in a family of Dandie Dinmont
Scholten-Sloof BE, Knol BW, Rijnberk A, Mol JA, Middleton DJ, Ubbink GJ.
Department of Clinical Sciences of Companion Animals, Faculty of
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
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
i.e. hyperadrenocorticotrophism, was caused by pituitary lesions which
functioning autonomously. In six of the seven animals there was a very
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
terriers with hyperadrenocorticotrophism had the biochemical
of de-novo neoplasms of proopiomelanocortin-producing cells, and there was
evidence for a genetic involvement in tumorigenesis.
PMID: 1487706 [PubMed - indexed for MEDLINE]