Cushing's Disease in Dogs: Symptoms, Diagnosis & Treatment
What Is Cushing's Disease?
Cushing's disease — properly called hyperadrenocorticism — is a condition in which the adrenal glands produce excessive amounts of cortisol, the body's primary stress hormone. Cortisol in normal amounts is essential: it regulates metabolism, immune function, blood pressure, and the stress response. But when cortisol is chronically elevated, it causes widespread, progressive damage to virtually every body system.
There are two primary forms of Cushing's disease in dogs:
- Pituitary-dependent hyperadrenocorticism (PDH): Accounts for 80–85% of cases. A tumor (usually a microadenoma) of the pituitary gland secretes excess ACTH, which drives both adrenal glands to overproduce cortisol. The adrenal glands enlarge bilaterally (on both sides).
- Adrenal-dependent hyperadrenocorticism (AT): Accounts for 15–20% of cases. A tumor on one adrenal gland autonomously produces excess cortisol, suppressing ACTH and causing the opposite gland to atrophy. Approximately 50% of adrenal tumors are malignant.
Cushing's disease is one of the most common endocrine disorders in middle-aged to older dogs. Predisposed breeds include Poodles, Dachshunds, Boxers, Yorkshire Terriers, Beagles, and Boston Terriers, though any breed can be affected.
Classic Signs of Cushing's Disease
The signs of Cushing's disease develop gradually over months to years and are often initially attributed to normal aging. The classic presentation includes a distinctive cluster of signs:
- Pot-bellied abdomen: One of the most visually striking signs. Chronically elevated cortisol causes redistribution of fat into the abdomen and weakening of abdominal muscles, creating a pendulous, enlarged belly even in dogs that are not significantly overweight overall.
- Polyuria and polydipsia (PU/PD): Excessive urination and excessive thirst. Cortisol impairs the action of antidiuretic hormone (ADH), causing the kidneys to produce large volumes of dilute urine. Owners notice dogs asking to go outside much more frequently, drinking from unusual water sources, or having house-training accidents they never had before.
- Bilateral symmetrical hair loss (alopecia): Hair loss that begins on the trunk and flanks, sparing the head and limbs. The remaining skin may become thin, darkly pigmented, and inelastic. Hair regrowth after clipping is severely delayed or absent.
- Calcinosis cutis: Calcium deposits form in the skin, particularly over the neck, back, and groin. This appears as firm, chalky plaques under the skin and is highly specific to Cushing's disease. It is caused by cortisol's interference with calcium metabolism.
- Muscle wasting: Cortisol breaks down muscle protein for energy (gluconeogenesis). Affected dogs lose muscle mass over time, particularly in the hind limbs and temporal muscles of the skull. Combined with the pot belly, this gives a characteristic "insurance symbol" silhouette.
- Excessive panting: Even at rest and in cool environments, Cushingoid dogs often pant persistently. This reflects metabolic changes, altered respiratory muscle function, and possibly central effects of cortisol excess.
- Increased appetite: Cortisol stimulates appetite. Cushing's dogs are typically ravenous and may beg, steal food, or raid waste bins.
- Susceptibility to infections: Cortisol suppresses immune function. Skin infections (pyoderma), urinary tract infections, and respiratory infections recur frequently and may resist normal treatment.
Diagnosis: Specific Tests Are Required
Cushing's disease cannot be diagnosed on clinical signs alone — the symptoms overlap significantly with diabetes mellitus, hypothyroidism, and kidney disease. Several tests may be required, and no single test is perfect. Your veterinarian will determine which sequence is most appropriate.
- Urine cortisol:creatinine ratio (UCCR): A useful screening test collected by the owner at home (first morning urine). A normal result effectively rules out Cushing's. However, many non-Cushingoid sick dogs also have elevated ratios, so a positive result requires confirmatory testing.
- Low-dose dexamethasone suppression test (LDDS): The most commonly used confirmatory test. A small dose of synthetic cortisol (dexamethasone) is given, and blood cortisol is measured 4 and 8 hours later. In normal dogs, dexamethasone suppresses cortisol output. In dogs with Cushing's, suppression fails to occur or occurs incompletely. The 8-hour pattern can also help differentiate PDH from AT.
