Surgical removal of the affected adrenal gland is the treatment of choice for patients with hyperadrenocorticism caused by
an adrenocortical tumor. If the tumor is inoperable, distant metastases are detected, or the patient is an unsuitable anesthetic
candidate, medical therapy can be used to control clinical signs.
In the United States, medical therapy is the mainstay of treatment of dogs with PDH. But in people, endoscopic removal of
the underlying pituitary tumor is the standard of care and is curative. A successful method for hypophysectomy (rather than
tumor removal) has been reported in dogs with hyperadrenocorticism, but it requires substantial expertise and is unlikely
to be routinely performed.4
Medical therapy controls the signs of hyperadrenocorticism; it does not cure the disease. Lifelong treatment will be necessary,
and owners need to commit to regular follow-up examinations. All of the options have side effects or limitations (Table 5), so provide clients with detailed information before initiating treatment.5
Table 5 Medical Therapy Options for Canine Hyperadrenocorticism
Because of negative experiences or poor responses, some veterinarians are reluctant to recommend treatment in dogs with hyperadrenocorticism.
Although studies have not documented improved longevity with therapy, the quality of life for both patients and clients appears
to be substantially improved if the disease is successfully controlled. Complications from untreated hyperadrenocorticism
include hypertension, diabetes mellitus, glomerulopathy, and thromboembolism; effective regulation of cortisol secretion may
protect patients from these debilitating problems.
When selecting a treatment for hyperadrenocorticism, consider likely efficacy, the cost of care (including monitoring), and
the risk of adverse events. In general, both ketoconazole and selegiline demonstrate low efficacy and are not widely regarded
as appropriate first-line therapies. Choosing between mitotane and trilostane requires careful thought; complications can
occur with both drugs, and regular patient evaluations will be necessary. In experienced hands, mitotane is often successful,
but its variable intestinal absorption, long half-life, and cytotoxic effects can be problematic. Deciding when to switch
from induction to maintenance therapy with mitotane can be difficult, and clients must promptly identify changes in thirst
and appetite to prevent overdose. In contrast, trilostane has more predictable pharmacokinetics and is not directly cytotoxic.
Daily medication costs may be higher with trilostane, but monitoring expenses may be lower.