Addison's disease in canines

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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]

Description[edit]

Addison’s disease, whether in dogs or humans, is an endocrine system disorder that occurs when the adrenal glands fail to produce enough hormones for normal function. The adrenal glands – located above the kidneys – secrete glucocorticoids such as cortisol [2] and mineralocorticoids such as aldosterone;[3] when proper amounts of these are not produced, the metabolic and electrolyte balance is upset.[4][5] Mineralocorticoids control the amount of potassium, salt and water in the body.[6][7][8] The disease is also known as hypoadrenocorticism, adrenal insufficiency, or hypocortisolism, and is fatal if left untreated.[9]

All causes for Addison's disease are not yet known. The usual causes are genetic, often related to autoimmune disorders, where the body attacks and kill its own tissue ("immune mediated destruction").[10] Other cases are caused by various disease processes,[8][10][11][12] including atypical Addison's -the failure of the pituitary gland to secrete ACTH, the hormone which stimulates the adrenal production of cortisol.[7]

The only preventable kind of Addisonian crisis is iatrogenic hypoadrenocorticism which is caused during abrupt cessation of a steroid medication.[13][14] During steroid treatment, the adrenal glands do not function fully. The body senses the levels of the exogenous steroids in the system and therefore does not signal for additional production.[15] The usual protocol for stopping steroid medications is not to eliminate them suddenly, but to withdraw from them gradually in a "tapering off" process, which allows the production to adjust to normal. If steroids are abruptly withdrawn, the dormant adrenal glands may not able to reactivate, and the body will need to have its adrenal glucocorticoid hormones replaced by medication.[15]

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,[11] 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.[8][11] Addison's disease is still relatively uncommon or underdiagnosed in dogs. Statistics gathered from a large veterinary hospital placed the number at 0.36 dogs per 1000. For an average veterinary practice with two veterinarians and 1500 canine patients, this would mean an average of one diagnosis of the disease each year.[11][16]

Susceptibility of certain breeds[edit]

Certain breeds are more susceptible than others to Addison's disease:[10][11]

Poodles, Leonbergers, and Nova Scotia Duck Tolling Retrievers are considered the most susceptible.[11] While Addison's is primarily a disease affecting female dogs, standard Poodles and Bearded collies of both sexes appear to be prone to the condition.[21]

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.[11][22]

Diagnosis[edit]

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.[10][23] Hypoglycemia can also be present, and initially may be confused with seizure disorders, insulin-secreting pancreatic tumor (insulinoma), food poisoning, parvovirus enteritis, gastric volvulus, spinal or joint problems, earning Addison's disease the nicknames of "the Great Mimic" and "the Great Imitator".[8][15] It is possible not to see any signs of the disease until 90% of the adrenal cortex is no longer functioning.[24]

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.[11] Therefore, the only accurate test for Addison's disease in canines is an ACTH stimulation test.[8][10][25] 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.[26]

In general, Addison's disease in canines is underdiagnosed,[27] and one must have a clinical suspicion of it as an underlying disorder for many presenting complaints. Females are overrepresented,[15] and the disease often appears in middle age (four to seven years), although any age or gender may be affected.[28] Dogs with Addison's disease may also have one of several autoimmune disorders.[28] Because it is an endocrine disorder, they may also suffer from neuropathy and some endocrine-related eye diseases.[29]

Addisonian crisis[edit]

If deterioration of the adrenal glands progresses far enough, a dog may experience an Addisonian crisis, an acute episode during which potassium levels increase (hyperkalemia), disrupting normal functions of the heart.[30] Arrhythmia can result and blood pressure may drop to dangerously low levels, while the dog's kidneys may cease to function properly.[6][7][31][32] Some 35% of canine Addison's cases are diagnosed as the result of an Addisonian crisis. It is a medical emergency.[10][25][24][33]

Whipworms[edit]

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.[15][30]

Pacific Rim[edit]

Breeds that began in the Pacific Rim, among them Akitas and Shiba Inus, tend to have higher potassium values in laboratory test, and elevated levels are not abnormal. Dogs who do not have Addison's disease will have normal values on ACTH tests.[15][30]

Typical and atypical Addison's[edit]

Layers of the adrenal cortex, or outer portion of the adrenal gland.

The adrenal outer layer, or cortex, has three layers; each produces a specific type of steroid.[6][15]

Adrenal Cortex Layers [14][34]
LayerProduces
Zona glomerulosaMineralocorticoids (aldosterone)
Zona fasciculataGlucocorticoids (cortisol)
Zona reticularisSex steroids (androgens)


In typical, or primary, Addison's, all of these layers stop functioning; the problem is with the adrenal gland.[10] But in atypical, or secondary, Addison's, the problem is not in the adrenal gland but in the pituitary gland; normally, its anterior portion produces a hormone, ACTH, (adrenocorticotropic hormone), that signals the zona fasciculata and zona reticularis to produce their steroids. When the pituitary is unable to produce ACTH, these zones stop production of their hormones. The zona glomerulosa is not controlled by ACTH, and remains able to produce a normal amount of mineralocorticoids [10] An atypical Addison's patient does not risk an Addisonian crisis and only needs to have medication to replace the glucocorticoid steroid cortisol.[11][15][25] One dog in every 42 diagnosed with Addison's disease will have the atypical or secondary form of the disease where mineralocorticoid production remains intact.[15]

Anatomy and physiology of animals Adrenal glands.jpgPituitary gland representation.PNG
Typical Addison's: problem with the adrenal glands.
Atypical Addison's: problem with the anterior pituitary.