Addison’s Disease

Addison’s disease occurs when the adrenal gland stops working and steroid hormones are not produced in adequate levels. Most commonly, Addison’s disease is manifest as a deficiency in both mineralocorticoids and glucocorticoids; occasionally however, dog’s with Addison’s disease will just be deficient in glucocorticoids. Addison’s disease usually results from the body’s immune system gradually destroying the adrenal tissue, why this occurs is not known. Occasionally Addison’s disease can also occur as a result of infection, haemorrhage or drugs which have damaged the adrenal glands. A hormone called adrenocorticotrophic hormone (ACTH) is released by the pituitary to stimulate the adrenal glands to produce cortisol; rarely therefore, dysfunction of the pituitary gland can result in Addison’s disease.

Addison’s disease is an uncommon disease in dogs and very rare in cats, with only a handful of cases reported in the veterinary literature. Addison’s is more common in females compared to males and more common in castrated males compared with intact males, this may be because of a protective effect of testosterone. Some breeds are also more commonly affected, these include the Standard Poodle, Leonberger, Great Dane and several others.

What are the signs of Addison’s disease?

The destruction of the adrenal gland is usually a gradual process so most dogs with Addison’s disease will have a waxing and waning episodes of lethargy, stomach upset and inappetence. If left untreated, these signs will worsen over time, and become more frequent and/or more severe. In it’s morst severe form, Addison’s disease can cause dogs to go into shock, with a so called ‘Addisonian crisis’. Often this is preceded by a period of non specific illness or waxing and waning disease.

An Addisonian crisis is precipitated by the combination of kidney effects as a result of mineralocorticoid deficiency (e.g. dehydration as a result of renal dysfunction and the accumulation of renal toxins such as urea and potassium) and the lack of glucocorticoids to cope with this stressful situation. Animals with Addisonian crisis usually present collapsed and can have very marked disturbances to their heart rate and rhythm as a result of high levels of potassium. A variety of other signs are also possible including abdominal pain, intestinal bleeding and occasionally seizures due to low blood sugar.

Because of the lack of mineralocorticoids blood tests usually reveal signs of renal dysfunction, such as high urea, creatinine and phosphate. Blood electrolytes may also be abnormal, often with low sodium levels and high potassium. The lack of glucocorticoids also means there may be a reduced stress response to illness, with lower numbers of white blood cells than expected.

Although the history, clinical examination and initial blood results may be very suggestive of Addison’s, they can sometimes be caused by renal disease and an ACTH stimulation test must be performed to allow a definitive diagnosis. ACTH is a hormone which stimulates the adrenal gland to produce glucocorticoids and is permissive in mineralocorticoid production, thus both normally rise dramatically after injection allowing an assessment of adrenal function. In Addison’s disease this response is usually very low and the lack of response allows us to be sure of the diagnosis.

Animals with glucocorticoid deficiency, but normal mineralocorticoids have very vague signs and as such represent a diagnostic challenge. Normally these signs have been progressing gradually over a long period and include gastrointestinal signs, such as vomiting and diarrhoea, weakness, lethargy and reduced activity. Because of the vague signs associated with ‘atypical’ hypoadrenocorticism an ACTH stimulation test may be performed as part of the investigation for a wide variety of presenting signs such as gastrointestinal disease or lethargy.