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Addison's disease is also
known as hypoadrenocorticism. It is a disease that results
from the reduction in corticosteroid secretion from the adrenal
gland. The adrenal gland is a small gland located near the
kidney that secretes several different substances that help
regulate normal body function. Some of the most important
products that it secretes are called glucocorticoids and mineralocorticoids.
There is another disease called Cushing's disease (hyperadrenocorticism)
that occurs when the adrenal gland produces too much of these
hormones. Addison's disease is not as common as Cushing's
disease, but it still occurs with regular frequency in the
dog population. It is difficult to recognize initially, but
once it is diagnosed, it can be successfully treated.
Glucocorticoids and Mineralocorticoids
The adrenal gland produces both glucocorticoids and mineralocorticoids.
Glucocorticoids such as cortisol have an effect on sugar,
fat, and protein metabolism. They are partially responsible
for the reaction known as fight or flight response during
stressful periods. Mineralocorticoids such as aldosterone
have an influence on the electrolytes sodium and potassium
in the body. They help regulate these electrolytes particularly
in stressful situations. When the adrenal glands stop functioning,
these hormones are not produced and the metabolism and electrolyte
balance of the animal gets out of whack creating the symptoms
and complications of Addison's disease.
Who gets Addison's disease and what are the symptoms?
Addison's is primarily a disease of young to middle-aged female
dogs, however, a dog of any age and either sex can develop
the disease. It does not appear to be more common in any one
particular breed. Cats can develop this disease, but it is
extremely rare. The symptoms of Addison's disease are very
vague and many animals may have symptoms for a long time before
the disease is diagnosed. Some of the more common symptoms
include lethargy, anorexia, vomiting, and muscle weakness.
The symptoms may wax and wane further complicating the diagnosis.
The other presentation for this disease is an episode called
an 'Addisonian crisis.' In this scenario, the animal collapses
in a state of shock due to an imbalance of electrolytes and
metabolism during a period of stress. This episode may be
the first time the owner suspects disease and may be fatal,
if not treated promptly.
What causes the adrenal glands to stop producing corticoids?
There are several different reasons the adrenal glands fail.
By far, the most common is destruction of the glands by the
body. This process where the body attacks and kills its own
tissue is known as 'immune mediated destruction.' Other causes
can be infections in the gland from granulomatous diseases
such as histoplasmosis or blastomycosis, or through other
means such as infarcts, tumors, or amyloidosis of the gland.
Another cause of Addison's can be the failure of the pituitary
gland to secrete ACTH, which is a hormone that stimulates
the adrenal gland to work. The hypothalamus can also stop
producing CRH, which is a hormone that controls the adrenal
gland. Failure of the pituitary gland or hypothalamus is usually
a result of a tumor, inflammation, or injury.
How is hypoadrenocorticism diagnosed?
Diagnosis is confirmed by a blood test called the ACTH stimulation
test. However, because the disease is not very common and
has a wide variety of symptoms, the ACTH test is usually done
after several other tests are used to rule out more common
diseases.
If the animal comes into the hospital in an Addisonian crisis
with electrolyte imbalances, and responds to therapy, then
a presumptive diagnosis of Addison's disease is made and once
the animal recovers, it can be confirmed with an ACTH challenge
test.
If however, the animal presents with a history of weight loss,
lethargy, or muscle weakness, the symptoms of many diseases,
a chemistry profile and blood count are usually performed
first to look at a number of body systems. Dogs with Addison's
disease often have elevated blood urea nitrogen (BUN) and
an elevated creatinine, as well as decreased blood glucose.
The blood count may show a chronic anemia. If the blood work
goes along with the symptoms, then an ACTH challenge test
is performed.
The dog is given an injection of the adrenal stimulating hormone
ACTH. A normal dog will respond by having an increase in blood
cortisol. If a dog with Addison's disease is given ACTH, the
dog will not have an increase in blood cortisol and the diagnosis
of Addison's disease is confirmed.
How is Addison's disease treated?
Once the disease is diagnosed, the treatment is fairly straightforward.
The standard treatment involves replacing the mineralocorticoids
and glucocorticoids in the body. The drug most commonly used
to accomplish this is Florinef (fludrocortisone). Florinef
is usually given twice a day. Initially, the blood sodium
and potassium levels are monitored to help obtain the correct
dose. After the animal is regulated, then the levels are rechecked
2 to 3 times a year and adjustments in dosing are made as
needed.
A newer option in the treatment of Addison's disease has recently
been made available. The new medication is an injectable medication
called DOCP. The injection is long acting and only needs to
be given every 25 days. DOCP was available years ago, but
was taken off the market and recently reintroduced as an approved
drug for dogs. DOCP has been intensively tested and been shown
to provide better electrolyte regulation than Florinef. Some
animals on DOCP may also need to be placed on a low maintenance
dose of prednisone. Novartis is manufacturing this drug and
more information on DOCP can be obtained by calling their
customer service number at 1-800-332-2761.
References and Further Reading
Bonagura, J. Kirk's Current Veterinary Therapy XII. W.B. Saunders Co. Philadelphia, PA; 2000.
Bonagura, J. Kirk's Current Veterinary Therapy XIII. W.B. Saunders Co. Philadelphia, PA; 1995.
Ettinger, S. Textbook of Veterinary Internal Medicine. W.B. Saunders Co. Philadelphia, PA; 1989.
Veterinary & Aquatic Services Department, Drs. Foster & Smith, Inc.
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