As this is an autoimmune disease with distruction of thyroid tissue, patients display hypothyroid symptoms. These include lethargy, weakness, hypoactivity, cold intolerance, bradycardia, myxedema, coarse skin and brittle hair. Bouts of hyperthyroidism sometimes occur due to thyrotoxicosis during follicular rupture.
Patients typically present with an enlarged, nontender thyroid gland, which is also known as a goiter. These goiters occur due to lymphocytic infiltration and fibrosis, rather than hypertrophy.
Most commonly, this disorder arises from various auto-antibodies which target thyroid peroxidase, thyroglobulin and TSH receptors. These antibodies then lead to an antibody-dependent cell-mediated cytotoxicity.
A common antibody present in Hashimoto's thyroiditis is anti-thyroid peroxidase, or TPO.
Another group of auto-antibody found in Hashimoto's thyroiditis are anti-thyroglobulin antibodies.
Upon histological examination, Hürthle cells can be seen in Hashimoto thyroiditis. These cells line atrophied colloid bodies and have eosinophilic, granular cytoplasm, along with metaplasia.
Lymphoid follicles can be seen in histological examination of patients with this disease. These are characterized by lymphoid aggregate with germinal centers.
Patients with the HLA-DR5 or HLA-DR3 haplotypes have a higher relative risk for developing this thyroid disorder.
Thyroid lymphomas are almost always the non-Hodgkin type. The risk of developing thyroid lymphoma is associated with Hashimoto thyroiditis.
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