Hypoadrenocorticism, sometimes referred to as Addison's disease, is a condition where there is decreased secretion of adrenocorticotropic hormone. In dogs, it's typically suffered by middle-aged female dogs. In some cases, this is a chronic deficiency for which there is no treatment, in others mineralocorticoid and glucocorticoid therapy is initiated. The causes for hypoadrenocorticism are usually unknown, but to some extent it is regarded as an autoimmune disease. refers to hypoadrenocorticism, or Addison's disease, when it occurs in canines. The first case of hypoadrenocorticism in dogs was recorded in 1953, over 100 years after it was described in humans by Thomas Addison.
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 and mineralocorticoids such as aldosterone; when proper amounts of these are not produced, the metabolic and electrolyte balance is upset. Mineralocorticoids control the amount of potassium, salt and water in the body. The disease is also known as hypoadrenocorticism, adrenal insufficiency, or hypocortisolism, and is fatal if left untreated.
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"). Other cases are caused by various disease processes, including atypical Addison's -the failure of the pituitary gland to secrete ACTH, the hormone which stimulates the adrenal production of cortisol.
The only preventable kind of Addisonian crisis is iatrogenic hypoadrenocorticism which is caused during abrupt cessation of a steroid medication. 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. 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 If steroids are abruptly withdrawn, the dormant adrenal glands may not able to reactivate, and the body will need to have its adrenal glucocorticoid hormones replaced by medication.
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, 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. 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.
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Signs and symptoms
The most common clinical manifestations are related to mental status and gastrointestinal function; they include lethargy, anorexia, vomiting, weight loss, and weakness. Additional findings may include dehydration, bradycardia, weak femoral pulses, and abdominal pain. Polyuria and polydipsia, diarrhea, and shivering are occasionally reported.
Addisonian crisis
If hyponatremia (low sodium) and hyperkalemia (high potassium) are severe, the resulting hypovolemia, prerenal azotemia, and cardiac arrhythmias may result in an Addisonian crisis. In severe cases, the patient may be presented in shock and moribund. Addisonian crisis must be differentiated from other life-threatening disorders such as diabetic ketoacidosis, necrotizing pancreatitis, and septic peritonitis.
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Causes
The adrenal outer layer, or cortex, has three layers; each produces a specific type of steroid.
Primary
Primary adrenocortical insufficiency is the more common form of hypoadrenocorticism. All layers of the adrenal gland stop functioning; the problem is with the adrenal gland. This causes a deficiency of both mineralocorticoid and glucocorticoid secretion. Most cases are classified as idiopathic, although immune-mediated adrenocortical destruction is a likely cause. Bilateral destruction of the adrenal cortex by neoplasia (e.g. lymphosarcoma), granulomatous disease, or arterial thrombosis can also cause primary adrenocortical insufficiency. The destruction is progressive, although variable in rate, ultimately leading to complete loss of adrenocorotical function. A partial deficiency syndrome may occur initially, with signs manifested only during times of stress (e.g., boarding, travel, surgery).
Secondary
In secondary hypoadrenocorticism, 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 An atypical Addison's patient does not risk an Addisonian crisis and only needs to have medication to replace the glucocorticoid steroid cortisol. 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.
Secondary adrenocortical insufficiency involves only a deficiency of glucocorticoid secretion. Destructive lesions (e.g. neoplasia, inflammation) in the pituitary gland or hypothalamus and chronic administration of exogenous glucocorticoids or megestrol acetate (cats) are the most common causes.
In some dogs with secondary hypoadrenocorticism, the disease progresses to the point where mineralocorticoid replacement is necessary, making them typical or primary Addison's patients, while others retain their ability to continue production of mineralocorticoids for years, requiring glucocorticoid replacement only.
Diagnosis
Hypoadrenocorticism is often tentatively diagnosed on the basis of history, physical findings, clinical pathology, and, for primary adrenal insufficiency, characteristic electrolyte abnormalities.
- Clinical Pathology - Abnormalities that may be identified on CBC, MBA, UA. Hyperkalemia, hyponatremia, and hypochloremia are the classic electrolyte alterations. The sodium/potassium ratio often is <27 (normal is between 27:1 and 40:1)and maybe <20 in animals with primary adrenal insufficiency.
