Cushing's Disease (Hyperadrenocorticism) in Poodles — Management Guide

A practical, evidence-based guide to diagnosis and long-term management of Cushing's (hyperadrenocorticism) in Poodles, including testing, trilostane therapy, monitoring and complications.

Quick Overview

• What it is: Canine Cushing's disease (hyperadrenocorticism, HAC) is a syndrome caused by chronic excess cortisol. In dogs the two main causes are a pituitary corticotroph tumor (pituitary-dependent HAC, PDH) and an adrenal gland tumor (adrenal-dependent HAC, ADH).
• Who's at risk: Middle-aged to older dogs. Poodles (especially Miniature and Toy Poodles, but Standard Poodles also reported) are among breeds over-represented for pituitary-dependent HAC.
• Prognosis: Many dogs respond well to medical therapy (trilostane) with improved quality of life; long-term prognosis depends on cause (PDH often lifelong medical management; unilateral benign adrenal tumor may be curable with adrenalectomy).

Pathophysiology — explained simply

Cortisol is a steroid hormone produced by the adrenal cortex under control of ACTH (adrenocorticotropic hormone) from the pituitary gland. In PDH a small pituitary tumor secretes excess ACTH, stimulating both adrenal glands to enlarge and overproduce cortisol. In ADH an adrenal tumor (benign adenoma or malignant carcinoma) directly produces cortisol independent of pituitary control. Chronic cortisol excess affects metabolism, the immune system, skin, bladder function, blood pressure and the cardiovascular system — producing the classic signs of Cushing's.

Breed-specific risk factors and prevalence

• PDH accounts for ~80–85% of naturally occurring HAC in dogs; ADH ~15–20%.
• Poodles (Miniature and Toy, and to a lesser degree Standard) are over-represented among dogs diagnosed with PDH in multiple epidemiologic series. Age of onset is usually middle-aged to older (median 8–10 years).
• No single gene identified as causal in Poodles; risk is likely polygenic and multifactorial.

There is no formal universally accepted staging system, but clinicians classify severity by clinical impact and comorbidities (mild/moderate/severe). Common signs:

• Polyuria and polydipsia (PU/PD) — most common early signs
• Polyphagia, pendulous abdomen (pot-belly), muscle wasting
• Generalized hair thinning (bilateral symmetric alopecia), poor hair regrowth, thin skin
• Recurrent skin infections (pyoderma), comedones
• Panting, lethargy, exercise intolerance
• Increased susceptibility to urinary tract infections
• Hypertension, proteinuria, increased risk of thromboembolism
• In advanced PDH with large pituitary tumors: neurologic signs (behavior change, circling, visual deficits, seizures)

Goal: confirm cortisol excess, then determine cause (PDH vs ADH).

1) Screening

• Urine cortisol-to-creatinine ratio (UCCR): sensitive but nonspecific; good initial screen when clinical suspicion is low. A normal UCCR makes HAC unlikely; an elevated UCCR requires further testing.

• Low-dose dexamethasone suppression test (LDDST): dexamethasone 0.01 mg/kg IV, cortisol at 0, 4 and 8 hours. LDDST is highly sensitive (~85–100%) and can also help differentiate PDH (partial suppression at 4 h with escape at 8 h or failure to suppress at both times) from ADH (no suppression).
• ACTH stimulation test: synthetic ACTH (cosyntropin) 5 μg/kg IV or IM (max 250 μg), cortisol measured baseline and 1 hour post-ACTH. The ACTH stim is less sensitive for naturally occurring PDH but is preferred to monitor dogs on trilostane and is useful to diagnose iatrogenic HAC or to detect atypical cases.

• LDDST pattern, endogenous plasma ACTH concentration (low in ADH due to negative feedback), abdominal ultrasound and adrenal imaging help. On ultrasound: bilateral adrenal enlargement suggests PDH; unilateral adrenal mass suggests ADH.
• If imaging is unclear, cross-sectional imaging (CT or MRI) of abdomen and brain is recommended. Pituitary MRI is indicated if neurologic signs are present or if pituitary macroadenoma is suspected.

• Consider internal medicine or endocrinology referral for equivocal cases, advanced imaging (MRI), or when surgical options are considered.

• No test is perfect: combine clinical picture, screening and confirmatory testing.
• Medications (ketoconazole, mitotane, trilostane, glucocorticoids), stress, and concurrent illness can affect results — discuss medication history with your vet.

Goals: reduce clinical signs, minimize cortisol excess, treat complications, and preserve quality of life.

Medical therapy (mainstay for PDH and many ADH cases)

• Trilostane (competitive inhibitor of 3β-hydroxysteroid dehydrogenase) is the most commonly used drug worldwide. Licensed products (e.g., Vetoryl) have clear dosing guidelines and product information.
• Typical dosing concepts: starting dose commonly in the range of 1–3 mg/kg once daily or a total daily dose of 2–6 mg/kg divided q12h depending on product label and clinician preference. Many clinicians favor twice-daily dosing for more stable control. Dose adjustments are made based on clinical response and monitoring tests.
• Clinical response: historically 70–85% of dogs show clinical improvement on trilostane; remission (complete resolution of signs) rates vary. Time to improvement is days to weeks for PU/PD and weeks to months for skin and haircoat recovery.
• Adverse effects: signs of hypoadrenocorticism (lethargy, vomiting, diarrhea, weakness), electrolyte changes (hyponatremia, hyperkalemia) are possible — monitoring is essential.

