Addison’s Disease or Hypoadrenocorticism

29 05 2011

Addison’s Disease or Hypoadrenocorticism

 

 

 

Hypoadrenocorticism or Addison’s disease is caused by a lack of corticosteroids and mineralocorticoid secretion from the adrenal glands.  In a normally functioning adrenal gland, corticosteroids are released during periods of stress and mineralocorticoids are released on a regular basis for the maintance of normal electrolyte levels involving sodium Na, Potassium K, and Chloride Cl.

 

Two types of hypoadrenocorticism exist.  Primary hypoadrenocorticism which results from a failure of the adrenal glands to secrete glucocorticoids (primarily cortisol) and mineralocorticoids (primarily aldosterone) from the adrenal cortex.  Secondary hypoadrenocorticism which is much less common, results from a failure of the pituitary gland to produce ACTH, a hormone that is responsible for stimulating glucocorticoid production from the adrenal glands.  With secondary hypoadrenocorticism, mineralocorticoid secretion (aldosterone secretion) is normal.

 

The most commonly affected breeds of dogs are young to middle-aged, typically 4 to 5 years of age, Great Danes, standard poodles, Portuguese Water Dogs, Nova Scotia duck tolling retrievers, Leonbergers, Rottweilers, Bearded collies, Wheaten and West Highland white terriers which have all been suggested to have a genetic predilection for hypoadrenocorticism.  Several other breeds appear to be predisposed for this disease including:  Airedale terrier, basset hound, German shepherd, German shorthaired pointer, Saint Bernard and the Springer spaniel although as yet a genetic relationship has not been established for these breeds.  Seventy percent of affected dogs are female.  Castrated male dogs are more commonly affected than are intact male dogs.

 

Common clinical signs may include sudden acute collapse, weakness, depression, inappetance, vomiting, weight loss and diarrhea.  Additionally the patient may have bradycardia (slow heart rate), hypothermia (low body temperatures), be shaking or shivering and exhibit abdominal painHematemesis (bloody vomiting), melena (blood in the stool) and hematochezia may occur infrequently.  Most dogs will have a waxing and waning of the clinical signs that will typically resolve with fluid and/or corticosteroid administration.

 

The classical diagnostic laboratory finding is the electrolyte alterations of hyponatremia (low sodium or Na levels) with Hyperkalemia (high potassium or K levels).  For primary hypoadrenocorticism a decrease in the sodium-potassium ratio from a normal 33:1 to a ration that is 25:1 or below, is typically diagnostic for acute hypoadrenocorticism. Other common laboratory abnormalities include hypoglycemia (low glucose levels), hypochloremia (low blood chlorine levels), hypocholesterolemia (low cholesterol levels), hypoalbuminemia (low levels of albumin in the blood) and azotemia (high blood ammonia levels).

 

On hematology these patients may exhibit anemia, eosinophilia (high levels of eosinophils, a certain white blood cell commonly seen in increased levels with allergies and parasitic infections), lymphocytosis (increase in the number of lymphocytes) or a lack of a stress leukogram in an ill patient.

 

Secondary or “atypical hypoadrenocorticism” may not exhibit the characteristic electrolyte alterations seen with primary hypoadrenocorticism.

 

Most addisonian patients will present with a urine specific gravity of less than 1.030 with concurrent isosthenuria (low levels of urine production) which in the face of azotemia may be incorrectly attributed to primary renal (kidney) failure.

 

A definitive diagnosis with atypical hypoadrenocortism is based on an ACTH stimulation test.  A post-ACTH plasma cortisol concentration of less than 2 µg/dl is consistent with hypoadrenocorticism.

 

Treatment consists of prednisone administration at initial doses of 0.5 to 1.0 mg/kg per day.  The dose of prednisone should be adjusted up to double the dosage rate the day before an anticipated stressful situation.  Patients in acute crisis should be placed on IV fluids preferably NaCL, sodium bicarbonate and given intravenous corticosteroids.

 

Mineralocorticoid supplementation with desoxycorticosterone pivalate (DOCP) should be administered as an intramuscular or subcutaneous injection every 25 days.  DOCP is available from Novartis Animal Health under the trade name Percorten-V®.    Alternatively, oral fludrocortisone acetate is available from Squibb under the trade name Florinef® and may be given at a starting dosage of 0.02 mg/kg per day.

Primary adrenal failure is suspected to be immune-mediated (situation were the body attacks itself) in most cases.  Immune-mediated destruction of the adrenal gland may occur concurrently with other immune-mediated endocrine disorders including:  hypothyroidism, diabetes mellitus and hypoparathyroidism.

Additional causes of primary adrenal failure included granulomatous destruction or hemorrhagic infarction of the adrenal gland, adrenalitis, neoplasia, amyloidosis and adrenal necrosis.  The use of several drugs may also result in primary hypoadrenocortism and include the use of:  mitotane, trilostane and ketoconazole.  The adrenal suppression caused by ketoconazole and trilostane may be reversible but adrenal failure resulting from mitotane is permanent.  .

Secondary hypoadrenocorticism may result from destructive lesions in the hypothalamus or pituitary gland secondary to neoplasia, inflammations or trauma.  An idiopathic (reason unknown) ACTH deficiency may also occur.  Chronic administration of glucocorticoids may also cause secondary adrenal failure through the suppression of ACTH production.

Life-long treatment is necessary.  With adequate treatment a dog may lead a long and happy life.

 

 

 

 

References:

 

Bonagura, John and David Twedt Editors.  Kirk’s Current Veterinary Therapy XIV.   W.B. Saunders. 2009. Pp. 231-235.

 

Ettinger, Stephen and Edward Feldman Editors.  Veterinary Internal Medicine.  5th Edition.  Vol. 2.  W.B. Saunders.  2000. Pp. 1488-1499.

 

Hoskins, Johnny.  “Testing for Addison’s Disease.”  DVM Newsmagazine.  January 2009. Pp. 8S-12S.

 

Kirk, Robert and Stephen Bistner.  Handbook of Veterinary Procedures and Emergency Treatment. W.B. Saunders and Co. 1981. P. 116-117.

 

Lathan, Patty and Catharine Scott-Moncrieff.  “Hypoadrenocorticism in Dogs.  NAVC Clinician’s Brief.  February.  2007.  Pp. 21-22.

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