CONDITION

Cushings Disease in Dogs

A hormonal condition where the body produces excess cortisol, affecting skin, appetite, thirst, body shape, and energy regulation.

Why this matters now

Cushing's disease — more precisely termed hyperadrenocorticism — occurs most commonly in middle-aged to older dogs, with the majority of cases diagnosed after the age of six. Certain breeds appear to be disproportionately represented, including Miniature Poodles, Dachshunds, Boxers, Boston Terriers, and various terrier breeds, though the condition can affect any breed. Approximately 80-85% of naturally occurring cases are pituitary-dependent, arising from a small tumour in the pituitary gland that overproduces adrenocorticotrophic hormone (ACTH), while the remaining 15-20% result from a functional adrenal tumour that produces cortisol independently. Iatrogenic Cushing's disease — caused by prolonged administration of corticosteroid medications — represents an additional category that may be encountered in dogs receiving long-term steroid therapy for other conditions. The insidious onset and gradual progression of clinical signs mean that the condition may develop over many months before being recognised, as individual changes are often attributed to normal ageing.

The clinical course of Cushing's disease tends to be slowly progressive, with signs developing incrementally over weeks to months. Early in the disease process, changes such as slightly increased water intake, mildly increased appetite, or occasional urinary accidents may be subtle enough to be dismissed as normal variation or age-related changes. As cortisol excess continues, the constellation of signs typically becomes more pronounced and recognisable — the characteristic body shape changes, skin alterations, and behavioural shifts gradually emerging over time. The rate of progression varies between individuals and may be influenced by the size and growth rate of the underlying tumour (in pituitary-dependent cases) or the hormone output of the adrenal mass. Without management, the chronic cortisol excess can contribute to secondary complications including diabetes mellitus, urinary tract infections, hypertension, and thromboembolic disease, each of which adds complexity to the overall clinical picture.

Signals & patterns

Early signals

Increased water intake and urination

Polydipsia (excessive drinking) and polyuria (excessive urination) are among the most frequently reported early signs, often noticed as the water bowl needing refilling more frequently, the dog seeking alternative water sources, or urinary accidents occurring in previously housetrained dogs. The increased urine production results from cortisol's interference with antidiuretic hormone action at the renal collecting ducts, producing a dilute urine that fails to concentrate normally. This may initially be subtle — perhaps an extra trip outside or slightly larger puddles — before becoming more obviously excessive over weeks to months.

Increased appetite

Polyphagia — a noticeably increased drive to eat — is a common early change that owners may initially view positively or attribute to a healthy appetite. Dogs may begin begging for food more persistently, attempting to eat items they previously ignored, scavenging, or becoming protective over food resources. This heightened appetite is driven by cortisol's stimulatory effects on appetite centres in the brain and its metabolic actions promoting gluconeogenesis and altering energy balance. Some owners report that their dog seems perpetually hungry despite consuming more food than usual.

Gradual abdominal enlargement

A progressively distended abdomen — sometimes described as a pot-bellied appearance — develops due to a combination of factors including hepatomegaly (liver enlargement from cortisol-induced glycogen accumulation), redistribution of body fat to the abdominal region, and weakening of the abdominal musculature from protein catabolism. This change tends to develop gradually over months, making it easy to attribute to weight gain or normal ageing. The abdominal distension may become apparent when viewing the dog from above or from the side, particularly when compared to photographs from earlier months.

Reduced activity and exercise tolerance

Dogs may show a gradual decline in energy levels, becoming less enthusiastic about walks, tiring more quickly during exercise, or spending more time sleeping. This lethargy reflects the systemic effects of cortisol excess on muscle metabolism and may also relate to the overall metabolic burden of the disease. Because the change typically develops slowly, it can be easily attributed to advancing age rather than recognised as a manifestation of an underlying endocrine disorder.

