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Hyperadrenocorticism arises from overproduction of glucocorticoid hormones by one or both of the adrenal glands (Cushing’s disease) or from chronic or excessive administration of steroid medications (Cushing’s syndrome)
Pituitary-dependant hyperadrenocorticism (PDH) develops when a tumour of the pituitary gland produces high levels of adrenocorticotropic hormone (ACTH), overstimulating the adrenal glands. PDH is the most common cause (85%) of Cushing’s disease in the dog and whilst most pituitary tumours are small, about 30% can be large enough to cause neurological signs as they enlarge.
Adrenal gland tumours occur in 15% of affected dogs, and half of these are malignant. Usually only one adrenal is affected and enlarged.
Iatrogenic hyperadrenocorticism arises from prolonged or excessive administration of steroids such as prednisone and dexamethasone. Since the pituitary gland constantly detects high levels of steroids in the blood, it decreases the production of ACTH, causing both adrenal glands to shrink. This may cause problems if the dog comes off steroid medications too quickly with a deficiency of naturally produced steroids within the body (Addisonian crisis)
Most affected dogs are middle-aged or older and miniature poodles, boxer and dachshund are especially predisposed.
Female large-breed dogs are more at risk from adrenal tumours.
Common signs include
- Increased thirst, urination and appetite
- Obesity often with a classic pot-belly appearance
- Thinning or darkening of the skin
- Urinary tract and skin infections
Less frequently seen are
- High blood pressure
- Congestive heart failure
- Acute breathing problems from blood clots within the lungs
Cushing’s syndrome is usually suspected based on a history of prolonged exposure to steroid medications.
Cushing’s disease requires laboratory tests as no clinical sign is specific for the disease. Routine bloods may show raised liver enzymes, cholesterol, blood sugar and white blood cells.
Several screening tests are used that involve measuring steroid levels in the blood after transient chemical stimulation or suppression of the adrenal glands. These include the ACTH stimulation test and low-dose dexamethasone suppression test. Both require day admission for obtaining blood samples at timed intervals.
Once Cushing’s has been diagnosed it is usually necessary to test to differentiate between PDH and adrenal tumours due to difference in treatment and prognosis. Such tests include the high-dose dexamethasone suppression test, abdominal X-rays and ultrasound, and CT or MRI imaging of the brain.
Unfortunately Cushing’s can often be difficult to diagnose as test results may not be clear-cut. The presence or absence of obvious clinical signs characteristic of Cushing’s are often used to further support or rule out the disease.
Cushing’s syndrome is treated by slow, tapered withdrawal of steroid medications. Too rapid a withdrawal can lead to Addisonian crisis.
PDH is usually treated with medications- mitotane or trilostane. Unfortunately radiation therapy is not available in Hong Kong.
Adrenal tumours may be surgically removable but are often so large or enmeshed with vital surrounding structures that medications are again used.
Treatment is complicated and usually involves frequent adjustments of drug doses and repeated lab tests. Also the drugs used are potentially toxic and require careful use and monitoring.
Most dogs with PDH improve with treatment but sadly the disease may still shorten the dog’s overall lifespan.