Hypoadrenocorticism (Addison’s Disease)
What Is It?
Hypoadrenocorticism, commonly called Addison’s Disease, is a metabolic disease in which the adrenal glands are not functioning appropriately. The adrenal glands are small glands located near the kidneys that produce two important substances for the body: glucocorticoids and mineralocorticoids. Glucocorticoids, such as cortisol, are important for metabolism of carbohydrates (sugars), fats, and protein, especially during stressful situations. Mineralocorticoids, such as aldosterone, are important for maintaining the body’s sodium, potassium, and water balance. In Addison’s disease, one or both of these are deficient. A “typical Addisonian” is deficient in both glucocorticoids and mineralocorticoids, while an “atypical Addisonian” is deficient only in glucocorticoids.
A deficiency of glucocorticoids typically causes gastrointestinal signs such as vomiting, diarrhea, lack of appetite, abdominal pain, and weight loss. In addition, changes in mentation, such as lethargy, are common. Other signs may include weakness, shivering, difficulty walking, dehydration, and an increase in water consumption and urination. If the body’s sodium and potassium abnormalities become too abnormal, a very severe condition called an Addisonian crisis may occur. This is characterized by a drop in blood pressure, abnormalities in the heart rhythm and rate, shock, collapse, and sometimes death. Clinical signs are more likely to occur during times of stress.
The cause of primary hypoadrenocorticism (most common) is unknown. It is likely an immune-mediated destruction of the adrenal cortex. It is estimated that 90% of the adrenal gland must be destroyed for clinical signs to develop. It is typically a disease of young to middle-aged female dogs, though dogs of any age can be affected. The most commonly affected breeds include Standard Poodles, Portuguese Water Spaniels, Labrador Retrievers, and Rottweilers. While most of these patients have both a deficiency of glucocorticoids and mineralocorticoids, atypical hypoadrenocorticism is used to describe those patients with only a glucocorticoid deficiency at the time of diagnosis. Secondary hypoadrenocorticism is also a deficiency of only glucocorticoids, but is caused by an abnormality of the pituitary gland in the brain. In addition, signs of secondary hypoadrenocorticism can develop when an animal that has been on supplemental corticosteroids suddenly stops therapy. This is termed iatrogenic hypoadrenocorticism. Though rare, hypoadrenocorticism does occur in cats as well.
The diagnosis of hypoadrenocorticism begins with a complete medical history and a thorough physical examination. Since signs of Addison’s disease are fairly nonspecific, your veterinarian will often consider several other diseases as possibilities for your pet’s clinical signs. Initially, a minimum database consisting of a serum chemistry profile, a complete blood count (CBC), and a resting cortisol level are performed. Additional tests to rule out other diseases may include a thyroid test, urinalysis, and imaging studies such as radiographs or ultrasound. An abnormal sodium to potassium ratio and cortisol level can be indicators that Addison’s disease is a possibility, though diseases of the gastrointestinal tract, liver, and urinary system can cause similar abnormalities.
The definitive test for Addison’s disease is the ACTH stimulation test. This involves injecting a synthetic hormone (adrenocorticotropic hormone or ACTH) into the body, then measuring the cortisol levels. In normal animals, this hormone would trigger the adrenal glands to release cortisol. In patients with Addison’s disease, the adrenal gland is not functioning properly and there will be no rise in cortisol levels.
Replacement of the glucocorticoids and mineralocorticoids is the mainstay of therapy for Addison’s disease. The preferred method involves a combination of an injectable mineralocorticoid called desoxycorticosterone pivalate or DOCP and an oral glucocorticoid called prednisone. The injection is given subcutaneously every 21-28 days (depending on your pet’s response) and the prednisone is given once to twice daily. Initially, electrolytes are checked at 12 and 25 days after starting therapy. Once stabilized, it is ideal to check the electrolytes every 3-6 months or sooner if there are any problems. An alternative medication is fludrocortisone acetate (Florinef) which has both mineralocorticoid and glucocorticoid properties. However, there is a wide range of dosages needed to manage pets with this medication, and owners often report unwanted side effects. If your pet is in an Addisonian crisis, fluid therapy and emergency glucocorticoid and mineralocorticoid replacement will be administered.
It is very important that your pet receives an increase in the prednisone dose during times of stress, as the body’s need for cortisol increases during these times. We typically recommend doubling the dose of prednisone during times of illness, boarding, grooming, traveling, or surgery.
Addison’s disease cannot be cured, but most pets with Addison’s disease respond well to medical treatment and have normal life spans. Medication and monitoring for this disease can be costly, especially for large or giant breed dogs. If your pet has been diagnosed with Addison’s disease, be sure to talk with your veterinarian about both the short and long term medical needs for a pet with Addison’s disease.
Please do not hesitate to contact us if you have any questions regarding your pet’s condition.
Content prepared by St. Francis Animal Hospital, 1227 Larpenteur Ave. West, Roseville MN. 55113