Panting

Increased or inappropriate panting — occurring at rest, in cool environments, or at times when the dog would not normally pant — is a frequently observed early sign that may precede more obvious changes. The mechanism is thought to involve cortisol's effects on the respiratory centre, redistribution of body fat including within the thorax and abdomen compressing the diaphragm, and hepatomegaly reducing thoracic space. Owners often describe their dog as seeming to pant 'for no reason,' particularly noticeable during the night or in air-conditioned environments.

Later signals

Skin and coat changes

Progressive skin changes represent some of the most visible later signs of Cushing's disease, including bilateral symmetrical hair loss (alopecia), thin and fragile skin that tears easily or bruises with minimal trauma, poor wound healing, and recurrent skin infections. The hair loss typically affects the trunk and flanks while sparing the head and extremities, and the remaining coat may become dull, dry, and slow to regrow after clipping. In some dogs, comedones (blackheads) develop, and calcinosis cutis — hard, mineralised plaques within the skin — may appear, particularly along the dorsal midline, axillae, or inguinal regions. These skin changes result from cortisol's catabolic effects on collagen, elastin, and hair follicle cycling.

Recurrent infections

The immunosuppressive effects of chronic cortisol excess can manifest as repeated urinary tract infections, skin infections (pyoderma), ear infections, or respiratory infections that may respond to treatment but recur frequently. Urinary tract infections are particularly common due to the combination of immunosuppression, dilute urine (which provides a less hostile environment for bacterial growth), and sometimes incomplete bladder emptying from abdominal muscle weakness. These infections may be relatively asymptomatic due to cortisol's anti-inflammatory properties masking the usual signs of infection.

Muscle wasting and weakness

Progressive loss of muscle mass, particularly noticeable over the temporal muscles of the head and the muscles of the limbs, reflects the protein catabolic effects of sustained cortisol excess. Dogs may develop difficulty climbing stairs, jumping, or rising from rest, and the combination of muscle weakness with abdominal distension creates a characteristic body shape. Ligament laxity may also develop, and in severe cases dogs may exhibit a plantigrade stance (walking on their hocks) in the hind limbs due to weakening of the ligamentous support structures.

Neurological signs (pituitary macroadenoma)

In a subset of dogs with pituitary-dependent Cushing's disease, the pituitary tumour may grow large enough to extend beyond the sella turcica and compress surrounding brain structures. This can produce neurological signs including altered mentation, circling, head pressing, vision changes, seizures, and behavioural changes. The onset of these signs may be gradual or relatively acute and may occur at any point during the disease course, including after medical management has been initiated. The proportion of pituitary tumours that become clinically significant macroadenomas varies across studies but represents an important consideration in long-term management.

Click to read about the biological mechanisms

How this is usually investigated

Investigating suspected Cushing's disease involves a staged approach combining clinical assessment, routine blood and urine testing, specific endocrine function tests, and diagnostic imaging. The diagnostic process can be complex because no single test provides a definitive diagnosis in all cases, and each test has characteristic strengths and limitations that influence its interpretation.

Routine haematology and biochemistry

Purpose: Baseline blood work often provides the first clues suggestive of Cushing's disease. A characteristic pattern may include a stress leucogram (mature neutrophilia, lymphopaenia, eosinopaenia, monocytosis), markedly elevated alkaline phosphatase (ALP) — often due to the steroid-induced isoenzyme — elevated alanine aminotransferase (ALT), elevated cholesterol and triglycerides, and mildly elevated blood glucose. While none of these findings are specific to Cushing's disease individually, the constellation of changes can raise clinical suspicion.
Considerations: Many of these biochemical changes can occur with other conditions or as effects of certain medications, so they are supportive rather than diagnostic. Dogs receiving exogenous corticosteroids may show identical blood work patterns. The degree of elevation does not necessarily correlate with disease severity, and some dogs with confirmed Cushing's disease may have relatively modest biochemical changes, particularly early in the disease course.

