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Hashimoto’s thyroiditis or chronic lymphocytic thyroiditis is an autoimmune disease where the body’s own T-cells attack the cells of the thyroid. It was the first disease to be recognised as an autoimmune disease.[citation needed]
This disorder is believed to be the most common cause of primary hypothyroidism in North America. It occurs far more often in women than in men (10:1 to 20:1), and is most prevalent between 45 and 65 years of age.
In European countries, an atrophic form of autoimmune thyroiditis (Ord’s thyroiditis) is more common than Hashimoto’s thyroiditis.
The family history of thyroid disorders is common, with the HLA-DR5 gene most strongly implicated conferring a relative risk of 3 in the UK. In addition Hashimoto’s thyroiditis may be associated with CTLA-4 gene since the CTLA-4 antigen acts as an inhibitor to T-Cell activation.
The genes implicated vary in different ethnic groups and the incidence is increased in patients with chromosomal disorders, including Turner, Down’s, and Klinefelter’s syndromes.
The underlying specifics of the immune system destruction of thyroid cells is not clearly understood. Various autoantibodies may be present against thyroid peroxidase, thyroglobulin and TSH receptors, although a small percentage of patients may have none of these antibodies present. A percentage of the population may also have these antibodies without developing Hashimoto’s thyroiditis.
In many cases, Hashimoto’s thyroiditis results in hypothyroidism, although in its acute phase, it can cause a transient hyperthyroidism thyrotoxic state known as hashitoxicosis.
Physiologically, antibodies against thyroid peroxidase and/or thyroglobulin cause gradual destruction of follicles in the thyroid gland. Accordingly, the disease can be detected clinically by looking for these antibodies in the blood. It is also characterized by invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes. It is associated with non-Hodgkin lymphoma.
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