Glucocorticoid deficient hypoadrenocorticism in dogs: 18 cases (1986-1995)

• Published in: Journal of the American Veterinary Medical Association Vol. 209; no. 12; p. 2076
• Main Authors: Lifton, S J, King, L G, Zerbe, C A
• Format: Journal Article
• Language: English
• Published: United States 15-12-1996
• Subjects: Adrenal Cortex Function Tests - veterinary; Adrenal Insufficiency - drug therapy; Adrenal Insufficiency - physiopathology; Adrenal Insufficiency - veterinary; Adrenocorticotropic Hormone; Animals; Dog Diseases - drug therapy; Dog Diseases - physiopathology; Dogs; Female; Glucocorticoids - deficiency; Glucocorticoids - therapeutic use; Male; Retrospective Studies
• ISSN: 0003-1488
• DOI: 10.2460/javma.1996.209.12.2076

To characterize naturally developing glucocorticoid deficiency in dogs.
Retrospective case series.
18 dogs with glucocorticoid deficiency defined by an inadequate response to stimulation with adrenocorticotropic hormone (ACTH), a normal Na:K ratio (> 27), and no history of receiving corticosteroids for at least 6 weeks.
Information including signalment, body weight, clinical signs on admission, historical findings, physical examination findings, results of CBC and serum biochemical analyses, results of ACTH stimulation tests and other ancillary endocrine tests, diagnostic imaging findings, findings from other procedures such as endoscopy and surgery, and information on concurrent diseases, management, and outcome were retrieved from the medical records of dogs with glucocorticoid deficiency treated between 1986 and 1995 at the University of Pennsylvania's School of Veterinary Medicine and 2 dogs from private practices.
Most dogs were young (< 7 years) and represented larger breeds (> 20 kg). Clinical signs were nonspecific: lethargy, weight loss, and gastrointestinal disturbances including regurgitation with radiographic evidence of megaesophagus. Hypocholesterolemia, hypoalbuminemia, hypoglycemia, and a mild, nonregenerative anemia were common. Ten of the 18 dogs responded well to glucocorticoid supplementation alone, with only 2 dogs developing electrolyte abnormalities. Four (22%) of the dogs died, with death usually occurring as a result of secondary disease processes rather than hypoadrenocorticism.
An ACTH stimulation test should be considered as part of the diagnostic plan in dogs with signs of weight loss, inappetence, and intermittent vomiting and diarrhea. Glucocorticoid-deficient dogs may not require supplemental mineralocorticoids.