What is Addison’s Disease?
In animals with Addison’s disease there is a deficiency or reduction of the corticosteroid hormones released from the adrenal glands. We usually don’t know the direct cause of the hormone deficiency, but fortunately the disease can be managed with the administration of corticosteroid hormones even if the cause of it is unknown.
Clinical signs and symptoms
Patients are usually young (age 4-5 years) dogs but any age dog can be affected (this disease can occur in cats but is very rare). There is a genetic predisposition for Addison’s disease in the standard poodle and bearded collie. Female dogs are affected twice as often as males.
Symptoms start out vague and non-specific, they can include
- seeming “off” in some way
Un-diagnosed, this disease will progress to what is known as an Addisonian crisis. Symptoms of this are basically a shock episode
- dangerously low blood sugar levels
- extremely high potassium levels in the blood
- heart rate drops, resulting in arrhythmias
Without quick emergency veterinary treatment your dog may not survive this episode.
Diagnosing Addison’s Disease
Animals usually present during an Addisonian crisis and are in shock. Shock treatment is initiated, and blood work is completed.
Bloodwork will show
- elevations in renal values (BUN/Creatine)
- elevation in potassium levels
- low blood sugar levels
After your dog is stabilized, an ACTH stimulation test will need to done to confirm Addison’s disease. A blood sample is collected, then an injection of synthetic adrenocorticotropic hormone is given. A second blood sample is collected 1 hour later to measure and compare the pre and post response to the hormone injection. A non-Addisonian dog will show an increase in cortisol levels, whereas a dog with Addison’s will show no response to the hormone injection.
The most important aspect of treatment for hypoadrenocorticism is the replacement of the missing corticosteroid hormones. One way to do this is with oral fludrocortisone (Florinef®). Florinef is given usually twice a day at a dose determined by the patient’s sodium and potassium blood tests. At the beginning of treatment, electrolyte levels will need weekly monitoring by running blood tests. When levels seem stable, these blood tests are repeated two to four times per year depending on the veterinarian’s discretion. Occasionally it will be found that the dose of Florinef needed to control the Addison’s disease will increase. Florinef is an expensive medication, making this disease a bit pricey to treat.
What is Atypical Addison’s Disease?
Approximately one dog in 42 will have a special form of Addison’s disease. Most dogs get Addison’s disease when all three layers of the adrenal gland are destroyed and no corticosteroid hormones of any kind can be produced. With atypical Addison’s disease, the problem is limited to the layers that produce the glucocorticoids. This creates a patient who cannot regulate blood sugar normally but who is not at risk for an Addisonian crisis. Diagnosis is still done with the ACTH stimulation test. Treatment consists of supplementing glucocorticoid hormones, such as prednisone. Often these patients ultimately progress to the more typical Addison’s disease.
A similar deficiency in glucocorticoids can also occur when a pet has been on long-term oral glucocorticoids (such as prednisone) that has been stopped too abruptly. Long term glucocorticoid use leaves the outer layers of the adrenal cortex with nothing to do and there is also no stimulation from the pituitary gland since the medication is providing the body with more than enough glucocorticoids. Once the medication is withdrawn, the body is back to relying on its own adrenal glands for glucocorticoids but the gland has atrophied from lack of stimulation. This creates a deficiency in glucocorticoids similar to atypical Addison’s disease and is the reason why steroid hormones are typically tapered off rather than abruptly discontinued. True atypical Addison’s disease can be distinguished from overuse of medication by a plasma ACTH level (high in atypical Addison’s and low with medication overuse).