Addison's disease in canines refers to hypoadrenocorticism, or Addison's disease, when it occurs in canines. The first case of Addison’s disease in dogs was recorded in 1953, over 100 years after it was described in humans by Thomas Addison.[1]
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Addison’s disease is an endocrine system disorder that occurs when the adrenal glands – located above the kidneys – fail to produce enough hormones to keep the body functioning normally. The adrenal glands secrete glucocorticoids such as cortisol [2] and mineralocorticoids such as aldosterone;[3] when proper amounts of these are not produced, an animal's metabolic and electrolyte balances may be upset.[4][5] Mineralcorticoids control the amount of potassium, salt and water in the body.[6][7][8] This may occur when the animal's pituitary gland fails to secrete ACTH, the hormone which stimulates the adrenal glands' production of cortisol, or when a disorder causes the body to attack and kill its own tissue ("immune mediated destruction").[7] The disease is also known as hypoadrenocorticism, adrenal insufficiency, or hypocortisolism. Addison’s disease is fatal if left untreated. The only preventable kind of Addison's disease is that which is caused when a dog is abruptly taken off of a steroid medication.[9][10]
| Abrupt Withdrawal of Steroids [11] | |
|---|---|
| Layer | Produces |
| Zona glomerulosa | Mineralcorticoids (aldosterone) |
| Zona fasciculata | Glucocorticoids (cortisol) |
| Zona reticularis | Sex steroids (androgens) |
Use of steroids means that the adrenal glands do not function fully during the course of the medication. The body senses the levels of the exogenous steroids in the system and therefore does not signal for additional production. [12]
During this time, the adrenal glands go into a type of dormancy because the steroid medication is doing their work for them. The usual protocol for stopping steroid medications is not to eliminate them suddenly, but to withdraw from them gradually in a "tapering off" process. Doses become less and less frequent prior to the planned cessation of the medication.[12] This tells the body to signal the inactive adrenal glands to go back to producing adrenal hormones. In cases where steroids are abruptly withdrawn, the dormant adrenal glands may not able to be "awakened" and the body will need to have its adrenal glucocorticoid hormones replaced by medication; the mineralcorticoids are not affected by this and do not need replacement therapy. There would be no risk of an Addisonian crisis because mineralcorticoid production remains intact.[12][13]
All causes for Addison's disease are not yet known. Some are genetic, others appear to be autoimmune related; there are cases caused by various disease processes.[14][15][16][8]
It is thought Addison’s disease occurs much more frequently in dogs than in humans; in fact, it may occur one hundred times more often in the canine population. It mostly affects young to middle-aged female dogs,[14][9] as the average age at diagnosis being four years old (although it has been found in puppies and dogs up to twelve years old). About seventy percent of dogs that are diagnosed with Addison's disease are female.[14][9][8]
Nevertheless, Addison's disease is still relatively uncommon in dogs.[14][9]
Certain breeds are more susceptible than others to Addison's disease:[9][15][14]
Poodles, Leonbergers, and Nova Scotia Duck Tolling Retrievers are considered the most susceptible.[9]
Several breeds are relatively not susceptible, including American Pit Bull Terriers, American Staffordshire Terriers, Chihuahuas, Cocker Spaniels, Golden Retrievers, Lhasa Apso, Schnauzers, and Yorkshire Terriers.[14][21]
Symptoms of Addison's disease in canines can include vomiting, diarrhea, lethargy, lack of appetite, tremors or shaking, muscle weakness, low body temperature, collapse, low heart rate, and pain in the hind quarters.[9][15] Hypoglycemia can also be present, and intially may appear to be a seizure disorder or an insulin-secreting pancreatic tumor (insulinoma).[12][22] Symptoms can appear to be those of many other disorders, earning Addison's disease the nicknames of "the Great Mimic" and "the Great Imitator" because of this.[8][23][12] It is possible not to see any signs of the disease until 90% of the adrenal cortex is no longer functioning.[23]
Signs that a dog may have Addison's disease include elevated levels of potassium and unusually low levels of sodium (hyponatremia) and chloride (hypochloremia). However, not all dogs' electrolyte ratios are affected during an Addisonian episode.[14] Therefore, the only accurate test for Addison's disease in canines is an ACTH stimulation test.[15][13][8] While most corticosteroid drugs will invalidate the results of an ACTH test, Dexamethasone may be used in the event of an Addison's emergency without fear of compromising the results of the test.[24]
