Dept. of Reproduction and the Small Animal Clinic, School of Veterinary Medicine, University of California, Davis, CA 95616
Canine Hyperadrenocorticism Due to Adrenocortical Neoplasia: Pretreatment Evaluation of 41 Dogs
Article first published online: 5 FEB 2008
Journal of Veterinary Internal Medicine
Volume 5, Issue 1, pages 3–10, January 1991
How to Cite
Reusch, C. E. and Feldman, E. C. (1991), Canine Hyperadrenocorticism Due to Adrenocortical Neoplasia: Pretreatment Evaluation of 41 Dogs. Journal of Veterinary Internal Medicine, 5: 3–10. doi: 10.1111/j.1939-1676.1991.tb00922.x
- Issue published online: 5 FEB 2008
- Article first published online: 5 FEB 2008
This retrospective study identifies parameters that might separate dogs with hyperadrenocorticism caused by adrenocortical tumors from dogs with pituitary-dependent hyperadrenocorticism. Further, an attempt was made to identify factors that could separate dogs with adrenocortical adenomas from dogs with carcinomas. The records of 41 dogs with hyperadrenocorticism caused by adrenocortical neoplasia were reviewed. The history, physical examination, urinalysis, hemogram (CBC), chemistry profile adrenocorticotrophic hormone (ACTH) stimulation and low dose dexamethasone test results were typical of the nonspecific diagnosis of hyperadrenocorticism. The preceding information on the 41 dogs with adrenocortical tumors was compared with that from 44 previously diagnosed pituitary-dependent hyperadrenocorticoid dogs. There was no parameter which aided in separating these two groups of dogs.
Thirty dogs with adrenocortical tumors were tested with a high-dose dexamethasone test and none had suppressed plasma Cortisol concentrations 8 hours after IV administration of 0.1 mg/kg of dexamethasone. In 29 of the 41 adrenal tumor dogs, plasma endogenous ACTH was not detectable on at least one measurement (< 20 pg/ml). The remaining 12 dogs from this group had nondiagnostic concentrations (20–45 pg/ml). Thirteen of 22 dogs (59%) with adrenocortical carcinomas had adrenal masses identified on abdominal radiographs and seven of 13 dogs (54%) with adrenocortical adenomas had radiographically visible adrenal masses. Thirteen of 17 adrenocortical carcinomas (76%) and five of eight adenomas (62%) were identified with ultrasonography. Radiographs of the thorax and ultrasonography of the abdomen identified most of the dogs (8 of 11) with metastatic lesions.
In conclusion, the most sensitive tests in distinguishing dogs with pituitary-dependent hyperadrenocorticism from dogs with adrenocortical tumors were the plasma endogenous ACTH concentrations, abdominal radiography, and abdominal ultrasonography. None of these three tests alone, however, were completely reliable, suggesting the potential need for review of several tests when attempting to separate dogs with pituitary-dependent hyperadrenocorticism from those with adrenocortical tumors. Recognition of metastatic lesions with radiography and/or ultrasonography was the only parameter that separated dogs with adenomas from dogs with carcinomas.