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Canine Addison’s Disease by Margaret Muns, DVM,Veterinary Issues Editor
Hypoadrenocorticism (Addison’s disease) is a condition with a relatively low rate of occur- rence in the dog. However, it is still an important disease because of its life-threatening potential. What makes things more complex is the difficulty faced when trying to diag- nose dogs with Addison’s disease. The symptoms of the disorder are often vague and identical to those seen with more common disorders. Yet with accurate diagnosis and good management, affected dogs can be expected to live normal life spans.
Normal Adrenal Physiology
The adrenal glands are a major component of the normal dog’s endocrine system, which is responsible for hormone regulation. Located at the top of each kid- ney, the adrenals are divided into two main parts—the medulla and the cortex. The adrenal medulla produces the familiar hormone adrenaline. This is the hormone responsible for regulating an animal’s “flight or fight” response. By contrast, the adrenal cortex is the sight of steroid hormone production. Two major classes of ste- roid hormones are produced in the adrenal cortex—glu- cocorticoids and mineralocorticoids. Glucocorticoids are important regulators of metabolism, affecting virtually every cell in a dog’s body. Cortisol is the most important glucocorticoid hormone in the dog. Mineralocorticoids have a major role in regulating a dog’s blood pressure and electrolyte balance. Aldosterone is the most impor- tant canine mineralocorticoid.
Regulation of the adrenal hormone levels in a dog’s body occurs via a process called a “feedback loop” (see Fig. 1). The loop begins inside the animal’s brain when a gland called the hypothalamus releases a hormone called CRH (corticotrophin releasing hormone). This chemical stimulates the release of a second hormone called ACTH (adrenocorticotrophic hormone) from the nearby pituitary gland. When ACTH reaches the adrenal gland, the cortex responds by releasing steroid hormones. Once the level of steroid hormones reaches a certain level, the pituitary gland stops secreting ACTH.
Naturally occurring Addison’s disease happens when the adrenal gland fails. Typically this happens because of immune mediate destruction of the adrenal cortex.
Basically, for unknown reasons, the dog’s own immune system attacks the adrenal cortex. The destruction means that the adrenal cortex cannot respond to stimu- lation by ACTH. This type of Addison’s disease is the most common in the dog and is typically referred to as primary hypoadrenocorticism.
Secondary hypoadrenocorticism is more rarely seen in dogs. This form of Addison’s disease happens when the pituitary gland does not produce enough ACTH. Pituitary trauma, tumors or defects can all cause sec- ondary Addison’s disease. More commonly, secondary disease happens because of long term use of steroid- containing drugs. These medications act like a form of negative feedback. The pituitary “sees” these medica- tions the same way as it does naturally occurring steroi- dal hormones. As a result, pituitary ACTH production is suppressed. If the medications are abruptly stopped, then the dog can go into an adrenal crisis, much like it could with primary Addison’s. For this reason it is important to always taper steroid medications slowly. This allows the pituitary-adrenal axis time to recover.
A third variety of Addison’s disease in the dog is atypi- cal hypoadrenocorticism. Dogs with atypical Addison’s are only glucocorticoid deficient. Later on, these dogs may develop mineralocorticoid deficiency. However, some will not. For example, some cases of primary Addison’s disease can be atypical in the early stages of the disease until enough of the adrenal cortex is destroyed to produce mineralocorticoid deficiency. By contrast, secondary Addison’s disease is always atypical because it is characterized primarily by glucocorticoid deficiency.
May/June 2005 The Australian Shepherd Journal 31