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Autoimmune thyroiditis, or Chronic Autoimmune thyroiditis, is a disease in which the body interprets the thyroid glands and its hormone products T3, T4 and TSH as threats, therefore producing special antibodies that target the thyroid’s cells, thereby destroying it. It presents with hypothyroidism or hyperthyroidism and the presence or absence of goiters. Specialists clinically separate autoimmune thyroiditis into two categories. If goiters are present, it is understood as Hashimoto’s Thyroiditis. On the other hand, if the thyroid is atrophic, but does not present goiters, it is denominated Atrophic Thyroiditis. If the symptoms of thyroiditis appear in women after birth, it is attributed to such and therefore called Postpartum Thyroiditis. The effects of this disease are not permanent but transient. Symptoms may come and go depending on whether the patient receives treatment, and whether the treatment is effective.
Thyroid autoantibodies appear mostly with the presence of lymphocytes in the targeted organ. There are three types of antibodies: Thyroid Peroxidase Antibodies (TPOAb), Thyroglobulin Antibodies ( TgAb), and Thyroid Stimulating Hormone Receptor Antibodies (TRAb). These antibodies affect different targets in the thyroid gland. The three main targets are as follows: Thyroglobulin, a protein specified in housing the thyroid hormones T3, T4 and TSH; the Thyroid Microsomal Antigen also known as Thyroid Peroxidase, an enzyme in charge of regulating how much hormone the gland should produce; and the Thyrotropin receptors. “A certain percentage of patients who are healthy may be positive for one or more thyroid antibodies.” Doctors who attend to such patients will most likely do routine follow-ups on the patient’s health since, even though it is highly unlikely that they will present any thyroid problems, there is still a chance that they will develop some type of dysfunction with time.
The exact cause for autoimmune thyroiditis is not known for certain, but researchers have found high correlations with aspects such as genetics, high iodine consumption, and age.
“Thyroid autoimmunity is familial.”  The disease is said to be inherited as a dominant trait since it has been reported that as many as fifty percent of the first degree relatives of patients with some type of autoimmune thyroiditis present thyroid antibodies in serum. Some studies have even related it to chromosome 21 because of its high correlation with patients with Down’s syndrome and familial Alzheimer’s disease. Still, this theory is doubted, since patients with Turner’s syndrome also present a high prevalence of autoimmune thyroiditis (up to fifty percent).
High Iodine Consumption 
Autoimmune thyroiditis has a higher prevalence in societies that have a higher intake of iodine in their diet, such as the United States and Japan. Also, the rate of lymphositic infiltration increased in areas where the iodine intake was once low, but had been given iodine supplementation. “The prevalence of positive serum tests in such areas rises to over forty percent within 0.5 to 5 years.”  When in the presence of excess iodine, the gland is unable to avoid its inhibitory effect on the biosynthesis of thyroid hormones. This is why when a person has excess iodine in his or her diet or is administered with additional supplementation in areas where sufficient iodine has been noted, it can induce reversible hypothyroidism.
It has been shown that “the prevalence of positive tests for thyroid antibodies increases with age, with a frequency as high as 33 percent in women 70 years old or older.”  The mean age of prevalence in women is higher than in men by one year, 58 and 59 years old respectively. Autoimmune thyroiditis can also affect children. Although it is very rare for children under the age of five, it can occur, and it accounts for around 40 percent of the cases in adolescents with goiters. In the case of hypothyroidism, patients over the age of 45 have more chances of developing autoimmune thyroiditis.
The symptoms for autoimmune thyroiditis may vary depending on whether it causes hyperthyroidism or hypothyroidism.
Hyperthyroidism can cause sweating, rapid heart rate, anxiety, tremors, fatigue, difficulty sleeping, sudden weight loss, and protruding eyes.
Hypothyroidism can cause weight gain, fatigue, dry skin, hair loss, intolerance to cold, and constipation.
There are various tests that can be made depending on the symptoms the patient presents. Doctors may search for TPOAb when the patient has symptoms that suggest hypothyroidism or when said patient will be started on a drug therapy associated with risks of developing hypothyroidism, such as treatments with lithium or Interpheron Alfa. This antibody is related to Hashimoto's thyroiditis and Grave’s disease. They may look for TgAb whenever a thyroglobulin test is performed to see if the antibody is present and likely to interfere. It can also be ordered in regular intervals after the patient has been diagnosed with thyroid cancer, and just like TPOAb, it can be associated with Hashimoto’s thyroiditis. In the case that the patient presents symptoms for hyperthyroidism, the doctors are more likely to test for TRAb, as well as monitoring the effects of anti- thyroid therapy, also associated with Grave’s disease.
It can refer to:
- Dayan, Dayan, Colin M; Dayan, Colin M., and Gilbert H. Daniels. (1996). "Chronic Autoimmune Thyroiditis". The New England Journal of Medicine. 335.2: 99–107.
- Weetman, A. P.; A. M. McGregor, JPublications. 48. (1982): 196-200. H. Lazarus & R. Hall (1982). "Thyroid Antibodies are Produced by Thyroid- Derived Lymphocytes.". Blackwell Scientific Publications. 48. (1982): 196-200 48: 196–200.
- "Thyroid Antibodies". Retrieved 4 April 2012.
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