Thyroid autonomy

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Under a thyroid autonomy is meant a carve of parts of the thyroid tissue from the thyroid stimulating loop ( hypothalamic - pituitary gland - thyroid gland ), so that the production of thyroid hormones does not take place as needed.

The incre- ment of the thyroid hormones is mainly dependent on this control circuit; However, some of the thyroid cells also produce thyroid hormones independently of this in healthy individuals (physiological basal autonomy). The increase in these autonomous functional components can, under certain conditions, lead to an overactive thyroid .

causes

Iodine deficiency can be seen as a major influencing factor for the autonomic tissues . In 1990 the first somatic heterozygous mutations in the Gs-alpha protein gene and in 1993 in the TSH receptor gene were discovered during unifocal thyroid autonomy . Both lead to a constitutive activation of the cAMP cascade in the mutated thyroid cell, thereby stimulating the cells' growth and hormone production. These gene mutations are not found outside of autonomous areas and are therefore considered to be causative. A connection between the gene mutations and iodine deficiency has not yet been proven. It is discussed, however, whether the increased exposure to radicals under iodine and selenium deficiency favors the mutations. In the meantime, around 30 point mutations are known that trigger autonomy. In addition to the more frequent somatic mutations, mutations were also observed that can be passed on to the offspring in an autosomal dominant mode of inheritance .

Diagnosis

For diagnosis is thyroid scintigraphy inevitable. Since the substances used in this investigation ( 99m Tc-pertechnetate or 131 iodine) only accumulate in active, i.e. hormone-producing, thyroid cells ( tracer substance ), there is no illustration of inactive thyroid tissue (suppressed TSH , therefore no hormone production). Autonomous thyroid tissue appears despite the lack of TSH (maximum suppression), as it is metabolically active regardless of the TSH level.

Scintigraphy of an autonomic adenoma
  • If one or more parts of the thyroid are excessively active, one speaks of " adenoma (s)". In the event that these sections produce more hormones than the body needs (decompensated adenoma (s) - hyperthyroidism ), the other parts of the thyroid gland are suppressed by the thyrotropic control circuit, so the tracer substance does not accumulate and thus only presents itself Depending on the number and distribution of the autonomic parts, a distinction is made between autonomous adenoma (“hot nodule”), multifocal autonomy (several to many “hot nodules”) and disseminated autonomy (increase in autonomic tissue distributed over the entire thyroid gland).
  • Suppression scintigraphy is used to differentiate between the physiological autonomy that is also present in healthy individuals and pathologically increased (compensated thyroid adenoma (s)) in euthyroid patients . Thyroid hormones are given in order to reduce the TSH level in the blood via the thyrotropic control circuit (and thus suppress the hormone production in non-autonomous thyroid tissue and consequently also the absorption of the tracer substance). Only the autonomous districts are then shown in the scintigram. A total Tc uptake (uptake) in the thyroid gland of more than three percent under suppressive conditions indicates a high risk of developing hyperthyroidism after exposure to iodine.

therapy

The therapy is based on the cause and the degree of autonomy. In the early phase and in the absence of overt hyperthyroidism , iodide may also be used in combination with thyroxine . If the autonomy has already led to manifest hyperthyroidism, thyreostatics are indicated in order to normalize the thyroid hormone level in the blood. The definitive therapy consists in an eradication of the pathologically increased autonomic tissue; Thyroid resection (surgery) and radioiodine therapy are suitable for this .

Individual evidence

  1. ↑ Herold 2007.
  2. ↑ a b R. Paschke et al.: Therapy of uni- or multifocal thyroid autonomy. In: Dtsch Arztebl. 2000; 97 (21), pp. A-1463 / B-1245 / C-1168.
  3. ↑ Studies on the influence of iodine deficiency on the development of thyroid autonomy and the role of oxidative stress under iodine deficiency. In: Universität Leipzig, Research Report 2004 - Projects ( Memento of the original from June 10, 2008 in the Internet Archive ) Info: The archive link has been inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. @1@ 2Template: Webachiv / IABot / www.uni-leipzig.de
  4. ↑ Oxidative stress in the thyroid glands of mice and rats with iodine and selenium deficiency. ( Memento of the original from June 10, 2008 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. University of Leipzig, Research Report 2006 - Projects @1@ 2Template: Webachiv / IABot / www.uni-leipzig.de
  5. ↑ W. Böcker, H. Denk, Ph. U. Heitz, H Moch: Pathology. 4th edition. Munich 2008, p. 399.
  6. ↑ P. Schumm-Draeger: Thyroid diagnosis and therapy: Update 2005. In: Bayerisches Ärzteblatt . 4/2005, pp. 236-243. (PDF; 444 kB).
  7. ^ R. Paschke, P. Georgi: Therapy of the uni- or multifocal thyroid autonomy: Closing words. In: Dtsch Arztebl. 2000; 97 (47), pp. A-3197 / B-2692 / C-2387.
  8. ↑ H. Vogt, H. Wengenmair et al.: Radioiodine therapy for combined thyroid autonomy: results after correction for disseminated parts. In: Nuclear Medicine. 2006; 45 3, pp. 101-104.