- ECG - The severity of the ECG abnormalities correlates with the severity of the hyperkalemia. Therefore the ECG can be used to identify and estimate the severity of hyperkalemia and to monitor changes in serum potassium during therapy.
- Diagnostic imaging - Abdominal ultrasound may reveal small adrenal glands, suggesting adrenocortical atrophy. However, finding normal-sized adrenal glands does not rule out hypoadrenocorticism. Rarely, megaesophagus is evident on radiographs.
- ACTH stimulation test - Confirmation requires evaluation of an ACTH stimulation test. Basline plasma cortisol and urine cortisol/Cr ratios are unreliable for confirming the diagnosis. One major diagnostic criterion is abnormally decreased post-ACTH plasma cortisol. Normal plasma cortisol after ACTH stimulation rules out adrenal insufficiency.
The ACTH stimulation test does not distinguish between primary adrenal insufficiency and secondary insufficiency or adrenocortical destruction caused by mitotane overdose. Differentiation between primary and secondary adrenal insufficiency can be made by periodically measuring serum electrolytes, baseline endogenous ACTH, or possibly serum or plasma aldosterone during the ACTH stimulation test.
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. 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". It is possible not to see any signs of the disease until 90% of the adrenal cortex is no longer functioning.
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. Therefore, the only accurate test for Addison's disease in canines is an ACTH stimulation test. 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.
In general, Addison's disease in canines is underdiagnosed, and one must have a clinical suspicion of it as an underlying disorder for many presenting complaints. Females are overrepresented, and the disease often appears in middle age (four to seven years), although any age or gender may be affected. Dogs with Addison's disease may also have one of several autoimmune disorders. Because it is an endocrine disorder, they may also suffer from neuropathy and some endocrine-related eye diseases.
Addisonian crisis
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. Arrhythmia can result and blood pressure may drop to dangerously low levels, while the dog's kidneys may cease to function properly. Some 35% of canine Addison's cases are diagnosed as the result of an Addisonian crisis. It is a medical emergency.
Whipworms
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.
Pacific Rim
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.
Treatment
Aggressiveness of therapy depends on the clinical status of the patient and the nature of the insufficiency (glucocorticoid, mineralocorticoid, or both). Many dogs and cats with primary adrenal insufficiency are presented in Addisonian crisis and require immediate, aggressive therapy. In contrast, secondary insufficiency often has a chronic course.
Hypoadrenocorticism is treated with fludrocortisone (trade name Florinef) or a monthly injection of Percorten-V (desoxycorticosterone pivalate, DOCP) and prednisolone or Zycortal. Routine blood work is necessary in the initial stages until a maintenance dose is established. 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.
If the owner knows about an upcoming stressful situation (shows, traveling etc.), the animals 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. Most dogs with hypoadrenocorticism have an excellent prognosis after proper stabilization and treatment.
Addisonian crisis
Treatment is directed towards (1) correcting hypotension, hypovolemia, electrolyte imbalances, and metabolic acidosis; (2) improving vascular integrity, and (3) providing an immediate source of glucocorticoids. Rapid correction of hypovolemia is the first priority.
Most patients show dramatic improvement within 24 to 48 hours of appropriate fluid and glucocorticoid therapy. Over the ensuing 2 to 4 days, a gradual transition from IV fluids to oral water and food is undertaken, and maintenance mineralocorticoid and glucocorticoid therapy is initiated. Failure to make this transition smoothly should raise suspicion of insufficient glucocorticoid supplementation, concurrent endocrinopathy (e.g. hypothyroidism), or cocurrent illness (especially renal damage).
Epidemiology
Hypoadrenocorticism is typically a disease of young to middle-aged (mean, 4 years; range, 2 months to 12 years) female dogs. No significant breed predilection exists, although genetics probably play a role in Standard Poodles and Portuguese Water Spaniels. The disease is rare in cats. There exists no apparent gender predisposition in cats, but young to middle-aged cats (average, 6 years) are most often affected.
Certain breeds are more susceptible than others to Addison's disease:
Poodles, Leonbergers, and Nova Scotia Duck Tolling Retrievers are considered the most susceptible. 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.
Several breeds are relatively not susceptible, including American Pit Bull Terriers, American Staffordshire Terriers, Cocker Spaniels, Lhasa Apso, Schnauzers, and Yorkshire Terriers.
Source of the article : Wikipedia
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