title: The endocrinologic changes in critically ill chronic obstructive pulmonary disease patients.
abstract: BACKGROUND
  Alterations in the neuroendocrine system occur during critical illness. Chronic obstructive pulmonary disease (COPD) itself causes hormonal changes. The aim of this study was to determine neu roendocrine hormones of COPD patients with acute respiratory failure and to investigate the relationship between hormonal changes, mortality, and morbidity.
  
  
  METHODS
  We enrolled 21 patients (13 F/8 M) with COPD exacerbation requiring artificial airway support. Blood samples were collected on admission to the ICU, and on the day of hospital discharge. Eighteen healthy people were included as controls.
  
  
  RESULTS
  Female patients had lower luteinizing hormone (LH), follicle stimulating hormone (FSH), and free triiodothyronine (fT3), and higher prolactin (PRL) levels than controls on admission to the ICU (FSH: 70.3 vs. 29.3 mlU/mL; LH: 26.6 vs. 6.8 mlU/mL; fT3: 2.9 vs. 2.0 pg/mL; PRL: 12.4 vs. 21.3 ng/mL). Male patients had low testosterone and TSH and high PRL but only changes in TSH and PRL reached statistical significance (testosterone: 3.5 vs. 1.5 ng/mL, TSH: 1.1 vs. 0.5 ulU/mL, PRL: 9.7 vs. 14.2 ng/mL). Female patients had lower fT3 than males (fT3(female): 2.7 vs. fT3(male): 2.0 pg/mL). On follow-up, significantly elevated FSH and fT3 and decreased estradiol concentrations were documented among recovered women (FSH: 28.4 vs. 46.6 mlU/mL, fT3(,): 2.0 vs. 2.6 pg/mL, E(2): 27.7 vs. 19.0 pg/mL). Patients had high C-reactive protein levels and acute physiologic and chronic health evaluation II scores. Mortality rate was 9.5% and a negative correlation between E(2) and duration of noninvasive mechanical ventilation and length of hospital stay was found in male patients.
  
  
  CONCLUSIONS
  Men and women with acute respiratory failure in the presence of COPD develop significant changes in the neuroendocrine axis. Hormonal suppression vanishes with disease improvement.
authors.affiliation: Marmara University School of Medicine, Department of Internal Medicine and Critical Care Unit, Istanbul, Turkey. turkayakbas@yahoo.com
authors.forename: Türkay
authors.initials: T
authors.lastname: Akbaş
authors.forename: Sait
authors.initials: S
authors.lastname: Karakurt
authors.forename: Göksenin
authors.initials: G
authors.lastname: Unlügüzel
authors.forename: Turgay
authors.initials: T
authors.lastname: Celikel
authors.forename: Sema
authors.initials: S
authors.lastname: Akalin
mesh_terms: D018806:APACHE; D000208:Acute Disease; D000368:Aged; D000369:Aged, 80 and over; D016638:Critical Illness; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006728:Hormones / Q000097:blood*; D006801:Humans; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D008875:Middle Aged; D011388:Prolactin / Q000097:blood; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D012131:Respiratory Insufficiency / Q000150:complications; D013739:Testosterone / Q000097:blood; D013972:Thyrotropin / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D006728:Hormones; D014284:Triiodothyronine; D013739:Testosterone; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013972:Thyrotropin