• An adrenal cytotoxic drug that causes selective adrenal cortical necrosis. Still used by some clinicians. Induction and maintenance dosing protocols exist (induction: ~50–75 mg/kg/day divided until clinical/biochemical control; maintenance lower), but mitotane has more systemic effects and risk and has largely been supplanted by trilostane in many regions.

• Adrenalectomy: Unilateral adrenalectomy is indicated for unilateral adrenal tumors without metastatic disease. When successful, it can be curative. Risks include hemorrhage, perioperative hypoadrenocorticism, and anesthetic risk. Preoperative stabilization and postoperative steroid support are crucial.
• Transsphenoidal hypophysectomy: Available at specialized centers for PDH. In experienced hands this can be curative in many cases (remission rates reported up to ~70–80% in selected cohorts). Requires specialized surgical expertise and long-term follow-up.

• Stereotactic or conventional radiotherapy to pituitary macroadenomas may be used when surgery isn't an option and the tumor causes neurologic signs.

• Ketoconazole, aminoglutethimide, and mitotane have been used historically. Selegiline is generally not effective for classical PDH in dogs.

Monitoring combines clinical assessment and lab testing. The ACVIM consensus recommends individualized monitoring; typical practical schedule:

• Baseline: CBC, chemistry (including electrolytes), urinalysis, and blood pressure before starting therapy.
• After starting or changing trilostane: recheck within 7–14 days. Many clinics perform an ACTH stimulation test (baseline and 1 hr post-ACTH) at a standardized time relative to trilostane dosing (commonly 4–6 hours after dosing) to assess adrenal reserve. Also check electrolytes.
• Once stable: monitor every 3–6 months (clinical review and labs), and sooner if signs change. Annual rechecks are common for long-term stable dogs.
• For dogs on trilostane be alert to signs of hypocortisolism and check electrolytes; if hyponatremia or hyperkalemia develop, treat urgently.

• Do ACTH stimulation tests at a consistent time after the trilostane dose (clinician should document timing) so results are comparable.
• Monitor for secondary problems (diabetes, urinary infections, hypertension, proteinuria). Blood pressure and urine culture (if recurrent UTIs) are useful.

• Common: urinary tract infections, skin infections, dermatologic fragility, hypertension, proteinuria, diabetes mellitus, pancreatitis, thromboembolic events.
• Hypoadrenocorticism (Addisonian crisis) is an important potential complication of trilostane or mitotane therapy — recognize early (vomiting, diarrhea, weakness, collapse) and seek emergency care.
• Large pituitary tumors can cause neurologic deterioration — seizure, obtundation — urgency for specialty evaluation.

• Dogs with PDH often do well with medical therapy for months to years; many owners report substantial improvement in activity, appetite, and skin condition. Long-term survival is influenced by age at diagnosis, presence of comorbid disease (e.g., diabetes), and whether the tumor is pituitary macroadenoma or adrenal carcinoma with metastasis.
• Adrenal tumors that are benign and successfully resected may be cured; malignant adrenal carcinoma carries a worse prognosis.

• Medication timing: follow your vet's exact dosing schedule for trilostane. If a once-daily dose is used, give at the same time each day; if twice daily, space doses evenly.
• Monitor water intake, urine volume, appetite, energy and skin. Keep a diary of PU/PD, stool changes, vomiting episodes or mood changes to report at rechecks.
• Skin care: Poodles often have fragile skin — regular grooming, gentle shampoos, treating secondary infections promptly, and working with your vet on topical or systemic therapy when needed.
• Weight and muscle: maintain moderate exercise, high-quality diet, and address muscle loss with appropriate nutrition and physical activity once medically stabilized.
• Dental health: poor dentition contributes to systemic inflammation — regular dental care helps overall health.
• Avoid unnecessary steroid exposure: do not give glucocorticoids (including topical/inhaled forms) unless prescribed by your vet.

Seek immediate veterinary attention if your Poodle on treatment develops:

• Repeated vomiting, severe diarrhea, profound weakness, collapse — potential hypoadrenocorticism
• Severe panting, breathing difficulty or collapse
• Sudden neurologic signs (seizures, circling, disorientation, blindness) — possible pituitary tumor effects
• Dark or bloody urine, signs of blood clot (sudden limb lameness or respiratory distress)

• Early diagnosis and appropriate therapy substantially improve quality of life in many Poodles with HAC.
• Trilostane is the most commonly used medical therapy; monitoring for hypoadrenocorticism is essential.
• Distinguishing PDH from ADH is important because adrenalectomy or hypophysectomy may be curative in selected cases.
• Regular follow-up (clinical and laboratory) and prompt attention to complications will give your Poodle the best outcome.

• ACVIM Consensus Statement: Guidelines for the diagnosis and treatment of canine hyperadrenocorticism (Behrend et al., Journal of Veterinary Internal Medicine). https://pubmed.ncbi.nlm.nih.gov/24171802/
• Feldman EC, Nelson RW. Canine and Feline Endocrinology and Metabolism (textbook) — authoritative reference on HAC pathophysiology and management.
• Vetoryl (trilostane) product information (Dechra) — dosing and safety guidance: https://www.vetoryl.com

Frequently Asked Questions