Hypoadrenocorticism (HA), or Addison’s disease, describes a spectrum of conditions resulting in deficiencies of important adrenal hormones (i.e., cortisol and aldosterone). HA usually results from direct adrenocortical injury (primarily autoimmune disease) although the rapid withdrawal of adrenal suppressive medications (steroids), pituitary surgery, or cancer sporadically result in ACTH deficiency. The variable clinical signs correspond to a loss of the vital functions of cortisol in maintaining metabolism, immunity, and gastrointestinal health and of aldosterone in maintaining sodium and volume status. Recent studies suggest up to 25–30% of patients with HA have normal electrolytes (i.e., “atypical” HA).^46–48

The clinical signs of HA can occur in dogs of any age or breed. Most dogs are diagnosed in middle age, with a female predisposition inconsistently reported. Commonly affected breeds include the standard poodle, Portuguese water dog, and Great Dane. Often, sudden signs of volume depletion (shock) predominate in “typical” HA (cortisol deficiency with aldosterone deficiency), although the atypical form (clinical signs reflecting cortisol deficiency without electrolyte derangements) is more often chronic. Atypical HA is characterized by vomiting, lethargy, anorexia, and diarrhea; hypoalbuminemia and/or hypocholesterolemia are common laboratory findings.⁴⁹ The presence of a lymphopenia makes cortisol deficiency extremely unlikely.⁵⁰