thyroid antigens as foreign. The T cells are cytotoxic to thyroid epithelial cells (not good), and they stimulate B cells to make anti-thyroid antibodies (also not good), such as anti-peroxidase antibody, anti-thyroglobulin antibody, and anti-TSH-receptor antibody. The most sensitive and specific of these antibodies is anti-peroxidase antibody (the other antibodies can also be present in Graves disease). The most interesting (I think) is anti-TSH-receptor antibody. It blocks the action of TSH, leading to hypothyroidism!
Salient histologic features of Hashimoto disease include a whopping lymphoid infiltrate, often with germinal centers (as in the above image) and Hurthle cells, which are follicular epithelial cells with abundant, eosinophilic, granular cytoplasm (if you look closely, you can see some of these in the above image, especially around the perimeter at 2, 7, and 9 o’clock).
Patients with Hashimoto thyroiditis who are euthyroid may simply be observed clinically. Patients who are hypothyroid generally are given synthetic thyroid hormone (levothyroxine). Since the disease is a chronic, progressive, autoimmune process, treatment must continue for life.
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