PHOTOS 1-8: Cushing’s disease (hyperadrenocorticism) is classified as pituitary dependent, adrenocorticol dependent or iatrogenic. Pituitary dependent hyperadrenocorticism is usually caused by a functional adrenocorticotropic hormone (ACTH) secreting pituitary tumour. Excessive secretion of ACTH leads to bilateral adrenocorticol hyperplasia as well as excess cortisol secretion from the adrenal cortex. The normal feedback inhibition of ACTH by cortisol is absent, exacerbating the condition. Cushing’s disease typically develops in dogs over six years of age. Female dogs are more commonly diagnosed with adrenocorticol tumours that can also cause spontaneous hyperadrenocorticism. Adrenocorticol tumours causing hyperadrenocorticism secrete excessive amounts of cortisol irrespective of pituitary control. Iatrogenic hyperadrenocorticism is usually due to excessive administration of glucocorticoids. Glucocorticoids suppress circulating plasma ACTH concentrations leading to bilateral adrenocortical atrophy. PHOTOS 1-3, 6-7: Clinical signs of Cushing’s disease include ascites (pot belly), polyuria, polydipsia, polyphagia, panting, muscle weakness and lethargy. Hyperadrenocorticism causes insulin resistance which can lead to the development of diabetes mellitus. Furthermore, dogs with Cushing's disease often develop skin conditions such as comedomes, hyperpigmentation and seborrhea. PHOTOS 4-7: Endocrine alopecia causes the hair follicles to become atrophic, hyperpigmentation of skin, thinning of skin and hair loss. PHOTO 8: Mitotane is the medication of choice in dogs suffering from Cushing’s disease. Moderate doses selectively destroy glucocorticoid secreting cells of the adrenal cortex. It has several side effects however, most of which are associated with mineralcorticoids and glucocorticoid deficiencies. l-Deprenyl increases dopaminergic tone to the hypothalamic-pituitary axis thus decreasing pituitary ACTH secretion. Another medication, ketoconazole, inhibits the enzymes that are responsible for cortisol synthesis and can be used for dogs that are unable to tolerate mitotane. Trilostane has also been shown to be very effective in treating hyperadrenocorticism in dogs and may have fewer adverse effects that mitotane. Adrenal gland tumours can be treated by unilateral or bilateral adrenalectomy or radiation therapy.
REFERENCES: PHOTOS 1-7: Nelson, RW & Couto, CG (eds) 2009, ‘Small animal internal medicine’, 3rd ed, Mosby Elsevier, St. Louis, pp.810-812. PHOTO 8: 1. Tilley, LP & Smith, FWK 2004, ‘The 5-minute veterinary consult: canine and feline’, 3rd ed, Lippincott Williams & Wilkins, Philadelphia, pp. 602-604. 2. Neiger, R, Ramsey, I, O’Connor, J, Hurley, KJ & Moony, CT 2002, ‘Trilostane treatment of 78 dogs with pituitary-dependent hyperadrenocorticism’, The Veterinary Record, vol.150, no. 26, pp. 799-804. 3. Morgan, RV 2008 ‘Handbook of small animal practice’, 5th ed, Saunders Elsevier, Philadelphia, pp. 481-484.
Metadata assigned by Dr. M. van Schoor, Senior Lecturer, Dept. of Companion Animal Clinical Studies