Introduction:Addison’s disease is seen most commonly in young adult animals and results in low levels of aldosterone and cortisol. Aldosterone, a steroid hormone produced by the adrenal gland, is a member of a family of steroids known as mineralocorticoids. Aldosterone is necessary for proper water balance in the body, as well as for the balance of electrolytes (dissolved salt ions) such as potassium and sodium. Decreased aldosterone results in many different problems throughout the body. Also produced by the adrenal gland, cortisol is a member of a family of steroids known as glucocorticoids. Glucocorticoids are important in many functions of the body. Addison’s disease may be primary or secondary. In primary Addison’s disease, the patient lacks both mineralocorticoids and glucocorticoids. In secondary Addison’s disease, the patient lacks only glucocorticoids.
Causes: This disease is most commonly caused by a situation that results in the shrinkage of the adrenal gland. When the adrenal gland shrinks, the production of aldosterone and cortisol decrease and problems occur. Immune problems, decreased blood flow to the adrenal gland, and compression by nearby tumors are some of the many reasons the adrenal gland may decrease in size.
Clinical Signs: Typically, a dog with Addison’s disease may experience weight loss, weakness, loss of appetite, vomiting, diarrhea, increased thirst, and an increased need to urinate. Sometimes the symptoms follow a "waxing-waning course" (they tend to come and go). In severe or advanced cases, an Addisonian crisis may develop in which the animal may suddenly go into shock and possibly collapse. This should be considered a medical emergency! An animal can die during an Addisonian crisis!
Diagnosis: Diagnosis of Addison’s disease may be very difficult. This disease, which appears to mimic other diseases, tends to remain undiagnosed for some time in some patients. Some have nicknamed Addison’s disease "The Great Pretender."
A CBC and blood (serum) chemistry profile may be a very useful first step in the diagnosis. See pages D120 and D80 for additional information on CBC and chemistry profile. While these blood tests cannot diagnose Addison’s disease, they often are suggestive enough that a veterinarian will suspect the disease and conduct additional tests to confirm the diagnosis. The changes on a chemistry profile that are suggestive of Addison’s disease include increased calcium and potassium, and decreased glucose, sodium, and chloride levels.
Radiographs may also be taken as part of a diagnostic testing procedure. While radiographs cannot precisely diagnose the disease, they may provide hints which can lead a veterinarian to suspect the disease.
The current test of choice to specifically diagnose Addison’s disease is the ACTH stimulation test. This test measures cortisol levels before and after administration of ACTH. ACTH is a hormone which stimulates the adrenal gland to produce cortisol. The dog with Addison’s disease has very low levels of cortisol at first, and then shows little to no response to the ACTH administration.
Treatment: An acute crisis, especially if the animal has collapsed, should be considered a medical emergency which may require intensive treatment. Crisis treatment includes IV fluids, rapid-acting steroids, and other emergency management drugs.
Management of the disease includes supplementation with an oral glucocorticoid and possibly an oral mineralocorticoid, depending on the type of Addison’s disease.
Life-long monitoring is important in order to properly manage a patient with Addison’s disease. It is extremely critical to follow a veterinarian’s recommendations when managing a pet with this disease.
Prognosis: Unless the Addison’s disease is a complication of cancer, properly managed and carefully monitored pets with Addison’s disease have a good to excellent prognosis.