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Addison's Disease

Addison’s disease is a condition that occurs when the adrenal glands stop producing hormones.   The symptoms tend to be non-specific and may include lethargy, weakness, and gastrointestinal upset.  It is common for the signs to wax and wane over a period of time before a diagnosis is made.

Some dogs with Addison’s disease are not diagnosed until they are critically ill (an Addisonian crisis).  This life-threatening stage of the disease results in collapse and shock—it must be treated as an emergency.

There is no cure for Addison’s disease, but it can usually be treated with replacement hormones, giving the dog a normal life span and quality of life.  It is diagnosed (and monitored, once treatment has begun) with blood tests.  The drugs most commonly used to treat Addison’s disease are called prednisone, Florinef, and DOCP—a dog may require only one or a combination of these medications.

Most cases of Addison’s disease are diagnosed in middle-aged dogs (the median age of diagnosis is 4-5 years), although it has been reported in animals as young as 2 months and as old as 14 years.  Female dogs are disproportionately affected (about 70% of cases), with sexually intact females at greatest risk and intact males at the lowest risk.   About one third of cases are mixed-breed dogs, but there appears to be some breed predilection, with poodles, Portuguese water dogs, Great Danes, Leonbergers, German shepherds, and rottweilers among those thought to be predisposed.

The prognosis for dogs diagnosed with Addison’s disease is excellent as long as they are carefully managed.  They can be expected to live out a normal life span with few if any limitations, but they do require life-long medication.

The typical signs of Addison’s disease are vague and non-specific and are often seen in other, more common disorders.  They can also vary widely in severity.  Affected dogs may show lethargy, anorexia, vomiting, diarrhea, weight loss, shaking/shivering, or excessive thirst and urination.  A characteristic feature of Addison’s is that the signs tend to follow a waxing and waning course and improve dramatically when the animal is treated with fluids and/or steroids.

Additional clinical signs that your veterinarian may observe on physical examination include: poor body condition, weakness, dehydration, weak pulses, a slow heart rate, and blood in the stools.  Blood work may indicate:  anemia, electrolyte imbalances (i.e., elevated potassium, low sodium, and low chloride), low blood sugar, elevated calcium, acidosis, and elevation of liver and kidney values.

Approximately 35% of dogs with this disease present in what is known as Addisonian crisis; this is a true emergency and immediate treatment is required to save the dog’s life.  These animals have the classic signs of shock: mental dullness, pale mucous membranes, weak pulses, and cold extremities.  In addition, they have an abnormally slow heart rate due to elevated blood potassium levels.

Mechanisms and Causation

The adrenal glands are paired glands that sit near the kidneys.  They are made up of two layers, an outer cortex and an inner medulla, that are structurally and functionally distinct.  The cortex produces three types of hormone: mineralocorticoids, glucocorticoids, and androgens, which are collectively known as steroids.  Addison’s disease occurs when the adrenal cortices are destroyed and the body loses its ability to produce these hormones; the medical term for it is hypoadrenocorticism.   There may be no clinical signs of disease until 90% of the adrenal cortex has ceased to function.

It is not well understood what causes the destruction of the adrenal cortices.  In most cases the cause is thought to be autoimmune (the result of an over-active immune system) or idiopathic (unknown).  Rarely, there may be other causes, such as bleeding disorders, infectious disease, or metastatic cancer.  Addison’s disease may also occur when a dog that has being treated for a long period of time with steroids is abruptly withdrawn from the medication or when a drug called Lysodren is given, however, this form of the disease is usually reversible (fewer than 2% of these cases are permanent).


While the clinical signs may strongly suggest Addison’s disease, it can be definitively diagnosed only by means of a blood test called an ACTH stimulation test.  A baseline blood sample is drawn, then ACTH (a hormone that stimulates the adrenal glands) is given by injection and a second blood sample is taken 1-2 hours later.  The blood samples are analyzed to determine the level of adrenal hormone present; if the dog has shown little or no response to the ACTH administration, the test confirms Addison’s disease.


If an animal presents in Addisonian crisis, shock (i.e., low blood pressure and low blood volume) poses an immediate threat to his life and must be treated before the underlying disease is addressed.  The most critical aspect of the initial treatment is intravenous fluid replacement; this restores blood volume and pressure and also helps to correct some of the biochemical abnormalities.  An ACTH stimulation test should also be conducted at this time—it can be done concurrently with the fluid therapy.  Fluids are administered at a high rate (shock dose) for approximately the first hour, then lowered to a rate determined by individual needs once the dog’s heart rate, pulse quality, and attitude improve.  The dog often will improve rapidly with fluid therapy.  The heart rate and rhythm, electrolytes, and other parameters will begin to normalize over the next 12-24 hours.  During this time the dog will also begin to be treated with injectable steroids.  Most dogs that present to the clinic in a crisis will spend at least 24-48 hours in the hospital; the length of hospitalization will depend on the individual dog’s condition and response to therapy.

Maintenance treatment for Addisonian patients consists of life-long hormone replacement to compensate for the body’s inability to produce glucocorticoids and mineralocorticoids.  For dogs that present in crisis, this treatment can begin once they are stable and able to take food and water by mouth—for the others, it begins as soon as they are diagnosed.  Glucocorticoid replacement is accomplished with prednisone, given orally on a daily basis.

There are two options for mineralocorticoid replacement, an oral medication called fludrocortisone (Florinef) and an injectable one called DOCP (Percorten-V).  Florinef is usually more expensive than DOCP.  Florinef must be given daily, and it has some glucocorticoid activity in addition to its mineralocorticoid activity, so dogs that take it may or may not need to take prednisone as well (about 50% of dogs will need prednisone).  It is not unusual for a dog’s Florinef dose to rise gradually over the first 2 years or so of treatment, but it usually stabilizes after that.  DOCP injections are given approximately every 25 days, but DOCP has exclusively mineralocorticoid activity, so dogs that take this drug will usually require daily prednisone as well.  The response to DOCP is variable, so the actual dosing schedule must be tailored to the individual dog.

Stressful situations (e.g., travel, hospitalization, surgery) increase the body’s need for glucocorticoids, so you should keep a small supply of prednisone on hand to use as needed (your veterinarian will advise you on the appropriate dose for your dog).


Your veterinarian will recommend a specific monitoring plan for your dog, but typically it will include blood work every 5-7 days until the electrolytes have stabilized in the normal range (or for the first month if you are using DOCP), then monthly (or at the time of each subsequent DOCP injection) for the next 6 months and every 3-6 months thereafter.

An Addisonian dog needs to be carefully managed and faithfully medicated for the rest of his life, but as long as you do this, his prognosis is excellent for a normal lifespan and quality of life.