Hashimoto's thyroiditis
Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis and Hashimoto's disease, is an autoimmune disease in which the thyroid gland is gradually destroyed.[1][6] A slightly broader term is autoimmune thyroiditis, identical other than that it is also used to describe a similar condition without a goiter.[7][8]
"Hashimoto's disease" redirects here. For the encephalopathy, see Hashimoto's encephalopathy.Hashimoto's thyroiditis
Chronic lymphocytic thyroiditis, autoimmune thyroiditis, struma lymphomatosa, Hashimoto's disease
Painless goiter, weight gain, feeling tired, constipation, depression, dry skin, hair loss[1]
Family history, another autoimmune disease[1]
Levothyroxine, surgery[1][5]
2% at some point[4]
Early on, symptoms may not be noticed.[1] Over time, the thyroid may enlarge, forming a painless goiter.[1] Some people eventually develop hypothyroidism with accompanying weight gain, fatigue, constipation, depression, hair loss, and general pains.[1] After many years the thyroid typically shrinks in size.[1] Potential complications include thyroid lymphoma.[2] Furthermore, because it is common for untreated patients of Hashimoto's to develop hypothyroidism, further complications can include, but are not limited to, high cholesterol, heart disease, heart failure, high blood pressure, myxedema, and potential pregnancy problems.[9]
Hashimoto's thyroiditis is thought to be due to a combination of genetic and environmental factors.[4] Risk factors include a family history of the condition and having another autoimmune disease.[1] Diagnosis is confirmed with blood tests for TSH, T4, and antithyroid autoantibodies.[1] Other conditions that can produce similar symptoms include Graves' disease and nontoxic nodular goiter.[5]
Hashimoto's thyroiditis is typically treated with levothyroxine.[1][10] If hypothyroidism is not present, some may recommend no treatment, while others may treat to try to reduce the size of the goiter.[1][11] Those affected should avoid eating large amounts of iodine; however, sufficient iodine is required especially during pregnancy.[1] Surgery is rarely required to treat the goiter.[5]
Hashimoto's thyroiditis affects about 5% of Caucasians at some point in their lives.[4] It is the most common cause of hypothyroidism in iodine-sufficient areas of the world.[12] It typically begins between the ages of 30 and 50 and is much more common in women than men.[1][3] Rates of the disease appear to be increasing.[5] It was first described by the Japanese physician Hakaru Hashimoto in 1912.[13] In 1957, it was recognized as an autoimmune disorder.[14]
Genetics[edit]
Thyroid autoimmunity can be familial.[7] Many patients report a family history of autoimmune thyroiditis or Graves disease.[18] Twin studies have revealed a concordance of Hashimoto's disease in monozygotic twins.[12]
Prognosis[edit]
Overt, symptomatic thyroid dysfunction is the most common complication, with about 5% of people with subclinical hypothyroidism and chronic autoimmune thyroiditis progressing to thyroid failure every year. Transient periods of thyrotoxicosis (over-activity of the thyroid) sometimes occur, and rarely the illness may progress to full hyperthyroid Graves' disease with active orbitopathy (bulging, inflamed eyes). Rare cases of fibrous autoimmune thyroiditis present with severe shortness of breath and difficulty swallowing, resembling aggressive thyroid tumors, but such symptoms always improve with surgery or corticosteroid therapy. Although primary thyroid B-cell lymphoma affects fewer than one in 1000 persons, it is more likely to affect those with long-standing autoimmune thyroiditis,[61] as there is a 67- to 80-fold increased risk of developing primary thyroid lymphoma in patients with Hashimoto's thyroiditis.[62]
History[edit]
Also known as Hashimoto's disease, Hashimoto's thyroiditis is named after Japanese physician Hakaru Hashimoto (1881−1934) of the medical school at Kyushu University,[70] who first described the symptoms of persons with struma lymphomatosa, an intense infiltration of lymphocytes within the thyroid, in 1912 in the German journal called Archiv für Klinische Chirurgie.[3][71] This paper was made up of 30 pages and 5 illustrations all describing the histological changes in the thyroid tissue. Furthermore, all results in his first study were collected from four women. These results explained the pathological characteristics observed in these women especially the infiltration of lymphoid and plasma cells as well as the formation of lymphoid follicles with germinal centers, fibrosis, degenerated thyroid epithelial cells and leukocytes in the lumen.[3] He described these traits to be histologically similar to those of Mikulic's disease. As mentioned above, once he discovered these traits in this new disease, he named the disease struma lymphomatosa. This disease emphasized the lymphoid cell infiltration and formation of the lymphoid follicles with germinal centers, neither of which had ever been previously reported.[3]
Despite Dr. Hashimoto's discovery and publication, the disease was not recognized as distinct from Reidel's thyroiditis, which was a common disease at that time in Europe. Although many other articles were reported and published by other researchers, Hashimoto's struma lymphomatosa was only recognized as an early phase of Reidel's thyroiditis in the early 1900s. It was not until 1931 that the disease was recognized as a disease in its own right, when researchers Allen Graham et al. from Cleveland reported its symptoms and presentation in the same detailed manner as Hakaru.[3]
In 1956, Drs. Rose and Witebsky were able to demonstrate how immunization of certain rodents with extracts of other rodents' thyroid resembled the disease Hakaru and other researchers were trying to describe.[3] These doctors were also able to describe anti-thyroglobulin antibodies in blood serum samples from these same animals.
Later on in the same year, researchers from the Middlesex Hospital in London were able to perform human experiments on patients who presented with similar symptoms. They purified anti-thyroglobulin antibody from their serum and were able to conclude that these sick patients had an immunological reaction to human thyroglobulin.[3] From this data, it was proposed that Hashimoto's struma could be an autoimmune disease of the thyroid gland.
In 1957, it was recognized as an autoimmune disorder and was the first organ-specific autoimmune disorder identified.[14]
Following this recognition, the same researchers from Middlesex Hospital published an article in 1962 in The Lancet that included a portrait of Hakaru Hashimoto.[3] The disease became more well known from that moment, and Hashimoto's disease started to appear more frequently in textbooks.
Since those discoveries, a number of autoimmune diseases have been discovered, with several of them having to do with thyroid-specific antibodies.