Psychology Wiki
Advertisement

Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)


Hashimoto 4er.jpg|
Hashimoto's thyroiditis
ICD-10 E063
ICD-9 245.2
OMIM 140300
DiseasesDB 5649
MedlinePlus [1]
eMedicine med/949
MeSH {{{MeshNumber}}}

Hashimoto's thyroiditis or chronic lymphocytic thyroiditis is thyroid disorder and autoimmune disease where the body's own antibodies attack the cells of the thyroid.

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.

Causes[]

A combination of genetic and environmental factors initiate the autoimmune responce in Hashimoto's thyroiditis. 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.

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.

A wide variety of environmental triggers such as iodine, pure diet, infections, drugs and chemical pollutants can initiate Hashimoto's thyroiditis and contribute to the disease development in genetically susceptible individuals.

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.

Presentation[]

In many cases, Hashimoto's thyroiditis usually 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 characterised by invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes. It is associated with non-Hodgkin lymphoma.

Many patients do not show any symptoms initially. As the inflammation and destruction of the thyroid gland progress, less thyroid hormone is produced by the gland and person becomes hypothyroid and can get enlarged thyroid gland, called goiter.

In the early phase of the disease some people can experience hashitoxicosis which is characterized by release of too much thyroid hormone due to destruction of the thyroid gland. During this short events symptoms of Hashimoto's thyroiditis might include typical symptoms of hyperthyroidism.

Weight gain, weight loss, depression, mania, fatigue, panic attacks, low pulse, fast pulse, high cholesterol, reactive hypoglycemia, constipation, migraines, memory loss, infertility and hair loss are a few possible symptoms.

Treatment[]

Hypothyroidism caused by Hashimoto's Thyroiditis is treated with thyroid hormone replacement. A small pill taken once a day should be able to keep the thyroid hormone levels normal. This medicine will, in most cases, need to be taken for the rest of the patient's life.

Eponym[]

File:橋本通り.jpg

The explanation board of Hashimoto Dori in Kyushu University

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,[1] who first described the symptoms in 1912 in a German publication[2].

See also[]


References[]

  1. Who Named It doctor/1974
  2. H. Hashimoto: Zur Kenntnis der lymphomatösen Veränderung der Schilddrüse (Struma lymphomatosa). Archiv für klinische Chirurgie, Berlin, 1912, 97: 219−248.

External links[]



This page uses Creative Commons Licensed content from Wikipedia (view authors).
Advertisement