Use of ACTH stimulation tests to monitor the treatment of canine hyperadrenocorticism

Abstract

The case histories of 60 dogs with hyperadrenocorticism were reviewed. Fifty-four of the dogs were treated with mitotane at a mean daily dose rate of 48.8 mg/kg (range 25.6 to 84 mg/kg) for between four and 21 days. The mean weekly maintenance dose of mitotane was 48.8 mg/kg. An adrenocorticotrophic hormone (ACTH) stimulation test was performed before the treatment began, and in 30 cases at the end of the induction course, and the response to ACTH was measured at regular intervals thereafter. Nine of the treated dogs developed complete hypoadrenocorticism during treatment and required permanent mineralocorticoid replacement therapy. Twelve of the dogs had normal responses to an ACTH stimulation test before treatment, and the diagnosis of hyperadrenocorticism was based on the result of a low-dose dexamethasone suppression test. These 12 dogs had consistently lower cortisol levels before and after stimulation with ACTH and four of them developed complete hypoadrenocorticism. In general the clinical signs were well controlled when the cortisol levels were less than 105 nmol/litre before and after the stimulation test. Dogs in which the clinical signs recurred had cortisol levels between 210 and 580 nmol/litre after the test, a level which is within the normal pretreatment range. Twenty-seven of the treated dogs died and six of these deaths were attributable directly to the disease or therapy. The median survival time of the 54 treated dogs was 30 months; eight dogs died during the first 16 weeks of treatment, and the dogs which survived this period had a median survival time of 39 months (mean 50 months).

Use of ketoconazole to treat dogs with pituitary-dependent hyperadrenocorticism: 48 cases (1994–2007)

“…12,15,16 Adverse neurologic effects were also evident in 5% of mitotane-treated dogs. 3,7,8,11,12,16 Similar to findings in dogs treated with mitotane or trilostane, 3 survival time was significantly associated with age at diagnosis and serum cortisol concentration after ACTH stimulation after ketoconazole treatment. In view of the fact that ketoconazole has not been reported to affect mineralocorticoid activity, even at a dosage of 20 mg/kg every 12 hours, 28 the sodiumto-potassium ratio may not be appropriate for detecting secondary hypoadrenocorticism in dogs treated with ketoconazole.…”

“…Anorexia and vomiting appeared to be resolved by administration of ketoconazole with food or a temporary reduction in dose by 25% for 1 to 2 days. 4,7,8,11,[14][15][16] Adrenal necrosis in 1 trilostane-treated dog was also reported. 12,15,16 Adverse neurologic effects were also evident in 5% of mitotane-treated dogs.…”

“…1,2 Current treatments for dogs with PDH include a group of clinically evaluated drugs, only some of which effectively control the disorder. [3][4][5][6][7][8][9][10][11][12][13][14][15][16] Ketoconazole, cyproheptadine, aminoglutethimide, and L-deprenyl are used for treatment, but studies [17][18][19][20][21][22] in which the effectiveness of these drugs has been evaluated are limited and incomplete. [3][4][5][6][7][8][9][10][11][12][13][14][15][16] Ketoconazole, cyproheptadine, aminoglutethimide, and L-deprenyl are used for treatment, but studies [17][18][19][20][21][22] in which the effectiveness of these drugs has been evaluated are limited and incomplete.…”

Canine Pancreatic‐Specific Lipase Concentrations in Clinically Healthy Dogs and Dogs with Naturally Occurring Hyperadrenocorticism

“…Because of the retrospective nature of the study, the presence of confounding factors, including dyslipidemias, is unknown. Review of several long‐term evaluations of dogs with naturally occurring HAC2, 19, 20, 21, 22 did not identify a similar pattern of overrepresentation. Experimental studies in dogs also support a lack of association between glucocorticoid excess and pancreatitis 23, 24, 25, 26, 27, 28, 29.…”

Trilostane in Dogs

“…If the numbers of dogs from these 6 clinical trials are combined then only 39 dogs out of 244 dogs (16%) treated with trilostane developed adverse effects which may have been attributable to trilostane [18][19][20][21][22][23]. This prevalence of side effects compares favourably with those reported with mitotane (25 to 42%) [27,30,31].…”