title: Immunocytochemical localization of adrenocorticotropic hormone-immunoreactive cells of the pars intermedia in thoroughbreds.
abstract: OBJECTIVE
  To analyze and characterize adenoma and hyperplasia of the pars intermedia (PI) of Thoroughbred mares.
  
  
  METHODS
  165 Thoroughbred mares, without clinical signs of hyperadrenocorticism that had been euthanatized or had died, of causes such as sudden death, colic, pneumonia, or trauma, and were necropsied. Five of those horses, 17 to 25 years old, had a large pituitary gland at necropsy. Eight mares, 5 to 15 years old with normal-size pituitary gland, were selected at random for comparison.
  
  
  METHODS
  A morphologic comparison of the pituitary gland between horses with and without tumors of the PI was conducted by use of immunocytochemistry and morphometry.
  
  
  RESULTS
  In horses with normal pituitary gland, the PI was supplied by a vast capillary or sinusoidal plexus, which connected that in the pars distalis (PD) with that in the pars nervosa (PN). Cells of the PI stained slightly with ACTH antiserum, but some cells in the border region, which is contiguous to the PD, were strongly ACTH immunoreactive. At necrospy, horses with an enlarged pituitary gland also had adenoma of the pituitary gland involving the PI. Cells of the border region were hypertrophied and stained strongly with ACTH antiserum. The area and number of individual tumor cells of the border region of the PI of horses with adenoma were significantly increased, compared with those in horses with normal pituitary gland.
  
  
  CONCLUSIONS
  Cells of the PI-PD border region may secrete substantial quantities of ACTH, owing to stimulation by corticotropin-releasing factor. Adenoma and hyperplasia of the PI in Thoroughbred mares may be associated with hyperadrenocorticism.
authors.affiliation: Department of Veterinary Anatomy, College of Agriculture, Osaka Prefecture University, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Okada
authors.forename: T
authors.initials: T
authors.lastname: Shimomuro
authors.forename: M
authors.initials: M
authors.lastname: Oikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Nambo
authors.forename: Y
authors.initials: Y
authors.lastname: Kiso
authors.forename: Y
authors.initials: Y
authors.lastname: Morikawa
authors.forename: R M
authors.initials: RM
authors.lastname: Liptrap
authors.forename: S
authors.initials: S
authors.lastname: Yamashiro
authors.forename: P B
authors.initials: PB
authors.lastname: Little
authors.forename: F
authors.initials: F
authors.lastname: Sasaki
mesh_terms: D000236:Adenoma / Q000473:pathology / Q000662:veterinary*; D000324:Adrenocorticotropic Hormone / Q000032:analysis*; D000818:Animals; D005260:Female; D006734:Horse Diseases; D006736:Horses; D006965:Hyperplasia; D007150:Immunohistochemistry; D010902:Pituitary Gland / Q000166:cytology* / Q000473:pathology*; D010911:Pituitary Neoplasms / Q000473:pathology / Q000662:veterinary*; D012016:Reference Values
chemical_list: D000324:Adrenocorticotropic Hormone