Pituitary-dependent hyperadrenocorticism in a family of Dandie Dinmont terriers

Abstract

Adrenocortical function studies were performed in seven Dandie Dinmont terriers with pituitary-dependent hyperadrenocorticism. The ability of dexamethasone at a dose rate of 0.1 mg/kg body weight to suppress cortisol secretion was only moderate in four out of the six dogs tested. Concentrations of alpha-melanocyte-stimulating hormone in plasma were highly increased. Responses to stimulation with corticotrophin-releasing hormone and the dopamine-antagonist haloperidol, examined in three animals, were moderate or absent. These results indicate that adrenocortical stimulation, i.e. hyperadrenocorticotrophism, was caused by pituitary lesions which were functioning autonomously. In six of the seven animals there was a very close familial relationship and the coefficients of relationship and the coefficients of inbreeding were significantly higher than in a representative control population. It was concluded that these seven related terriers with hyperadrenocorticotrophism had the biochemical characteristics of de-novo neoplasms of proopiomelanocortin-producing cells, and there was evidence for a genetic involvement in tumorigenesis.

Correlation between impairment of glucocorticoid feedback and the size of the pituitary gland in dogs with pituitary-dependent hyperadrenocorticism

“…There is evidence that the earliest step may be an inherited aberration that plays an initiating or promoting role (Scholten-Sloof et al 1992). The clonai expansion of the genomically altered cell may be caused by either an intrinsic mutation resulting in a constitutive activation of cell replication or by extrinsic factors such as intrapituitary growth factors.…”

Transsphenoidal Hypophysectomy for Treatment of Pituitary‐Dependent Hyperadrenocorticism in 7 Cats

“…As in humans 16,17 and dogs, the treatment of PDH in cats may be aimed at eliminating the stimulus for the persisting hypersecretion of cortisol, ie, the pituitary lesion causing excessive secretion of adrenocorticotrophic hormone (ACTH). In dogs there is increasing evidence that these lesions are of primary pituitary origin and not the result of increased hypothalamic stimulation 18,19 . Early diagnosis of PDH, pituitary imaging, and intervention at the pituitary level may result in the successful treatment of feline PDH.…”

The Efficacy of L‐Deprenyl in Dogs with Pituitary‐Dependent Hyperadrenocorticism

“…The earliest stage may be an inherited aberration that plays an initiating or promoting role. 41 What other factors may contribute to tumor promotion is not known, although the results of the CT examination of the present study indicated that dopamine plays a minor role at best. The proportion of dogs (7 of 10) with hypophyseal enlargement at the start of the study was similar to that reported by Bertoy et al 42 In 4 dogs, a marked increase occurred in the size of the hypophysis after 4-6 months of L-Deprenyl treatment and 2 of these dogs had severe neurologic disturbances.…”