Euthyroid Sick Syndrome

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Classification according to ICD-10
E07 Other specified diseases of the thyroid gland
E07.8 Euthyroid Sick Syndrome
ICD-10 online (WHO version 2019)

Under a euthyroid sick syndrome (ESS), ( synonyms : non-thyroidal illness syndrome [NTIS], non-thyroidal illness (NTI), low T3 syndrome, low T3 syndrome, thyroid allostasis in critical illness, Tumors , uremia and starvation [TACITUS syndrome] ) are changes in the thyroid hormone metabolism without the presence of a disease or malfunction of the thyroid gland . This reactive response can result from allostatic reactions of the hypothalamic-pituitary-thyroid control circuit , dyshomeostatic changes, drug interference, and abnormal assay characteristics in critical illness.

The classic phenotype is observed in clinically euthyroid patients, test subjects or animals that are starving, hibernating or suffering from severe, non-thyroid-related general diseases. These include liver cirrhosis , heart failure , myocardial infarction one, bypass as part of a coronary heart disease , chronic renal failure , diabetic ketoacidosis , hypothermia , anorexia nervosa , burns, polytrauma and sepsis . Any trauma , surgery, special eating habits - such as malnutrition and malnutrition or fasting - can cause changes in the homeostatically regulated thyroid function within hours and lead to pathological findings known as non-thyroidal illness (NTI) or euthyroid sick syndrome (ESS ) are designated. The disorders of the classic euthyroid sick syndrome include a decreased concentration of the thyroid hormone T3 (low T3 syndrome), an increased reverse T3 concentration, and usually normal TSH and FT4 concentrations. In the case of very difficult processes, however, there is also a reduced setpoint of the control loop with low TSH and FT4 concentrations. This pattern arises from changes in the peripheral transport and metabolism of thyroid hormones, particularly with regard to deiodination , the regulation of TSH secretion and, in some cases, thyroid function itself. The classic pattern represents the response of the thyrotopic control loop to an allostatic load of type 1.

An alternative phenotype with a largely inverse hormonal pattern can occur in certain physiological and pathological situations such as pregnancy , obesity , endurance training and in some psychiatric illnesses. It is typically characterized by a high T3 syndrome, increased plasma protein binding of thyroid hormones and an increased setpoint of the control loop and results from an allostatic load of type 2.

Diagnosis

The interpretation of these pathological values ​​in euthyroid sick syndrome is made more difficult by various drugs that firstly reduce the biotransformation of peripheral T 4 into T 3 , e.g. B. iodine-containing X - ray contrast media , propranolol and amiodarone , and secondly drugs such as dopamine and corticosteroids , which inhibit the pituitary secretion of TSH, resulting in lowered TSH levels and consequently decreased thyroid T 4 secretion. This can make the differential diagnosis of latent hyperthyroidism more difficult , especially in the early phase of the critical illness .

Pathophysiology

In addition to a decrease in the concentration of thyroxine (T 4 ) and triiodothyronine (T 3 ) in the serum, an increase in the metabolically inactive reverse T 3 (rT 3 = reverse triiodothyronine ) can be observed as a result of a "step-down" deiodination of T 4 . Several studies have also observed an increased 3,5-T2 concentration.

Probably through direct effects on the hypothalamus, but possibly also via a negative feedback as a result of the increased 3.5-T2 concentration, it comes to further reduce the release of thyroid hormones, as in the pituitary gland , the secretion of thyroid stimulating hormone ( thyrotropin , TSH) and in the hypothalamus that of thyroliberin (thyrotropin releasing hormone (TRH)) is suppressed. Proinflammatory cytokines , glucocorticoids and metabolic metabolites are discussed as the cause of the direct effect .

Clinical consequences

The euthyroid sick syndrome could represent a protective mechanism by which autoaggressive immunological and metabolic reactions are to be slowed down and the energy and oxygen consumption of the critically ill organism is reduced. However, the hypothesis is also sometimes put forward that non-thyroidal illness syndrome is a central hypothyroidism that requires treatment. The contradicting study results may be due to the fact that too heterogeneous collectives were compared.

