Twenty-one normal dogs were assessed for baseline plasma cortisol concentrations as well as concentrations one hour after intramuscular administration of synthetic ACTH. These 21 dogs plus 10 additional clinically normal dogs also were assessed for baseline endogenous ACTH levels. Fifteen dogs suspected of having hyperadrenocorticism were then studied in the same fashion. Six of these dogs were normal in all four categories and were felt to be free of adrenal disease. Seven dogs had elevated one-hour post-stimulation plasma cortisol levels, elevated increments of change, normal or elevated resting plasma cortisol levels, and normal or elevated endogenous ACTH levels. These results were consistent with adrenal hyperplasia secondary to excessive pituitary secretion of ACTH. Six were successfully treated with o,p'DDD and one was euthanized and necropsied prior to therapy. This necropsy revealed adrenal cortical hyperplasia and a small pituitary gland tumor. The two remaining suspect hyperadrenal dogs had normal resting, post-stimulation, and increment of change plasma cortisols. Their endogenous plasma ACTH values were significantly below normal. These results were consistent with a functioning adrenal tumor. Both dogs had adrenal adenomas removed surgically. Sixteen dogs suspected of being hypoadrenal were also studied. Eight of these dogs were normal in all four categories. Seven dogs had depressed one-hour post-stimulation plasma cortisol values, depressed increments of change, elevated endogenous ACTH levels, and normal or depressed baseline plasma cortisol levels. These results confirmed primary adrenal cortical failure and below normal negative feedback to the pituitary. Six of these dogs have been successfully treated for hypoadrenocorticism. One dog was euthanized and necropsied prior to therapy and was found to have adrenal cortical atrophy. One additional dog had a depressed one-hour post-stimulaton plasma cortisol level, depressed increment of change, and an endogenous plasma ACTH level that was significantly decreased. This dog is consistent with pituitary failure to release ACTH and secondary adrenal cortical hypofunction. Five dogs in shock but without signs of hypoadrenocorticism also were assessed. These dogs had increased baseline plasma cortisol concentrations, which ruled out hypoadrenocorticism.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of the American Animal Hospital Association|
|State||Published - 1978|
ASJC Scopus subject areas