Canine hyperadrenocorticism (also called Cushing’s disease) is one of the most common endocrine disorders in dogs. The disease is associated with increased blood concentration of glucocorticoids, caused by excessive cortisol (the main glucocorticoid hormone in the dog) production or glucocorticoid administration (Herrtage 2004). In most cases (about 80 % of dogs with hyperadrenocorticism) the disease is caused by pituitary adenoma (secretory active benign tumor of the pituitary gland) that produces adrenocorticotropic hormone (ACTH). In these cases, ACTH overproduction persistently stimulates the adrenal glands to excessive production of cortisol (Behrend and Melian 2013; Galac et al. 2010). This form of the disease is called pituitary-dependent hyperadrenocorticism (Herrtage 2004). In most of remaining cases (15 – 20% of dogs with hyperadrenocorticism), the disease is caused by secretory active tumor (benign or malignant) of the adrenal gland that produces excessive amounts of cortisol (Behrend and Melian 2013; Galac et al. 2010). This form of the disease is called adrenal-dependent hyperadrenocorticism (Herrtage 2004). Other forms of hyperadrenocorticism include iatrogenic hyperadrenocorticism, and very rare cases of hyperadrenocorticism associated with sex steroid excess, ectopic ACTH syndrome (secretory active tumors in other organs producing excessive amounts of ACTH) and food-dependent hypercortisolemia (Galac et al. 2008; Galac et al. 2010; Greco 2007; Herrtage 2004; Syme et al. 2001). Hyperadrenocorticism occurs mainly in middle-aged and older dogs. There is a higher risk for the development of this disease in breeds such as Poodles, dachshunds, various small terrier breeds (such as Yorkshire Terriers, Jack Russell Terriers or Staffordshire Bull Terriers), beagles, boxers and German shepherds (Behrend and Melian 2013; Galac et al. 2010; Herrtage 2004).

Polyuria (excessive urine production) and polydipsia (increased thirst), polyphagia (increased appetite), weight gain, alopecia (hair loss; usually symmetrical), distended abdomen (caused by accumulation of abdominal fat and enlargement of the liver) with visible prominent abdomen blood vessels, muscle weakness (causing decreased physical activity, exercise intolerance, inability to climb stairs or jump into a car) and thin skin (caused by muscle and skin atrophy), hyperpigmentation (darkening of the skin), testicular atrophy or extension of anoestrus phase in intact female dogs are common clinical signs of canine hyperadrenocorticism (Behrend and Melian 2013; Galac et al. 2010; Herrtage 2004). Diabetes mellitus (insulin resistant), urinary tract infection, hypertension (persistent increased arterial blood pressure), and pulmonary thromboembolism (obstruction of pulmonary blood vessels by blood clots) are complications of Cushing’s disease in dogs (Behrend and Melian 2013; Galac et al. 2010; Johnson 2009).

Besides a clinical history and physical examination, diagnosis of canine hyperadrenocorticism requires demonstration of increased cortisol synthesis and disturbed functioning of the hypothalamic-pituitary-adrenal axis (Galac et al. 2010). There are several laboratory tests that are useful in the diagnosis of hyperadrenocorticism (including adrenal function tests) such as: determination of urinary cortisol concentration to urinary creatinine concentration ratio, ACTH stimulation test, dexamethasone suppression tests, and determination of plasma ACTH concentration. These tests are also useful in the differentiation between various forms of canine hyperadrenocorticism and monitoring of the therapy (Galac et al. 2010; Rijnberk and Kooistra 2010). It should be emphasized however, that other concurrent diseases, stress and drugs (e.g. glucocorticoids) affect the cortisol concentration, and that’s why each of these tests may give both false-positive and false-negative results (Herrtage 2004; Rijnberk and Kooistra 2010). Additionally, diagnostic imaging of the adrenal glands and the pituitary gland using ultrasonography, computed tomography, and magnetic resonance imaging, are useful in the diagnosis, form differentiation, and choice the way of treatment of hyperadrenocorticism in dogs (Behrend and Melian 2013; Galac et al. 2010).

