title: Activation of the hypothalamo-pituitary-adrenal axis in response to septic or non-septic diseases--implications for the euthyroid sick syndrome.
abstract: OBJECTIVE
  To determine whether cytokine release or activation of the hypothalamo-pituitary-adrenal (HPA) axis is predominantly involved in the development of the euthyroid sick syndrome (ESS).
  
  
  METHODS
  Prospective observational study.
  
  
  METHODS
  Intensive care unit at a tertiary care medical center in Germany.
  
  
  METHODS
  Nine patients with sepsis of different causes and eight patients with acute myocardial infarction.
  
  
  METHODS
  None.
  
  
  RESULTS
  Immediately on admission and on day 7 the following parameters were determined: total thyroxine (T4), free thyroxine (FT4), total triiodothyronine (T3), thyrotropin (TSH), interleukin-1 beta (IL-1 beta), interleukin-2 (IL-2), soluble interleukin-2 receptor (sIL-2R), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), serum cortisol and plasma adrenocorticotropin (ACTH). On admission, concentrations of all thyroid hormones and TSH were significantly lower in septic patients compared to non-septic patients, whereas all cytokines except IL-2 were significantly elevated in the sepsis group. By contrast, there was no difference in serum cortisol and plasma ACTH levels between the two groups. On day 7, T4 and T3 were still lower in the septic group, whereas IL-1 beta, sIL-2R and IL-6 were still elevated. Again, no differences were found with regard to cortisol and ACTH levels.
  
  
  CONCLUSIONS
  Euthyroid sick syndrome occurs very early during the course of septic diseases. Significantly decreased levels of total T4, FT4, T3 and TSH in septic patients suggest central suppression of TSH as well as inhibition of thyroid hormone release in ESS. The HPA axis is activated in septic patients and in non-septic patients and does not contribute to the development of ESS.
authors.affiliation: Klinik für Allgemeine Innere Medizin, Christian-Albrechts-Universität zu Kiel, Germany. hmoenig@1med.uni-kiel.de
authors.forename: H
authors.initials: H
authors.lastname: Mönig
authors.forename: T
authors.initials: T
authors.lastname: Arendt
authors.forename: M
authors.initials: M
authors.lastname: Meyer
authors.forename: S
authors.initials: S
authors.lastname: Kloehn
authors.forename: B
authors.initials: B
authors.lastname: Bewig
mesh_terms: D000328:Adult; D000368:Aged; D003422:Critical Care; D016207:Cytokines / Q000097:blood*; D005067:Euthyroid Sick Syndromes / Q000209:etiology* / Q000276:immunology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000150:complications / Q000276:immunology*; D011446:Prospective Studies; D018805:Sepsis / Q000097:blood / Q000150:complications / Q000276:immunology*; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood
chemical_list: D016207:Cytokines; D013972:Thyrotropin; D013974:Thyroxine