Pituitary-dependent hyperadrenocorticism in a family of Dandie Dinmont
terriers.

Scholten-Sloof BE, Knol BW, Rijnberk A, Mol JA, Middleton DJ, Ubbink GJ.

Department of Clinical Sciences of Companion Animals, Faculty of Veterinary
Medicine, University of Utrecht, The Netherlands.

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.

PMID: 1487706 [PubMed - indexed for MEDLINE]