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Canine hyperadrenocorticism
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Dogs with hyperadrenocorticism can often present with dermatological signs; this paper reviews the diagnosis and treatment of a common canine disease.
Fiona Scholz
BSc, BVMS, MANZCVS, Dip. ACVD, FANZCVS
Dr. Scholz is a founder and director of Veterinary Dermatology Specialists, a referral center based in Perth, Western Australia. After graduation from Murdoch University, she undertook an internship at Perth Veterinary Specialists and then commuted between the USA and her home in Australia whilst completing two residency programs. Dr. Scholz is the only dermatologist in Western Australia to achieve both Diplomate status with the American College of Veterinary Dermatologists and Fellowship status with the Australian and New Zealand College of Veterinary Scientists.
![Fiona Schulz](/sites/default/files/images/media/image/Schermafbeelding%202021-12-27%20om%2017.27.15.png)
Sam Crothers
BSc, BVMS, MANZCVS, Dip. ACVD, FANZCVS
Dr. Crothers graduated from Murdoch University and worked in a busy first opinion small animal practice in Perth before moving to California to complete a dermatology residency at the University of California Davis (UCD). She then worked as a clinical instructor at UCD before moving to Colorado State University as an Assistant Professor. Upon returning to Australia, she worked at the University of Melbourne Veterinary Hospital and in private practice before moving home to work at Veterinary Dermatology Specialists, where she is co-founder and director.
![Sam Crothers](/sites/default/files/images/media/image/Schermafbeelding%202021-12-27%20om%2017.27.44.png)
Key points
- Pituitary-dependent hyperadrenocorticism is the most common cause for spontaneously occurring hypercortisolism in dogs.
- The clinical signs of hyperadrenocorticism are wide and varied, but the various cutaneous changes are often obvious and dramatic.
- A variety of diagnostic procedures can be performed, but it is important to also identify the origin of the hyperadrenocorticism to appropriately guide the management and therapeutic plan.
- Treatment of hyperadrenocorticism should also encompass therapy for any intercurrent disorders in order to improve the patient’s quality of life.
Introduction
Canine hyperadrenocortisolism is a relatively common condition which may occur either spontaneously or via an iatrogenic route. The spontaneous etiologies include hypersecretion of endogenous glucocorticoids from a functional adrenal tumor or hypersecretion of corticotropin or corticotropin-like substances from an idiopathic functional pituitary tumor, whilst exogenous glucocorticoid administration can lead to iatrogenic disease. Approximately 85% of dogs with spontaneous hypercortisolism have pituitary-dependent hyperadrenocorticism (PDH), which results from excessive corticotropin secretion arising from either a microadenoma or a macroadenoma of the pituitary gland (1). Approximately 90% of all pituitary tumors are functional, with the hypersecretion of corticotropin resulting in bilateral adrenal hyperplasia.
The hypothalamic-pituitary-adrenal axis
The adrenal cortex is composed of three distinct anatomical regions, the zona glomerulosa, zona fasiculata and zona reticularis, with glucocorticoids being produced in the zona fasiculata under the control of the hypothalamic-pituitary-adrenal (HPA) axis. The hormone corticotropin (or adrenocorticotropic hormone, ACTH) is secreted by the adenohypophysis of the pituitary gland, with the primary function of stimulating the adrenal cortex. Secretion occurs in a pulsatile manner and is stimulated by stress, but is normally controlled by the negative feedback of serum glucocorticoid levels. Corticotropin in turn is controlled by release of corticotrophin releasing hormone (CRH), secreted by the hypothalamus, again in a pulsatile manner (2)(3). CRH secretion is inhibited by glucocorticoids and stimulated by serotonin and epinephrine.
Diagnosis
Since diagnosis of canine hyperadrenocorticism can be complex and none of the screening tests are 100% accurate, an integrated approach to the diagnosis is required. Signalment, history, clinical findings, screening tests and specific assays for the hypophyseal-adrenal axis should all be considered carefully in a collective manner to avoid misdiagnosis and to ensure concomitant disorders are not overlooked. [...]
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