Urinalysis and urine cortisol:creatinine ratio

Purpose: Urinalysis in dogs with Cushing's disease typically reveals a dilute urine (low specific gravity) reflecting the cortisol-mediated interference with urine concentrating ability. The urine cortisol:creatinine ratio (UCCR), measured on a morning urine sample collected at home, can serve as a sensitive screening test — a normal UCCR makes Cushing's disease unlikely, while an elevated ratio warrants further endocrine testing. Urine culture may also reveal subclinical urinary tract infections that are common in affected dogs.
Considerations: The UCCR has high sensitivity but low specificity, meaning many conditions causing physiological stress can produce elevated ratios. It is most valuable as a screening tool to exclude Cushing's disease rather than confirm it. The home-collected sample is important because veterinary visits can cause stress-related cortisol elevation that confounds the result. Proteinuria may also be detected and can be a consequence of cortisol-mediated glomerular changes.

Low-dose dexamethasone suppression test (LDDST)

Purpose: The LDDST is often considered the initial test of choice for diagnosing Cushing's disease. A low dose of synthetic glucocorticoid (dexamethasone) is administered and cortisol levels are measured at baseline and at four and eight hours afterward. In healthy dogs, the exogenous dexamethasone suppresses ACTH release, causing cortisol levels to fall, while dogs with Cushing's disease show failure of adequate suppression due to the autonomous nature of their cortisol overproduction. The four-hour sample may sometimes show a pattern of partial suppression followed by escape, which can provide additional information about whether the disease is pituitary-dependent.
Considerations: The LDDST requires an eight-hour in-hospital stay, which may cause some dogs stress that can influence results. False positive results can occur in dogs with significant non-adrenal illness (chronic illness effect), and results may be equivocal in dogs with mild or early disease. The test is generally more useful for confirming the presence of Cushing's disease than for definitively distinguishing between pituitary and adrenal forms, though certain suppression patterns can be suggestive.

ACTH stimulation test

Purpose: The ACTH stimulation test measures the adrenal glands' cortisol production capacity by administering synthetic ACTH and comparing baseline and post-stimulation cortisol levels one to two hours later. An exaggerated cortisol response suggests adrenal hyperfunction consistent with Cushing's disease. This test is also the primary method for monitoring dogs receiving trilostane therapy, as it assesses the degree of adrenal suppression achieved by treatment. It is additionally the only reliable test for diagnosing iatrogenic Cushing's disease, where the adrenal response is blunted rather than exaggerated.
Considerations: The ACTH stimulation test has somewhat lower sensitivity than the LDDST for diagnosing naturally occurring Cushing's disease, meaning a proportion of affected dogs may produce a normal result. It does not differentiate between pituitary-dependent and adrenal-dependent forms. The synthetic ACTH used (cosyntropin/tetracosactide) can be costly and may have limited availability in some regions. However, the shorter test duration (one to two hours versus eight hours) and its essential role in treatment monitoring make it a frequently used tool.

Abdominal ultrasonography

Purpose: Ultrasound examination of the abdomen allows direct visualisation of the adrenal glands, which is valuable for differentiating between pituitary-dependent and adrenal-dependent disease. In pituitary-dependent cases, both adrenal glands are typically symmetrically enlarged (bilateral adrenomegaly), while adrenal-dependent cases typically show one enlarged, often irregularly shaped adrenal gland with atrophy of the contralateral gland. Ultrasonography also allows assessment of other abdominal organs that may be affected, including liver size, bladder wall thickness, and any concurrent findings.
Considerations: Accurate adrenal gland assessment requires experience, as the glands can be challenging to visualise depending on the dog's body condition and temperament. Adrenal gland size alone does not confirm the diagnosis of Cushing's disease, as some normal dogs have adrenal glands above typical reference ranges. Incidental adrenal masses (incidentalomas) may be detected in dogs being investigated for other reasons, requiring careful interpretation in context. Ultrasonographic assessment of the adrenal glands does not replace endocrine function testing but complements it in establishing the form of the disease.

Options & trade-offs

Management of Cushing's disease varies depending on the underlying cause (pituitary-dependent versus adrenal-dependent), the severity of clinical signs, the dog's overall health status, and individual circumstances. The approaches involve different mechanisms, monitoring requirements, and consideration profiles, and the choice between them involves weighing multiple factors specific to each patient.

