title: Effect of trilostane and mitotane on aldosterone secretory reserve in dogs with pituitary-dependent hyperadrenocorticism.
abstract: BACKGROUND
  Maximal aldosterone secretion in healthy dogs occurs 30 minutes postadrenocorticotropin (ACTH; 5 μg/kg IV) stimulation. The effect of trilostane and mitotane on aldosterone at that time is unknown.
  
  
  OBJECTIVE
  To assess the effect of trilostane and mitotane in dogs with pituitary-dependent hyperadrenocorticism on aldosterone secretory reserve. To determine if aldosterone concentration correlates with electrolyte concentrations.
  
  
  METHODS
  Serum collected from 79 client-owned dogs and 33 stored samples.
  
  
  METHODS
  Client-owned dogs had ACTH stimulation tests with cortisol concentrations measured at 0 and 60 minutes and aldosterone concentrations measured at 0, 30, and 60 minutes. Stored samples had aldosterone concentrations measured at 0 and 60 minutes. Ten historical clinically healthy controls were included. All had basal sodium and potassium concentrations measured.
  
  
  RESULTS
  The aldosterone concentrations in the mitotane- and trilostane-treated dogs at 30 and 60 minutes post-ACTH were significantly lower than in clinically healthy dogs; no significant difference was detected in aldosterone concentration between 30 and 60 minutes in treated dogs. However, a significantly higher percentage of dogs had decreased aldosterone secretory reserve detected at 30 minutes than at 60 minutes. At 30 minutes, decreased secretory reserve was detected in 49% and 78% of trilostane- and mitotane-treated dogs, respectively. No correlation was detected between aldosterone and serum electrolyte concentrations.
  
  
  CONCLUSIONS
  Decreased aldosterone secretory reserve is common in trilostane- and mitotane-treated dogs; it cannot be predicted by measurement of serum electrolyte concentrations. Aldosterone concentration at 30 minutes post-ACTH stimulation identifies more dogs with decreased aldosterone secretory reserve than conventional testing at 60 minutes.
authors.affiliation: Department of Clinical Sciences, College of Veterinary Medicine, Auburn University, Auburn, AL.
authors.forename: L E
authors.initials: LE
authors.lastname: Reid
authors.forename: E N
authors.initials: EN
authors.lastname: Behrend
authors.forename: L G
authors.initials: LG
authors.lastname: Martin
authors.forename: R J
authors.initials: RJ
authors.lastname: Kemppainen
authors.forename: C R
authors.initials: CR
authors.lastname: Ward
authors.forename: J C
authors.initials: JC
authors.lastname: Lurye
authors.forename: T C
authors.initials: TC
authors.lastname: Donovan
authors.forename: H P
authors.initials: HP
authors.lastname: Lee
mesh_terms: D000450:Aldosterone / Q000097:blood* / Q000378:metabolism; D000818:Animals; D013196:Dihydrotestosterone / Q000031:analogs & derivatives* / Q000627:therapeutic use; D004283:Dog Diseases / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D004285:Dogs; D005260:Female; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D008939:Mitotane / Q000627:therapeutic use*; D047748:Pituitary ACTH Hypersecretion / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology / Q000662:veterinary*; D011188:Potassium / Q000097:blood; D012964:Sodium / Q000097:blood
chemical_list: D013196:Dihydrotestosterone; D000450:Aldosterone; D008939:Mitotane; D012964:Sodium; C009954:trilostane; D011188:Potassium; D006854:Hydrocortisone
keywords: Cushing's disease; Lysodren; Pituitary-dependent hyperadrenocorticism; Vetoryl