Individual evidence

  1. ↑ Dietrich JW, Landgrafe G, Fotiadou EH. TSH and Thyrotropic Agonists: Key Actors in Thyroid Homeostasis. J Thyroid Res. 2012; 351864. doi: 10.1155 / 2012/351864 . PMID 23365787
  2. ↑ a b c Apostolos Chatzitomaris, Rudolf Hoermann, John E. Midgley, Steffen Hering, Aline Urban, Barbara Dietrich, Assjana Abood, Harald H. Klein, Johannes W. Dietrich: Thyroid Allostasis - Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain , Stress, and Developmental Programming . In: Frontiers in Endocrinology . 8, July 20, 2017. doi : 10.3389 / fendo.2017.00163 . PMID 28775711 .
  3. ↑ G. Rothenbuchner, U. Loos , WR Kiessling, J. Birk, and EF Pfeiffer, “The influence of total starvation on the pituitarythyroid-axis in obese individuals,” Acta Endocrinologica, Supplement, vol. 173, p. 144, 1973.
  4. ↑ JW Dietrich, A. Ackermann, A. Kasippillai, Y. Kanthasamy, T. Tharmalingam, A. Urban, S. Vasileva, TA Schildhauer, HH Klein, A. Stachon, S. Hering: Adaptive changes in thyroid metabolism as risk indicators in trauma . In: Trauma and Occupational Disease . September 19, 2019. doi : 10.1007 / s10039-019-00438-z .
  5. ^ Leslie J. De Groot: Dangerous Dogmas in Medicine: The Nonthyroidal Illness Syndrome. In: The Journal of Clinical Endocrinology & Metabolism . Vol. 84, No. 1, pp. 151-164, PMID 9920076 .
  6. ^ B. McIver, C. Gorman: Euthyroid sick syndrome: an overview. In: Thyroid. 1997; 7; 1, pp. 125-132. PMID 9086580
  7. ↑ Jan R. Stockigt: Guidelines for diagnosis and monitoring of thyroid disease: nonthyroidal illness. In: Clinical Chemistry. (1996); 42, 1, pp. 188-192. PMID 8565225 (PDF; 903 kB).
  8. ↑ JW Dietrich, Müller P, Schiedat F, Schlömicher M, Strauch J, Chatzitomaris A, Klein HH, Mügge A, Köhrle J, Rijntjes E, Lehmphul I: Nonthyroidal Illness Syndrome in Cardiac Illness Involves Elevated Concentrations of 3,5-Diiodothyronine and Correlates with atrial remodeling . In: European Thyroid Journal . 4, No. 2, June 2015, pp. 129-37. doi : 10.1159 / 000381543 . PMID 26279999 . PMC 4521060 (free full text).
  9. ^ The role of cytokines and cortisol in the non-thyroidal illness syndrome following acute myocardial infarction.  ( Page no longer available , search in web archives )  Info: The link was automatically marked as defective. Please check the link according to the instructions and then remove this notice. In: European Journal of Endocrinology. (2000); 142, pp. 236-242. PMID 10700717 (PDF; 236 kB).@1@ 2Template: Dead Link / eje-online.org  
  10. ↑ JM Tibaldi, MI Surks: Effects of nonthyroidal illness on thyroid function. In: Med Clin North Am. 1985 Sep; 69 (5), pp. 899-911. PMID 3932793 .
  11. ↑ LJ De Groot: Non-thyroidal illness syndrome is a manifestation of hypothalamic-pituitary dysfunction, and in view of current evidence, should be treated with appropriate replacement therapies. In: Crit Care Clin. 2006, 22, pp. 57-86, PMID 16399020 .
  12. ↑ JW Dietrich, A. Stachon, B. Antic, HH Klein, S. Hering: The AQUA-FONTIS Study: Protocol of a multidisciplinary, cross-sectional and prospective longitudinal study for developing standardized diagnostics and classification of non-thyroidal illness syndrome . In: BMC Endocrine Disorders. 8 (13), PMID 18851740 .

literature

  • Beatrice R. Amann-Vesti: Clinical pathophysiology: 239 tables . Thieme, Stuttgart / New York 2006, ISBN 3-13-449609-7 .

Web links

  • M. den Brinker, KF Joosten, TJ Visser, WC Hop, YB de Rijke, JA Hazelzet, VH Boonstra, AC Hokken-Koelega: Euthyroid sick syndrome in meningococcal sepsis: the impact of peripheral thyroid hormone metabolism and binding proteins. In: The Journal of clinical endocrinology and metabolism. Volume 90, Number 10, October 2005, pp. 5613-5620, doi: 10.1210 / jc.2005-0888 , PMID 16076941 .