What Every Standard Poodle Fancier Should Know (3/95)

Addison's disease was first described as a human affliction in 1855 by Dr. Thomas Addison (even back then, medical doctors could be rather egocentric!). The more scientific name for this disease is hypoadrenocorticism which refers to an insufficient production of certain essential hormones by the adrenal glands.

Let the physiology lesson begin! Every Standard Poodle begins life with two adrenal glands. The adrenal glands sit directly in front of each kidney within the abdominal cavity and they are responsible for producing several important hormones including adrenaline, estrogen and testosterone (most of these two hormones are actually produced within the testicles and ovaries), cortisone, and aldosterone. Addison's disease is defined as a substantial decrease in the production of cortisone and aldosterone. The adrenal glands are the primary source of these two hormones and neither man nor beast can live without adequate levels of both of them. Cortisone has an effect on virtually every tissue in the body. It is essential for the normal function of every organ within the body and is responsible for a normal appetite and sense of well-being. Aldosterone's main function is the regulation of sodium and potassium levels within the body. In the absence of aldosterone, the blood potassium level increases and the blood sodium level decreases, both of which may be life threatening abnormalities. The adrenal glands need to be told to make cortisone and aldosterone. Hormones produced in two areas of the brain (the pituitary gland and the hypothalamus) stimulate the adrenal glands to manufacture these hormones. So, Addison's Disease can be caused by a problem within the adrenal glands themselves or within specific areas of the brain. The type of Addison's disease recognized in Standard Poodles is caused by problems within the adrenal glands themselves.

Addison's disease can occur in any breed of dog. A familial or inherited predisposition for the disease has been described in Standard Poodles, Labrador retrievers, and Portuguese water dogs. (You're no alone out there!) The cause of Addison's disease is incompletely understood, however, an immune mediated etiology is suspect. What this means is that the individual's own immune system is somehow triggered to attack and destroy its own body's normal tissues; in this case certain hormone-producing cells within the adrenal glands are destroyed. The disease is most common in middle aged female dogs as is the case for most autoimmune disorders.

Most dogs with Addison's disease initially have rather vague waxing and waning symptoms including a decrease in appetite, increased thirst, some vomiting and/or diarrhea, lethargy, and weight loss. In my own experience with Addisonian Standard Poodles, bloody diarrhea and muscle spasms may also be part of the history.

In the course of a thorough physical examination of an Addisonian patient, the veterinarian may notice depression, weakness, dehydration, weak pulses, thin body condition, and a slow heart rate (the slow heart rate is caused by an elevated blood potassium level). In the most extreme cases, the patient may present in a state of circulatory collapse and shock. The veterinarian may see none or all of these symptoms dependent mostly upon how long the patient has been Addisonian.

The diagnosis of Addison's disease begins with a blood and urine test. The urine is typically quite dilute rather than well concentrated. Blood test abnormalities may include increases in blood levels of potassium, blood urea nitrogen, creatinine, and calcium and decreases in sodium and glucose. If a chest x-ray is taken, the heart shadow may appear small. The definitive diagnosis of Addison's disease is made by measuring the level of cortisone within the blood stream before and after chemical stimulation of the adrenal glands. This is known as an ACTH response test . An Addisonian patient will have extremely low levels of circulating cortisone both prior to and after adrenal gland stimulation and, thus, the diagnosis is made. All in all, confirming the diagnosis of Addison's disease involves minimal testing and is, in the overall scheme of things, relatively inexpensive to diagnose.

Because the symptoms are so vague, the biggest pitfall with Addison's disease is it's recognition. The symptoms may wax and wane, so the pet owner often talks himself or herself out of a veterinary visit. If basic blood test abnormalities are mild, the veterinarian may not think about Addison's disease and, therefore, may fail to run and ACTH response test. If the patient presents in a state of collapse and weakness, the veterinarian may automatically administer cortisone thereby eliminating the possibility of getting accurate results from an ACTH response test. The most famous Addisonian in the world, John F. Kennedy, had waxing and waning symptoms for years before his physicians finally thought about testing for Addison's disease!

Treatment for Addison's disease involves life-long replacement therapy with cortisone and aldosterone. The cortisone is typically replaced with physiologic doses of prednisone (about one fifth the dose used to treat a flea allergy dermatitis!). Prednisone is inexpensive and, at the recommended dosage, has no side effects. Aldosterone replacement is achieved with a daily oral medication called florinef or an injectable preparation known as desoxycorticosterone pivalate. You may prefer to call it DOCP! DOCP has not yet been approved by the FDA (approval is anticipated sometime this year) for use in dogs, but veterinarians do have access to this drug. For now, I simply have an owner sign a special consent form before administering the DOCP to their pet. It is extremely safe and is given as a single injection to the dog approximately once every 25 days. It is expensive, but less so than florinef, which will cost the owner of an Addisonian Standard Poodle anywhere from $80.00 to $120.00 per month (get that pet insurance now!). In some cases, emergency therapy for the Addisonian patient may be necessary and included intravenous fluid therapy, cortisone administration, and treatment for circulatory shock.

The good thing about Addison's disease is that, if the diagnosis is made early enough, it is wonderfully treatable. With proper administration of medication and careful monitoring, the prognosis is excellent and there is no anticipated decrease in the patient's life expectancy. Recognition of the disease and cost of the medication seem to be the biggest obstacles to a successful outcome.

The history, symptoms, physical examination abnormalities, disease diagnosis, treatment, and prognosis in Addisonian Standard Poodles are not significantly different than for other breeds of dogs. The only difference I have noted is the very young age of onset for Standard Poodles as compared to other Addisonians I have met. Although not scientifically studied, my clinical impression is that Standard Poodles show an increased breed predisposition to a large spectrum of autoimmune diseases including Addison's disease, hemolytic anemia, thrombocytopenia, and hypothyroidism. Standard Poodle breeders might consider the notion of blood screening clinics in an attempt to pinpoint the genetic pathways these disorders are following within the breed. As distressful as the results might be, the knowledge obtained would be invaluable in preserving the long-term health and success of this wonderful breed.