Hashimoto's thyroiditis or chronic lymphocytic thyroiditis is an autoimmune disease in which the thyroid gland is attacked by a variety of cell- and antibody-mediated immune processes. It was the first disease to be recognized as an autoimmune disease. It was first described by the Japanese specialist Hakaru Hashimoto in Germany in 1912.
Hashimoto's thyroiditis very often results in hypothyroidism with bouts of hyperthyroidism. Symptoms of Hashimoto's thyroiditis include weight gain, depression, mania, sensitivity to heat and cold, paresthesia, chronic fatigue, panic, bradycardia, tachycardia, congestive heart failure, high cholesterol, reactive hypoglycemia, constipation, migraines, muscle weakness, joint stiffness, menorrhagia, myxedematous psychosis, cramps, memory loss, vision problems, infertility and hair loss.[citation needed]
The thyroid gland may become firm, large, and lobulated in Hashimoto's thyroiditis, but changes in the thyroid can also be nonpalpable. Enlargement of the thyroid is due to lymphocytic infiltration and fibrosis rather than tissue hypertrophy. Physiologically, antibodies against thyroid peroxidase (TPO) 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.[citation needed]
A 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 (Cytotoxic T-lymphocyte Associated-4) gene polymorphisms that result in reduced functioning of the gene's products, which are associated with negative regulation of T-lymphocyte activity. Downregulatory gene polymorphisms affecting CTLA4 are also associated with autoimmune pathology seen in development of Type I diabetes.The strong genetic component underscoring this theory is borne out in studies on monozygotic twins, with a concordance of 38-55%, with an even higher concordance of circulating thyroid antibodies not in relation to clinical presentation (up to 80% in monozygotic twins). Neither result was seen to a similar degree in dizygotic twins, offering strong favour for high genetic aetiology.
Preventable environmental factors, including high iodine intake, selenium deficiency, as well as infectious diseases and certain drugs, have been implicated in the development of autoimmune thyroid disease in genetically predisposed individuals.The genes implicated vary in different ethnic groups and the incidence is increased in patients with chromosomal disorders, including Turner, Down's, and Klinefelter syndromes usually associated with autoantibodies against thyroglobulin and thyroperoxidase. Progressive depletion of these cells as the cytotoxic immune response develops leads to higher degrees of primary hypothyroidism, presenting with a poverty of T3/T4 levels, and compensatory elevations of TSH.
Recent research suggests a potential role for HHV-6 (possibly variant A) in the development or triggering of Hashimoto's thyroiditis.
Hashimoto's thyroiditis - Wikipedia, the free encyclopedia
Hashimoto's Thyroiditis: Symptoms, Causes, and Treatments
