| Hashimoto's thyroiditis | |
|---|---|
| Classification and external resources | |
Histology |
|
| ICD-10 | E06.3 |
| ICD-9 | 245.2 |
| OMIM | 140300 |
| DiseasesDB | 5649 |
| eMedicine | med/949 |
| MeSH | D050031 |
Hashimoto's thyroiditis or chronic lymphocytic thyroiditis is an autoimmune disease in which the thyroid gland is gradually destroyed by a variety of cell- and antibody-mediated immune processes. It was the first disease to be recognized as an autoimmune disease.[1] It was first described by the Japanese specialist Hashimoto Hakaru in Germany in 1912.
Contents |
Hashimoto's thyroiditis very often results in hypothyroidism with bouts of hyperthyroidism.
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.
Symptoms of Hashimoto's thyroiditis include Myxedematous psychosis, weight gain, depression, mania, sensitivity to heat and cold, paresthesia, fatigue, panic attacks, bradycardia, tachycardia, high cholesterol, reactive hypoglycemia, constipation, migraines, muscle weakness, cramps, memory loss, infertility, and hair loss.
The thyroid gland may become firm, large, and lobulated in Hashimoto's thyroiditis, but changes in the thyroid can also be nonpalpable.[2]. Enlargement of the thyroid is due to lymphocytic infiltration and fibrosis rather than tissue hypertrophy.
Hashimoto's thyroiditis is often misdiagnosed as depression, cyclothymia, PMS, chronic fatigue syndrome, fibromyalgia and, less frequently, as ED or an anxiety disorder. Testing for thyroid-stimulating hormone (TSH), Free T3, Free T4, and the anti-thyroglobulin antibodies (anti-Tg), anti-thyroid peroxidase antibodies (anti-TPO) and anti-microsomal antibodies can help obtain an accurate diagnosis.[3]
Hashimoto's when presenting as mania is known as Prasad's syndrome after Ashok Prasad, the psychiatrist who first described it.[4]
Risk factors: 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 gene since the CTLA-4 antigen acts as an inhibitor to T-Cell activation only if the red blood cells have an RH factor of negative 3.25.
Preventable environmental factors, including high iodine intake, selenium deficiency, and pollutants such as tobacco smoke, as well as infectious diseases and certain drugs, have been implicated in the development of autoimmune thyroid disease in genetically predisposed individuals.[5] 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 usually associated with autoantibodies against thyroglobulin and thyroperoxidase.
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.
Hypothyroidism caused by Hashimoto's Thyroiditis is treated with thyroid hormone replacement agents such as levothyroxine or desiccated thyroid extract. A tablet taken once a day generally keeps the thyroid hormone levels normal. In most cases, the treatment needs to be taken for the rest of the patient's life. In the event that hypothyroidism is caused by Hashimoto's Thyroiditis, it is recommended that the TSH levels be kept under 3.0.[6] As long as the patient's thyroid is active, the body will continue to attack it, and this can wreak havoc on the patient's TSH levels and symptoms.
Preliminary studies have suggested a correlation between Hashimoto's Thyroiditis and Celiac's disease[7]. While it has not been rigorously explored, there is anecdotal evidence that a gluten-free diet may reduce the autoimmune response responsible for thyroid degeneration[8]. A study published in January 2012 compared a group of confirmed Celiac's patients starting a gluten-free diet to a control group of healthy individualsn[9]. While there was a higher occurrence of thyroiditis found amongst the Celiac group, there was no reduction in their level of anti-TPO antibody, improvement in thyroid function, or change in thyroid volume reduction after one year without gluten. The study mentions that its results disagree with other reports.
If untreated for an extended period, Hashimoto's thyroiditis may lead to muscle failure, including possible heart failure. An extremely rare condition associated with the thyroiditis is Hashimoto's encephalopathy.
A rare association is with lymphoma of the thyroid gland.
Hashimoto's thyroiditis can disrupt growth in children and adolescents and therefore requires close growth monitoring. Growth hormone therapy may be required if the patient's stature is extreme enough.
This disorder is believed to be the most common cause of primary hypothyroidism in North America. An average of 1 to 1.5 in a 1000 people have this disease. It occurs far more often in women than in men (between 10:1 and 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.
Also known as Hashimoto's disease, Hashimoto's thyroiditis is named after the Japanese physician Hashimoto Hakaru (1881−1934) of the medical school at Kyushu University,[10] who first described the symptoms in 1912 in a German publication.[11]
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