title: Adrenal axis functions in patients with familial Mediterranean fever.
abstract: OBJECTIVE
  Familial Mediterranean fever (FMF) is a hereditary disease characterized by recurrent attacks of fever with peritonitis, arthritis, pleuritis or erysipelas-like rash. It is unclear what effects of FMF itself on endocrine system and hormones are. None of the FMF patients without amyloidosis have been reported to have any endocrine disorders, except those who developed colchicine-induced diabetes insipidus. There is a large body of evidence to show that cytokines (IL-1, IL-6 and TNF-alpha) activate the hypothalamic-pituitary-adrenal (HPA) axis. We have designated this study to investigate the HPA axis in FMF patients without amyloidosis.
  
  
  METHODS
  Twenty-one patients with FMF were included. ACTH stimulation test was performed on the healthy subjects and during attack period in the patients. In the patient group, same test was repeated during remission period.
  
  
  RESULTS
  Peak cortisol levels were significantly higher in the attack period than those in the remission period of patients (p<0.05).
  
  
  CONCLUSIONS
  The cytokines play a role on the activation of the HPA axis; we thought the axis would be affected in this disease. The response of cortisol to 250 mug ACTH was significant in attack period when compared with remission period. This result reveals that HPA axis is more activated in an FMF attack. Previous studies suggest that the adrenal hormones increase in acute inflammatory events, and eventually, the changes on these hormones are related to TNF and IL-6 levels. During the FMF attack, HPA axis may be stimulated by cytokines. It seems that HPA axis is regulated normally in FMF patients.
authors.affiliation: Department of Nephrology, Erciyes University, Kayseri, Turkey. tsav@erciyes.edu.tr
authors.forename: Tansu
authors.initials: T
authors.lastname: Sav
authors.forename: Sav
authors.initials: S
authors.lastname: Tansu
authors.forename: Omer
authors.initials: O
authors.lastname: Ozbakir
authors.forename: Ozbakir
authors.initials: O
authors.lastname: Omer
authors.forename: Fahrettin
authors.initials: F
authors.lastname: Kelestimur
authors.forename: Kelestimur
authors.initials: K
authors.lastname: Fahrettin
authors.forename: Sebnem
authors.initials: S
authors.lastname: Gursoy
authors.forename: Gursoy
authors.initials: G
authors.lastname: Sebnem
authors.forename: Mevlut
authors.initials: M
authors.lastname: Baskol
authors.forename: Baskol
authors.initials: B
authors.lastname: Mevlut
authors.forename: Mustafa
authors.initials: M
authors.lastname: Kula
authors.forename: Kula
authors.initials: K
authors.lastname: Mustafa
authors.forename: Munis
authors.initials: M
authors.lastname: Dundar
authors.forename: Dundar
authors.initials: D
authors.lastname: Munis
mesh_terms: D000293:Adolescent; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000328:Adult; D001799:Blood Sedimentation; D002097:C-Reactive Protein / Q000032:analysis; D018450:Disease Progression; D010505:Familial Mediterranean Fever / Q000097:blood / Q000276:immunology / Q000503:physiopathology*; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D008297:Male; D010913:Pituitary-Adrenal System / Q000503:physiopathology*
chemical_list: D005340:Fibrinogen; D000324:Adrenocorticotropic Hormone; D002097:C-Reactive Protein; D006854:Hydrocortisone