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ACTH-independent hyperadrenocorticism due to food-dependent hypercortisolemia in a dog: a case report.
- Source :
-
Veterinary journal (London, England : 1997) [Vet J] 2008 Jul; Vol. 177 (1), pp. 141-3. Date of Electronic Publication: 2007 Jun 14. - Publication Year :
- 2008
-
Abstract
- In addition to adrenocortical tumours, aberrant expression of functional hormone receptors in the adrenal cortex may cause adrenocorticotrophic hormone (ACTH)-independent hyperadrenocorticism. Here we report on a 6 year old Vizsla dog in which ACTH-independent hyperadrenocorticism was associated with meal-induced hypercortisolemia. Diagnosis was based on history, physical findings, biochemical changes, and elevation of the urinary corticoid/creatinine ratio (UCCR) on two consecutive days (11 and 8.3 x 10(-6), reference range <8.3 x 10(-6)). Basal plasma ACTH concentration was found by repeated measurements to be suppressed (<1 ng/L, reference range 5-85 ng/L) and administration of corticotrophin releasing hormone (CRH) resulted in a minor increase (to 6 ng/L), consistent with ACTH-independent hyperadrenocorticism. Ultrasonography and computed tomography revealed two uniformly enlarged adrenal glands. Magnetic resonance imaging of the pituitary area showed a non-enlarged, normally enhancing pituitary gland. Based on these results, expression of functional aberrant adrenocortical receptors was suspected and the possibility of food-dependent hyperadrenocorticism was explored. The UCCR on two separate occasions rose from 11 and 8 x 10(-6) before a meal to 25 and 23 x 10(-6) at 3 h after ingestion of a meal, respectively. There was a corresponding increase in plasma cortisol concentration (from 90 to 150 nmol/L), while plasma ACTH concentration remained low or undetectable. Consistent with the diagnostic criteria for food-dependent hyperadrenocorticism in humans, administration of octreotide completely prevented meal-induced hypercortisolemia. The dog was treated successfully with the cortisol-synthesis-inhibitor trilostane (2h before meal), and at 26 months after the final diagnosis the dog is still in good condition. The combination of (1) low plasma ACTH concentration in the absence of an adrenocortical tumour, (2) an increase of >100% in UCCR after ingestion of a meal, (3) prevention of the meal-induced increase in plasma cortisol concentration by octreotide, and (4) reversal of signs of hypercortisolism by administration of trilostane a few hours before the meal led to the diagnosis of food-dependent hyperadrenocorticism in this dog.
- Subjects :
- Adrenocortical Hyperfunction blood
Adrenocortical Hyperfunction diagnosis
Adrenocortical Hyperfunction urine
Animals
Diagnosis, Differential
Dog Diseases blood
Dog Diseases urine
Dogs
Male
Adrenocortical Hyperfunction veterinary
Adrenocorticotropic Hormone blood
Dog Diseases diagnosis
Eating
Hydrocortisone blood
Postprandial Period
Subjects
Details
- Language :
- English
- ISSN :
- 1090-0233
- Volume :
- 177
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Veterinary journal (London, England : 1997)
- Publication Type :
- Academic Journal
- Accession number :
- 17572120
- Full Text :
- https://doi.org/10.1016/j.tvjl.2007.04.008