Addison's disease, or hypoadrenocorticism, is a well-recognized syndrome caused by the inadequate production of glucocorticoids and/or mineralocorticoids from the adrenal glands.

Immune-mediated destruction of the adrenal cortices leading to primary adrenocortical failure is believed to be the most common cause of hypoadrenocorticism. Other causes of adrenocortical destruction include mycobacterial infection, fungal infection, treatment with o,p'-DDD, hemorrhage, and neoplasia. Secondary hypoadrenocorticism can occur when the hypothalamic-pituitary-adrenal axis malfunctions due to brain neoplasia or inflammation, or the adrenals atrophy from exogenous steroid administration. Secondary hypoadrenocorticism causes glucocorticoid deficiency but aldosterone levels usually remain adequate (normal electrolytes). There is also evidence that primary adrenal disease, on occasion, can cause glucocorticoid deficiency without concurrent mineralocorticoid deficiency.

Because of the often vague nature of clinical signs and inconsistent laboratory abnormalities, Addison's disease is often overlooked in the differential diagnosis.

Most reports of dogs with Addison's disease (both typical and atypical) have noted a higher prevalence in young to middle-aged, female dogs. In one study, the majority were larger-breed dogs with body weight >20 kg. Familial hypoadrenocorticism has been reported in several breeds including the Standard Poodle, Bearded Collie, Leonberger, Nova Scotia Duck Tolling Retriever, Portuguese Water Dog, Old English Sheepdog, Labrador Retriever, Standard Schnauzer, Soft-Coated Wheaton Terrier, Basset Hound, English Springer Spaniel, German Shorthaired Pointer, Doberman Pinscher, Newfoundland and West Highland White Terrier. Any breed or mixed breed of dog can be affected. The condition can also occur in combination with autoimmune thyroiditis, a situation called Schmidt's syndrome in people. Addison's disease is quite rare in cats.

• Typical Clinical Presentations
  Historically, dogs with Addison's disease have vague complaints such as intermittent anorexia, vomiting, diarrhea, weakness, lethargy, depression and weight loss. In the acute form of the disease, weakness and depression can progress to collapse, hypovolemic shock, and bradycardia.
• Unusual Clinical Presentations
  Megaesophagus. Dogs with both typical and atypical Addison's disease have reportedly had poor esophageal contractility leading to mega-esophagus. Regurgitation may be their only complaint on presentation. Some dogs present with aspiration pneumonia as a result. Thus, all dogs with megaesophagus should be evaluated for hypoadrenocorticism.
  Hypoglycemia. About 16-33% of affected dogs are hypoglycemic. This can present as weakness, ataxia and disorientation, or even acute collapse with seizures.
  Gastrointestinal hemorrhage. Melena and/or hematemesis have been reported in both typical and atypical Addison's cases.
  Pure aldosterone deficiency. Although rarely seen, some dogs with abnormal electrolytes and normal ACTH stimulation tests have been confirmed to be aldosterone deficient. Once all other causes of hyponatremia and hyperkalemia are ruled out, aldosterone levels are measured before and after ACTH stimulation. In some cases, this rare manifestation of Addison's disease is confirmed at necropsy.