TRAK

from Wikipedia, the free encyclopedia

Thyrotropin receptor autoantibodies ( TRAK , also TSH receptor autoantibodies , TSHR-AK ) are antibodies (hence autoantibodies ) formed by the body against the thyrotropin receptor (TSH receptor ), which develop similar effects on the thyrotropin receptor as actually there binding hormone thyrotropin (TSH).

Effect on the thyroid gland

TRAK are different from most other autoantibodies (in other autoimmune diseases ) because they are directly responsible for the clinical symptoms of the disease, and not just as a by-product of the disease. TRAK are responsible for the clinical symptoms of Graves' disease , as they lead to uncontrolled stimulation of the receptor and thus the thyroid gland at the TSH receptor ( overactive thyroid gland ).

Significance for diagnostics

This direct connection between TRAK and Graves' disease makes it a suitable diagnostic tool for the disease. The presence of TRAK in a patient's blood is virtually indicative of a diagnosis of Graves' disease. If no TRAK can be detected in a patient with an overactive thyroid, then other reasons (non-autoimmune cause) are responsible for this overactive (e.g. a so-called autonomous adenoma ).

Further differentiation of the TRAK

In thyroid research, the TRAK are further subdivided:

  • in those with stimulating properties (thyroid s timulating antibodies, T S Ab or s TRAb )
  • and those with blocking properties (thyroid b locking / i nhibiting antibodies, T B Ab or i TRAb ).

In most patients with Graves' disease, at least in Europe, the stimulating antibodies occur. The importance of the blocking antibodies is still controversial.

In routine diagnostics, only the TRAK are determined by the laboratory doctor. There is usually no distinction between TSAb and TBAb . Positive TRAK in the blood confirm the diagnosis of Graves' disease , whereby this laboratory examination is only one part of the diagnostic procedure in addition to physical examination, ultrasound of the thyroid gland and other methods.

If further differentiation of TRAK is required from a clinical point of view, TSAb can be treated with special procedures, e.g. B. so-called bioassays can be determined in which the stimulating effect of the antibodies on the TSH receptor is seen by measuring the cAMP formed.

More recent findings

According to the latest studies, the concentration of the TRAK is also associated with the course of Graves' disease. Patients with very high TRAK values ​​have a risk of over 90 percent of relapse after drug therapy. The reverse is not true. Patients with low TRAK levels can also get a relapse of the disease. Some authors therefore suggest that if the patient has high TRAK values, a so-called definitive therapy (surgery, radioiodine therapy) should be sought as soon as possible. However, this has not yet been proven by prospective studies and is viewed rather cautiously by others.

TRAK and endocrine orbitopathy

According to the latest studies, TRAK and endocrine orbitopathy (EO) are related to a similar relationship as TRAK and Graves' disease. EO is a presumably autoimmune disease of the eye socket, which is closely related to Graves' disease and usually occurs together with thyroid disease (but not always at the same time). If the EO is severe, high TRAK concentrations can also be detected in the blood. It could also be shown that TSH receptors are also expressed in the orbit. Whether the TRAK is the cause of the disease in EO or just a by-product of the autoimmune process is still the subject of research. The TRAK are also of diagnostic importance for EO, ​​especially for predicting the severity of the disease.

See also

literature

  • Axel M. Gressner, Torsten Arndt: Lexicon of Medical Laboratory Diagnostics . Springer Verlag, 2nd edition Berlin / Heidelberg 2013, p. 215 (on Google Books )
  • Harald Schicha, Otmar Schober: Nuclear medicine: basic knowledge and clinical application . Schattauer Verlag, 7th edition Stuttgart 2013, p. 181 (on Google Books )
  • Peter C. Heinrich, Matthias Müller, Lutz Graeve: Löffler / Petrides Biochemistry and Pathobiochemistry . Springer Verlag, 9th edition Berlin / Heidelberg 2014, p. 526 (on Google Books )
  • Gynter Mödder: Diseases of the Thyroid . Springer Verlag, 3rd edition Berlin / Heidelberg 2003, p. 40 (on Google Books )
  • M. Luster (ed.): Thyroid 2013: The thyroid in all phases of life - from clinical standard to individual medicine . Lehmanns Media, Berlin 2013, p. 50 f. (on Google Books )
  • MJ Seibel, B. Weinheimer, R. Ziegler: Thyroid 1999: The thyroid and its relationship to the organism . Walter de Gruyter, Berlin 2000 (on Google Books )
  • Walter Siegenthaler, Hubert E. Blum: Clinical pathophysiology . Georg Thieme Verlag, Stuttgart 2006, p. 277 (on Google Books )
  • Michael Freissmuth, Stefan Offermanns, Stefan Böhm: Pharmacology and Toxicology: From the Molecular Basics to Pharmacotherapy . Springer Verlag, 2nd edition Berlin / Heidelberg 2016, p. 620 (on Google Books )
  • Stefan Fischli, Giatgen A. Spinas: Endocrinology and metabolism compact . Georg Thieme Verlag, 2nd edition Stuttgart 2011, p. 43 (on Google Books )
  • JR Siewert, M. Rothmund, V. Schumpelick: Practice of Visceral Surgery: Endocrine Surgery . Springer Medizin Verlag, Heidelberg 2007, p. 111 (on Google Books )

Web links