- ACTH stimulation test: Measures cortisol before and after synthetic ACTH administration. Useful for confirming Cushing's and essential for monitoring dogs on treatment (particularly those on mitotane).
- Abdominal ultrasound: Once biochemical Cushing's is confirmed, ultrasound evaluates the adrenal glands. Bilaterally enlarged glands suggest PDH. A unilateral mass suggests AT. This guides treatment decisions.
- Full blood panel and urinalysis: Characteristic changes (elevated alkaline phosphatase, elevated cholesterol, dilute urine, often UTI) support the diagnosis and establish baseline organ function before treatment.
Treatment: Prescription Medications and Ongoing Monitoring
Treatment decisions depend on the underlying cause, tumor size, the dog's overall health, and owner commitment to monitoring. All treatments require close veterinary supervision.
- Trilostane (Vetoryl): The current first-line medical treatment for PDH and some AT cases. Trilostane blocks an enzyme in the adrenal cortex, reducing cortisol synthesis. It is a prescription drug requiring careful dose titration. Dogs must be monitored with ACTH stimulation tests 10 days after starting treatment, after dose changes, and every 3–6 months long-term. Potential side effects include life-threatening hypoadrenocorticism (too little cortisol) if the dose is too high.
- Mitotane (Lysodren): An older alternative that destroys adrenal cortical tissue. Requires an induction phase with daily dosing, followed by weekly maintenance. Also requires ACTH stimulation monitoring. Has a narrower safety margin than trilostane and requires owners to be familiar with signs of hypoadrenocorticism crisis (weakness, vomiting, collapse).
- Surgery: Adrenalectomy is the definitive treatment for AT when the tumor is accessible and the dog is a suitable surgical candidate. Pituitary surgery (transsphenoidal hypophysectomy) is performed at specialist referral centers for PDH.
- Radiation therapy: For large pituitary tumors (macrotumors) causing neurological signs, radiation may shrink the tumor and alleviate pressure on surrounding brain structures.
There are no evidence-based herbal, homeopathic, or dietary treatments for Cushing's disease. Products sold as "natural Cushing's remedies" — including melatonin, lignans, and various herbal blends — have not been validated in controlled clinical trials and should not replace veterinary treatment. Using them in place of proper medical management allows progressive organ damage to continue.
Long-Term Monitoring Is Essential
Dogs with Cushing's disease require lifelong monitoring, regardless of which treatment is chosen. Regular ACTH stimulation tests, urine cultures (to detect recurrent UTIs), blood pressure monitoring, and periodic imaging are part of standard management. The prognosis is good for dogs with PDH receiving appropriate treatment — median survival times of 2 years or more are documented. Dogs with benign AT treated surgically can achieve long-term remission.
Key Takeaways
- Cushing's disease is caused by chronically excessive cortisol — 85% of cases originate from a pituitary tumor, 15% from an adrenal tumor.
- Classic signs: pot belly, excessive thirst and urination, symmetrical hair loss, skin calcium deposits, muscle wasting, and persistent panting.
- Diagnosis requires specific blood tests (LDDS or ACTH stimulation) and abdominal ultrasound — symptoms alone are not enough.
- Treatment is with prescription medications (trilostane or mitotane) that require careful dose monitoring — never attempt to treat Cushing's at home.
- No herbal or supplement products have proven efficacy for Cushing's disease; using them instead of medical treatment causes harm.
- Lifelong veterinary monitoring is essential — dogs on treatment need ACTH stimulation tests every 3–6 months.
References
Behrend EN, et al. (2013). Diagnosis of spontaneous canine hyperadrenocorticism: 2012 ACVIM consensus statement. Journal of Veterinary Internal Medicine. PubMed
Feldman EC. (2011). Evaluation of twice-daily lower-dose trilostane treatment administered orally in dogs with naturally occurring hyperadrenocorticism. Journal of the American Veterinary Medical Association. PubMed
