What Is Cushing's Disease?
Cushing's disease — or more formally, hyperadrenocorticism — is a condition in which the adrenal glands produce excessive amounts of cortisol. Cortisol is an essential stress hormone that in normal amounts regulates immune function, metabolism, and the response to physical and emotional stress. However, chronically elevated cortisol causes widespread harm across virtually every body system, producing the characteristic constellation of signs seen in affected dogs.
Cushing's disease is most commonly seen in middle-aged to older dogs, and small to medium breeds such as Poodles, Dachshunds, Staffordshire Bull Terriers, Jack Russell Terriers, and Yorkies appear overrepresented. However, it can occur in any breed or size of dog.
The Three Forms of Cushing's Disease
Understanding which form of Cushing's disease a dog has is critical, because the treatment approach differs significantly between them.
Pituitary-Dependent Hyperadrenocorticism (PDH)
PDH accounts for approximately 85% of all Cushing's disease cases in dogs. It is caused by a tumour — almost always a benign microadenoma — of the pituitary gland at the base of the brain. This tumour produces excessive amounts of adrenocorticotrophic hormone (ACTH), which in turn over-stimulates both adrenal glands, causing them to enlarge and produce too much cortisol. Because both adrenal glands are affected, PDH is a bilateral condition.
Adrenal-Dependent Hyperadrenocorticism (ADH)
Adrenal tumours account for the remaining 15% of cases. These are primary tumours of one adrenal gland that independently produce excessive cortisol regardless of pituitary signals. Approximately half of adrenal tumours are benign (adenomas) and half are malignant (carcinomas). Because the tumour produces cortisol autonomously, ACTH levels from the pituitary are actually suppressed, and the opposite adrenal gland typically atrophies.
Iatrogenic Cushing's Disease
Arguably the most common cause of Cushing's-like signs in dogs is iatrogenic — meaning it is caused by the administration of corticosteroid medications such as prednisolone, dexamethasone, or topical steroids (including eye and ear drops used over a prolonged period). The body responds to externally supplied corticosteroids by suppressing its own production, but the signs of cortisol excess still appear. Iatrogenic Cushing's resolves once the steroid medication is gradually withdrawn, though this must always be done slowly and under veterinary supervision to avoid an adrenal crisis.
Recognising the Signs
The clinical signs of Cushing's disease develop slowly and are often attributed to normal ageing. Common signs include:
- Pot belly or pendulous abdomen — caused by redistribution of fat and weakening of abdominal muscles
- Polyuria and polydipsia (PU/PD) — excessive drinking and urination, often the first signs noticed by owners
- Polyphagia (PP) — ravenous appetite
- Bilateral symmetrical alopecia — hair loss affecting both sides of the trunk equally, typically sparing the head and limbs
- Thin, fragile skin with prominent blood vessels visible through it
- Calcinosis cutis — calcium deposits in the skin, appearing as firm, chalky plaques, particularly along the back and neck
- Muscle wasting and weakness
- Panting, even at rest or in cool conditions
- Recurrent urinary tract infections
Diagnosing Cushing's Disease
Diagnosis involves both confirming the presence of cortisol excess and then identifying which form is responsible. No single test is perfect, and clinical judgement is essential throughout.
Low-Dose Dexamethasone Suppression Test (LDDST)
The LDDST is the preferred screening test for Cushing's disease in dogs. A small dose of dexamethasone is given by injection, and cortisol levels are measured at baseline, four hours, and eight hours later. In a healthy dog, dexamethasone suppresses cortisol production. In a dog with Cushing's disease, cortisol fails to suppress appropriately. The LDDST has good sensitivity for detecting PDH and can also provide early evidence of the underlying cause based on the suppression pattern observed at the four-hour mark.
High-Dose Dexamethasone Suppression Test (HDDST)
The HDDST uses a higher dose of dexamethasone and is used primarily to differentiate PDH from adrenal-dependent disease. In PDH, higher doses of dexamethasone can usually override the pituitary tumour's resistance and produce some cortisol suppression. In adrenal tumours, the cortisol production is autonomous and will not suppress even at high doses.
Abdominal ultrasound is a vital part of the diagnostic workup, allowing direct visualisation of the adrenal glands. Bilateral enlargement points towards PDH, while a single enlarged or irregular gland with a small, atrophied opposite gland is strongly suggestive of an adrenal tumour.
Treatment Options
Trilostane (Vetoryl)
For PDH, and increasingly for medically managed adrenal tumours, Trilostane — marketed as Vetoryl — is the treatment of choice in the United Kingdom. Trilostane works by blocking an enzyme in the adrenal gland that is essential for cortisol synthesis, thereby reducing cortisol output without destroying the gland itself. It is given orally once or twice daily with food.
Regular monitoring is essential during Trilostane therapy, beginning with an ACTH stimulation test performed four to six hours after the pill is given, at approximately ten days, four weeks, and three months after starting treatment, then every three to six months thereafter. The goal is to bring cortisol levels into the target range, neither too high (inadequate control) nor too low (risk of hypoadrenocorticism, or Addison's disease).
Surgical Adrenalectomy
Dogs with adrenal tumours may be candidates for surgical removal of the affected adrenal gland. When performed by an experienced surgeon in a well-stabilised patient, the outcomes can be excellent, particularly for benign adenomas. However, surgery carries significant risks in Cushing's patients and is not appropriate for all cases.
Prognosis and Quality of Life
With appropriate treatment, the majority of dogs with PDH enjoy a significantly improved quality of life, often for several years after diagnosis. Calcinosis cutis, coat regrowth, and resolution of PU/PD typically occur gradually over weeks to months. Owners should be prepared for a monitoring-intensive initial period, but this usually settles into a manageable long-term routine. Close collaboration with your vet throughout treatment is essential for the best possible outcome.