Canine Hyperadrenocorticism (Cushing's Disease): Welfare and Management
Cushing's Disease in Dogs: A Common but Treatable Condition
Hyperadrenocorticism (HAC) — commonly called Cushing's disease — is one of the most common endocrine disorders in dogs, caused by chronic excess cortisol production. With an estimated prevalence of 1-2 per 1,000 dogs, it primarily affects middle-aged to older dogs of certain breeds. Without treatment, Cushing's disease causes progressive welfare deterioration through multiple body systems. Effective treatment dramatically improves quality of life.
Types and Causes
Pituitary-dependent HAC (PDH, 80-85%): Benign pituitary adenoma secretes excess ACTH, driving bilateral adrenal cortical hyperplasia and overproduction of cortisol. Generally responsive to medical treatment.
Adrenal-dependent HAC (ADH, 15-20%): Unilateral adrenocortical tumour (adenoma or carcinoma) produces cortisol autonomously. Surgical adrenalectomy is curative for benign tumours; carcinomas have guarded prognosis.
Iatrogenic HAC: Caused by chronic exogenous corticosteroid administration. Treatment is gradual steroid withdrawal.
Clinical Signs and Welfare Impacts
Chronic cortisol excess causes the classic 'pot-bellied' Cushingoid appearance alongside significant welfare compromise:
- Polyuria and polydipsia (PU/PD) — often the first sign owners notice; frequent urination disrupts sleep and causes house-soiling distress
- Polyphagia (ravenous appetite) with weight gain despite muscle wasting — causes constant hunger discomfort
- Pendulous abdomen from muscle weakness and fat redistribution
- Bilateral symmetrical alopecia and thin, fragile skin ('paper skin')
- Calcinosis cutis — calcium deposits causing itchy, painful skin lesions
- Exercise intolerance and muscle weakness
- Hypertension with associated retinal changes and cardiac effects
- Increased infection susceptibility (UTI, skin infections)
Diagnosis
ACTH stimulation test and low-dose dexamethasone suppression test confirm diagnosis. High-dose dexamethasone suppression test and abdominal ultrasound differentiate PDH from ADH.
Medical Treatment
Trilostane (Vetoryl): Licensed, first-choice treatment for PDH. Inhibits adrenal steroidogenesis. Requires regular monitoring (ACTH stimulation tests at 10 days, 4 weeks, 3 months, then 3-6 monthly). Dose adjustment ensures adequate control without hypoadrenocorticism (over-treatment). Improves quality of life dramatically in well-controlled patients.
Mitotane (Lysodren): Alternative for PDH and ADH; destroys adrenocortical cells. Requires careful monitoring; risk of hypoadrenocorticism. Effective but less commonly used since trilostane availability.
Prognosis and Quality of Life
Well-managed Cushing's disease allows dogs to achieve excellent quality of life. Median survival with treatment is 2-3 years (with concurrent diseases accounting for most deaths). Owners consistently report dramatic quality of life improvements following successful treatment — reduced PU/PD, improved activity, better coat, and restored appetite regulation.
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