Pharmacological or surgical (adrenalectomy – removal of the adrenal tumor; hypophysectomy – removal of the pituitary gland) treatment, depending on the form of the disease and its characteristics and severity (i.e. pituitary-dependent or adrenal-dependent Cushing’s disease; unilateral or bilateral adrenal tumor with or without pulmonary metastases), are used in the therapy of canine hyperadrenocorticism (Herrtage 2004; Behrend and Melian 2013; Galac et al. 2010). Treatment of iatrogenic hyperadrenocorticism caused by treatment with glucocorticoids requires glucocorticoid dose reduction in a stepwise manner. A too rapid dose reduction or sudden complete cessation of administration of these drugs leads to iatrogenic hypoadrenocorticism caused by glucocorticoid induced suppression of the hypothalamic-pituitary-adrenal axis. This suppression leads to atrophy of the adrenal zona fasciculata and zona reticularis, and after long-term glucocorticoid therapy several months may be required for recovery (Behrend and Melian 2013; Galac et al. 2010). It should also be emphasized that both pharmacological and surgical treatment of hyperadrenocorticism may lead to development of iatrogenic hypoadrenocorticism (Behrend and Melian 2013; Galac et al. 2010; Gójska-Zygner et al. 2011).


Behrend E.N., Melian C. Hyperadrenocorticism in Dogs. In: Rand J., Behrend E.N., Gunn-Moore D. and Campbell-Ward M.L. (eds.) Clinical Endocrinology of Companion Animals. Wiley-Blackwell, Ames, 2013, pp. 43-64.

Galac S., Kars V.J., Voorhout G., Mol J.A., Kooistra H.S. ACTH-independent hyperadrenocorticism due to food-dependent hypercortisolemia in a dog: A case report. Veterinary Journal, 2008, 177, 141-143.

Galac S., Reusch C.E., Kooistra H.S., Rijnberk A. Adrenals. In: Rijnberk A. and Kooistra H.S. (eds.) Clinical Endocrinology of Dogs and Cats. An Illustrated Text. 2 nd ed. Schlütersche Verlagsgesellschaft, Hannover, 2010, pp. 93-154.

Gójska-Zygner O., Lechowski R., Zygner W. Canine iatrogenic persistent hypoadrenocorticism after short-term treatment of hyperadrenocorticism with trilostane – a case report. Veterinarski Arhiv, 2011, 81, 699-705.

Greco D.S. Hyperadrenocorticism Associated with Sex Steroid Excess. Clinical Techniques in Small Animal Practice, 2007, 22, 12-17.

Herrtage M.E. Canine hyperadrenocorticism. In: Mooney C.T. and Peterson M.E. (eds.) BSAVA Manual of Canine and Feline Endocrinology. 3 rd ed. British Small Animal Veterinary Association, Gloucester, 2004, pp. 150-171.

Johnson L.R. Pulmonary Thromboembolism. In: Silverstein D.C. and Hopper K. (eds.) Small Animal Critical Care Medicine. 1 st ed. Saunders Elsevier, St. Louis, 2009, pp. 114-117.

Rijnberk A., Kooistra H.S. Protocols for Function Tests. In: Rijnberk A. and Kooistra H.S. (eds.) Clinical Endocrinology of Dogs and Cats. An Illustrated Text. 2 nd ed. Schlütersche Verlagsgesellschaft, Hannover, 2010, pp. 305-314.

Syme H.M., Scott-Moncrieff J.C., Treadwell N.G., Thompson M.F., Snyder P.W., White M.R., Oliver J.W. Hyperadrenocorticism associated with excessive sex hormone production by an adrenocortical tumor in two dogs. Journal of the American Veterinary Medical Association, 2001, 219, 1725-1728.

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