In general, Addison's disease in canines is underdiagnosed,[25] and one must have a clinical suspicion of it as an underlying disorder for many presenting complaints. Females are overrepresented,[12] and the disease often appears in middle age (four to seven years), although any age or gender may be affected. Genetic continuity between dogs and humans helps to explain the occurrence of Addison's disease in both species.[26]
Dogs with Addison's disease may also have one of several autoimmune disorders.[26] Because it is an endocrine disorder, dogs with Addison's disease may also suffer from neuropathy and some endocrine-related eye diseases.[27]
If deterioration of the adrenal glands progresses far enough, a dog may experience an Addisonian crisis, a type of acute episode during which potassium levels elevate (hyperkalemia) and disrupt normal functions of the heart.[22] Arrhythmia can result and blood pressure may drop to dangerously low levels, while the dog's kidneys may cease to function properly.[6][7][28][29] Some 35% of canine Addison's cases are diagnosed as the result of an Addisonian crisis. It is a medical emergency.[15][23][30][13]
Laboratory tests for dogs with whipworms can exhibit the same low sodium and high potassium values found in Addison's disease; their ACTH values, however, will be normal.[12][22]
Breeds that began in the Pacific Rim, among them Akitas and Shiba Inus, can tend to have higher potassium values in laboratory tests. For these breeds, the elevated levels are not abnormal. Dogs who do not have Addison's disease will have normal values on ACTH tests.[12][22]
The adrenal outer layer, or cortex, has three layers; each produces a specific type of steroid.[12][6]
| Adrenal Cortex Layers [11][31] | |
|---|---|
| Layer | Produces |
| Zona glomerulosa | Mineralcorticoids (aldosterone) |
| Zona fasciculata | Glucocorticoids (cortisol) |
| Zona reticularis | Sex steroids (androgens) |
In typical Addison's, all of these layers stop functioning; the problem is with the adrenal gland.[15] But in atypical Addison's, the problem is not in the adrenal gland but in the pituitary gland. The gland produces a hormone, ACTH, (adrenocorticotropic hormone), that signals the zona fasciculata and zona reticularis to produce their steroids. When the anterior portion of the pituitary is unable to produce ACTH, there is nothing to activate the zona fasciculata and zona reticularis and they stop production of their respective hormones. The zona glomerulosa remains able to produce a normal amount of mineralcorticoids because it is not controlled by ACTH.[15] An atypical Addison's patient does not face the risk of an Addisonian crisis and only needs to have medication to replace the glucocorticoid steroid cortisol.[12][13][14] One dog in every 42 diagnosed with Addison's disease will have the atypical or secondary form of the disease where mineralcorticoid production remains intact.[12]
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Typical Addison's
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Atypical Addison's
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In some dogs with atypical (secondary) Addison's, the disease progresses to the point where mineralcorticoid replacement is necessary (making them typical or primary Addison's patients), while others retain their ability to continue production of mineralcorticoids for years, requiring glucocorticoid replacement only.[32][33]
Hypoadrenocorticism is treated with fludrocortisone (trade name Florinef)[34][35] or a monthly injection called Percorten-V (desoxycorticosterone pivalate, DOCP) and prednisolone.[36][37][38] Routine blood work is necessary in the initial stages until a maintenance dose is established.[9][15]
Most of the medications used in the therapy of hypoadrenocorticism cause excessive thirst and urination. It is absolutely vital to provide fresh drinking water for a canine suffering from this disorder.[9]
If the owner knows about an upcoming stressful situation (shows, traveling etc.), patients generally need an increased dose of prednisone to help deal with the added stress. Avoidance of stress is important for dogs with hypoadrenocorticism. Physical illness also stresses the body and may mean that the Addison's medication(s) need to be adjusted during this time.[39] Most dogs with hypoadrenocorticism have an excellent prognosis after proper stabilization and treatment.[8][13][9][23]