title: Morphology of the pituitary gland in ferrets (Mustela putorius furo) with hyperadrenocorticism.
abstract: Pituitary tumours are the cause of hyperadrenocorticism in a variety of species, but the role of the pituitary gland in hyperadrenocorticism in ferrets is not known. In this species, the disease is mediated by the action of excess gonadotrophins on the adrenal cortex and is characterized by an excessive secretion of sex steroids. In this study, the pituitary gland of four healthy control ferrets, intact or neutered, and 10 neutered ferrets with hyperadrenocorticism was examined histologically following immunohistochemical labelling for adrenocorticotrophic hormone, alpha-melanocyte-stimulating hormone, growth hormone, thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, and prolactin. Immunohistochemistry revealed that somatotrophs, thyrotrophs and lactotrophs were the most abundant cell types of the pars distalis of the pituitary gland in the healthy ferrets. The distribution of corticotrophs was similar to that in the dog and man. In ferrets, as in dogs, the melanotrophic cell was almost the only cell type of the pars intermedia. Gonadotrophs were found in the pars distalis of neutered, but not intact ferrets. All the ferrets with hyperadrenocorticism had unilateral or bilateral alterations of the adrenal gland. In addition, in the pituitary gland of two of these ferrets a tumour was detected. These tumours were not immunolabelled by antibodies against any of the pituitary hormones, and had characteristics of the clinically non-functional gonadotroph tumours seen in man. In some of the other ferrets low pituitary immunoreactivity for gonadotrophic hormones was detected, which may have been due to the feedback of autonomous steroid secretion by the neoplastic transformation of the adrenal cortex. It is concluded that initially high concentrations of gonadotrophins resulting from castration may initiate hyperactivity of the adrenal cortex. The low incidence of pituitary tumours and the low density of gonadotrophin-positive cells in non-affected pituitary tissue in this study suggest that persistent hyperadrenocorticism is not dependent on persistent gonadotrophic stimulation.
authors.affiliation: Division of Avian and Exotic Animal Medicine, Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 8, 3584 CM Utrecht, The Netherlands.
authors.forename: N J
authors.initials: NJ
authors.lastname: Schoemaker
authors.forename: M H
authors.initials: MH
authors.lastname: van der Hage
authors.forename: G
authors.initials: G
authors.lastname: Flik
authors.forename: J T
authors.initials: JT
authors.lastname: Lumeij
authors.forename: A
authors.initials: A
authors.lastname: Rijnberk
mesh_terms: D000236:Adenoma; D000311:Adrenal Glands / Q000473:pathology; D000308:Adrenocortical Hyperfunction / Q000209:etiology / Q000473:pathology* / Q000662:veterinary*; D000818:Animals; D002369:Castration / Q000009:adverse effects; D005260:Female; D005289:Ferrets; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D010902:Pituitary Gland / Q000473:pathology*; D010911:Pituitary Neoplasms / Q000209:etiology / Q000473:pathology / Q000662:veterinary