HistoryThis section has been translated automatically.
Hakaru Hashimoto 1912
DefinitionThis section has been translated automatically.
Most frequent, painless, autoimmunological inflammation of the thyroid gland (autoimmunological thyroiditis), which can last for years, with partial or complete destruction of the thyroid gland. There is a familial disposition as well as a frequent association with other autoimmune diseases. Most frequent cause of hypothyroidism (Caturegli P et al. 2014).
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ClassificationThis section has been translated automatically.
Forms of progression of Hashimoto's thyroiditis
- Atrophic form: In this case, atrophy of the organ occurs. In Germany the majority of patients suffer from this variant of the disease.
- Hypertrophic form: In this case the thyroid gland enlarges; formation of a goiter
Furthermore, a distinction can be made between fibrotic, IgG4-associated, juvenile, hashitoxicosis and painless thyroiditis (sporadic or postpartum).
Occurrence/EpidemiologyThis section has been translated automatically.
Hashimoto's thyroiditis is one of the most common autoimmune diseases in humans and the most common cause of primary hypothyroidism. In a larger survey study, elevated antibodies were found in 10 % of the subjects in a population sample, subclinical hypothyroidism in 4.3 % and clinically manifest hypothyroidism in 0.3 %. In another study, clinical and subclinical hypothyroidism was found in 10 % of the subjects. The prevalence of Hashimoto's thyroiditis in Western Europe is reported to be 1-2 %; however, subclinical courses are more frequent and are 6-8 %.
EtiopathogenesisThis section has been translated automatically.
The exact cause that leads to the onset of Hashimoto's thyroiditis is not yet sufficiently understood and, as in Graves' disease, it is manifold. Discussed are genetic predisposition (family history of frequent cases, the concordance in monozygotic twins is 30-60%), infections (bacteria, viruses: mononucleosis, zoster), iodine exposure, drugs(nivolumab, lithium), hormonal changes (puberty, childbirth, menopause), psychological stress.
The formation of microsomal antibodies against thyroid peroxidase(anti-TPO, MAK) and antibodies against thyroglobulin(Tg-AK) takes place in a side reaction. In 10-20% of patients no antibodies are formed. Therefore, missing antibodies do not exclude the presence of Hashimoto's thyroiditis. In contrast to Graves' disease, antibodies do not cause the disease. The thyroid hormones T3 and T4 are insufficiently produced and released in a reduced manner as the inflammation progresses. Hashimoto's thyroiditis is one of the most common causes of hypothyroidism.
ManifestationThis section has been translated automatically.
Affected are mainly women between the 30-50 LJ. w:m= 2(5):1.
Clinical featuresThis section has been translated automatically.
Initially, lymphocytic thyroiditis is usually symptomless; however, a diffusely enlarged, rarely slightly painful goiter may develop, possibly with signs of hyperthyroidism. This passive hyperthyroidism is called "hashitoxicosis" and is characterized by:
- Sweating, racing heart, high blood pressure (hypertension), weight loss, diarrhoea, increased anxiety, restlessness and restlessness ("always in the fast lane"), trembling hands, muscle weakness, muscle tremors, insomnia, nervousness and ravenous appetite.
As the autoimmunological inflammation progresses, there is increasing destruction of the organ by cytotoxic T cells. It gradually becomes non-functional.
The clinical signs of hypothyroidism develop with:
- Fatigue, memory and concentration disorders, general physical exhaustion, lack of resilience, weight gain, sensitivity to cold, depression, susceptibility to infections, sleep disorders, joint and muscle pain, diffuse effluvium, dry skin, brittle fingernails, flatulence, constipation, menstrual disorders in women, tingling and falling asleep of the hands and forearms at night (carpal tunnel syndrome), loss of libido, increase in blood lipids, cardiac arrhythmias, oedema, hearing loss, rough voice.
Hashimoto's thyroiditis often occurs together with other autoimmune diseases. For example, with vitiligo (Baldini E et al. 2017), alopecia areata, celiac disease, diabetes mellitus type 1, Addison's disease, hypoparathyroidism (Radetti G 2014). Such constellations are called polyendocrine autoimmune syndromes.
LaboratoryThis section has been translated automatically.
HistologyThis section has been translated automatically.
Lymphocytic (cytotoxic T cells) infiltration of the thyroid parenchyma. In the late stage increasing fibrotic transformation with atrophy of the glandular body.
DiagnosisThis section has been translated automatically.
Sonography of the thyroid gland including color Doppler: inhomogeneous sound pattern of the shrunken thyroid parenchyma.
Possible sintigram: reduced radionuclide uptake.
Internal therapyThis section has been translated automatically.
Hashimoto's thyroiditis is one of the most common causes of hypothyroidism in adults; it is not curable. The most important therapeutic measure in Hashimoto's thyroiditis is the treatment of hypothyroidism with L-thyroxine (levothyroxine). Glucocorticoids and other immunosuppressive drugs are useless. Close monitoring is important. The positive effect of selenium in AIT with euthyroidism is discussed (dosage: 200 µg/day) (Zagrodzki P et al. 2014). Increased hormone requirements during pregnancy. A sufficient LT4-substitution must be ensured.
Progression/forecastThis section has been translated automatically.
The course of Hashimoto's thyroiditis varies greatly from individual to individual. It often develops insidiously with many uncharacteristic symptoms that are difficult to detect, especially at the beginning of the disease. In the late stages of atrophy and fibrosis of the organ with hypothyroidism, a normal life expectancy can be assumed with correct LT4 substitution.
Note(s)This section has been translated automatically.
A variant of Hashimoto's thyroiditis is the IgG4-associated fibrosing Riedel's goiter (E06.5), which infiltrates the area around the thyroid gland as a so-called "iron-hard" goiter.
LiteratureThis section has been translated automatically.
- Baldini E et al (2017) Vitiligo and Autoimmune Thyroid Disorders. Front endocrinol (Lausanne)8:290.
- Caturegli P et al (2014) Hashimoto thyroiditis: clinical and diagnostic criteria. Autoimmune Rev 13:391-397.
- Kobayashi T et al (2018) Patients With Antithyroid Antibodies Are Prone To Develop Destructive Thyroiditis Patients With Antithyroid Antibodies Are Prone To Develop Destructive Thyroiditis by Nivolumab: A Prospective Study. J Endocr Soc 2:241-251.
- Radetti G (2014) Clinical aspects of Hashimoto's thyroiditis. Endocr Dev 26:158-170.
- Zagrodzki P et al (2014) The importance of selenium in Hashimoto's disease.Postepy Hig Med Dosw (Online) 68:1129-37.
Incoming links (22)Amicrobial intertriginous pustulose; Antiphospholipid antibodies; Anti-tpo antibody; Autoimmune diseases; Autoimmune hepatitis; Chronic mucocutaneous candidiasis; Dermatitis herpetiformis; Hashimoto's thyroiditis; Hepatitis c; Hypothyroidism acquired; ... Show all
Outgoing links (10)Alopecia areata (overview); Anti-tpo antibody; Hypothyroidism and skin changes; Lithium hydroxide (inci); Mononucleosis infectious; Nivolumab; Riedel's goiter; Tak; Vitiligo (overview); Zoster;
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