Trilostane (medical management)

Trilostane is a competitive inhibitor of 3-beta-hydroxysteroid dehydrogenase, an enzyme essential for cortisol synthesis in the adrenal cortex. By blocking this enzyme, trilostane reduces cortisol production without destroying adrenal tissue. It is administered orally, typically once or twice daily, and the dose is individually titrated based on clinical response and ACTH stimulation test results. Trilostane is currently the most widely used medical management for both pituitary-dependent and adrenal-dependent Cushing's disease in dogs, with most dogs showing clinical improvement in water intake, appetite, and activity levels within the first few weeks of treatment.

Trade-offs: Trilostane requires regular monitoring through ACTH stimulation tests and clinical assessments, particularly during the initial dose-finding period, which involves ongoing veterinary visits and associated costs. Over-suppression of cortisol production (iatrogenic hypoadrenocorticism) is a recognised risk that can range from mild and transient to life-threatening adrenal crisis, requiring owner awareness of signs warranting prompt attention. The medication is typically lifelong, as it manages rather than cures the condition, and dose adjustments may be needed over time as the disease evolves. Individual variability in drug metabolism means that some dogs require considerably higher or lower doses than standard starting recommendations.

Mitotane (medical management)

Mitotane (o,p'-DDD) is an adrenolytic drug that selectively destroys the cortisol-producing zones of the adrenal cortex. Treatment involves an initial induction phase with daily dosing until cortisol production is sufficiently reduced, followed by a lower maintenance dose administered once or twice weekly. Mitotane was historically the primary medical treatment for Cushing's disease before trilostane became widely available, and it remains an option in certain clinical scenarios, including cases where trilostane proves insufficient or where complete adrenalectomy of the cortisol-producing zones is desired.

Trade-offs: Mitotane carries a risk of permanent adrenal destruction if dosing is excessive or monitoring inadequate, which can result in permanent hypoadrenocorticism (Addison's disease) requiring lifelong mineralocorticoid and glucocorticoid supplementation. The induction phase requires careful monitoring for signs of cortisol depletion, and the drug's narrow therapeutic margin demands close veterinary oversight. Gastrointestinal side effects (anorexia, vomiting, diarrhoea) are relatively common during the induction phase. Mitotane is a cytotoxic agent requiring careful handling, and its availability varies by region.

Adrenalectomy (surgical)

Surgical removal of the affected adrenal gland is the primary treatment consideration for adrenal-dependent Cushing's disease caused by an adrenal tumour. If the tumour is unilateral and has not invaded surrounding structures, adrenalectomy can potentially provide a definitive resolution of the cortisol excess. The surgery is technically demanding due to the deep retroperitoneal location of the adrenal glands and their close association with major blood vessels, particularly the vena cava. Pre-operative medical management to reduce cortisol levels and address associated complications (such as hypertension and hypercoagulability) may improve surgical outcomes.

Trade-offs: Adrenalectomy is a major surgical procedure with significant perioperative risks, including haemorrhage (particularly with right-sided tumours due to vena cava proximity), thromboembolism, and post-operative hypoadrenocorticism as the atrophied contralateral adrenal gland recovers function. The procedure requires specialist surgical expertise and advanced perioperative monitoring capabilities, typically available only at referral centres. Not all adrenal tumours are amenable to surgical removal — those with vascular invasion, local infiltration, or evidence of metastasis may be considered non-resectable. Post-operative recovery requires intensive monitoring and temporary supplementation with glucocorticoids until the remaining adrenal gland resumes adequate function.

Radiation therapy (pituitary tumour)

Radiation therapy directed at the pituitary gland may be considered for dogs with pituitary-dependent Cushing's disease, particularly those with macroadenomas causing neurological signs or those not responding adequately to medical management. Both conventional fractionated radiation therapy and stereotactic radiosurgery approaches have been described. The goal is to reduce the size and functional capacity of the pituitary tumour, thereby reducing ACTH secretion and subsequent cortisol production. The hormonal effects of radiation may take weeks to months to become apparent, and concurrent medical management is typically continued during this period.

Trade-offs: Radiation therapy for pituitary tumours requires specialised equipment and expertise available only at select veterinary referral centres, and the financial investment is substantial. Multiple anaesthetic episodes may be required for fractionated protocols, and potential side effects include transient worsening of neurological signs during treatment, late radiation effects on surrounding brain tissue, and temporary or permanent damage to remaining normal pituitary function. The response to radiation therapy is variable, with some dogs showing excellent tumour control and clinical improvement while others respond incompletely. Long-term follow-up with repeated imaging may be necessary to monitor tumour response.

Monitoring without active treatment

In some circumstances, the decision may be made to monitor the dog's clinical signs without initiating specific treatment for the Cushing's disease. This approach may be considered when clinical signs are mild and progressing slowly, when the dog has concurrent conditions that complicate treatment, when the risks of treatment are judged to outweigh the potential benefits for that individual, or when owner circumstances preclude the monitoring requirements of active treatment. Monitoring typically involves regular clinical assessments and management of secondary complications (such as urinary tract infections) as they arise.

Trade-offs: Without treatment to reduce cortisol levels, the clinical signs of Cushing's disease typically continue to progress over time, and the risk of secondary complications (diabetes mellitus, thromboembolic events, infections, hypertension) remains present. The quality of life implications of ongoing cortisol excess vary between individuals, with some dogs maintaining reasonable comfort for extended periods while others deteriorate more rapidly. This approach requires ongoing reassessment to determine whether the balance of considerations has shifted in favour of initiating treatment.

Common misconceptions

Misconception:

"Cushing's disease is just a cosmetic issue that only affects how the dog looks."

Reality:

While the visible changes of Cushing's disease — hair loss, potbellied appearance, thin skin — are often the most immediately apparent, the condition involves systemic effects on virtually every organ system. Chronic cortisol excess affects the immune system (increasing infection susceptibility), the musculoskeletal system (causing muscle wasting and ligament laxity), the cardiovascular system (promoting hypertension and hypercoagulability), and metabolic regulation (predisposing to diabetes mellitus). The internal consequences of unmanaged cortisol excess can significantly affect a dog's overall health and comfort, extending well beyond the cosmetic changes that first draw attention.

Misconception:

"If the dog is eating well and seems happy, Cushing's disease doesn't need to be managed."

Reality:

The increased appetite associated with Cushing's disease can create a misleading impression of wellbeing, as dogs may appear enthusiastic about food and daily routines despite significant internal metabolic disruption. Cortisol's anti-inflammatory properties can also mask discomfort that might otherwise be apparent, and dogs are generally adept at maintaining normal behaviour patterns despite underlying physiological compromise. The progressive nature of the condition means that complications may develop gradually and insidiously, potentially reaching a point where they become clinically significant before the external appearance changes dramatically enough to prompt concern.

Misconception:

"A single blood test can definitively diagnose or rule out Cushing's disease."

Reality:

The diagnosis of Cushing's disease is often described as one of the more challenging endocrine diagnoses in veterinary medicine, and no single test provides definitive confirmation or exclusion in all cases. Each diagnostic test has specific sensitivity and specificity profiles, and results can be influenced by concurrent illness, stress, medications, and the stage of disease. The diagnostic process typically involves integrating findings from clinical examination, routine blood work, urinalysis, specific endocrine function tests, and imaging to build a composite picture. False positive and false negative results occur with all available tests, and in some cases the diagnosis is reached through a combination of supportive evidence rather than a single definitive result.

Living with Cushing's disease involves an ongoing relationship between observation, monitoring, and adjustment that evolves over time as the dog responds to management and as the disease itself may change. Understanding the patterns of cortisol excess — how they manifest in appetite, thirst, energy levels, skin condition, and body shape — can help build a more nuanced picture of each individual dog's experience. The condition often coexists with other age-related processes, and distinguishing what is attributable to cortisol excess versus other concurrent factors can be an evolving consideration throughout the management journey.

Last reviewed: 24 April 2026 · Dr Alastair Greenway MRCVS