Addison disease, also known as hypoadrenocorticism, is a type of adrenal gland disease that results from the atrophy of the adrenal glands and is characterized by insufficient production of the hormone cortisol. Adrenocortical hormones are vital for life. Aldosterone is the most important naturally occurring mineralocorticoid, while cortisol represents the most important glucocorticoid. Both hormones are synthesized from cholesterol.3 Cortisol is the principal glucocorticoid secreted by the adrenal cortex which helps metabolize nutrients, mediate physiologic stress, and regulate the immune system. Intense heat or cold, infection, trauma, exercise, obesity and debilitating diseases influence cortisol production.
Addison disease is the opposite of Cushing disease in which cortisol is overabundant. However, in Addison disease, cortisol production is not the only problem, because other adrenal hormones will also be insufficiently produced by the pituitary gland or the hypothalamus. Female dogs are more frequently affected than male dogs. Older male dogs may develop cognitive disturbances characterized by aggression and seem to bite out of the blue.4 Although hypoadrenocorticism used to be regarded a rare canine endocrine disease, it is believed now to be underdiagnosed.
Naturally occurring hypoadrenocorticism is an uncommon canine disease.3 Two iatrogenic (doctor-caused) forms of Addison disease may occur in dogs with adrenal damage. One form is caused by corticosteroids for inflammatory conditions. Some of the patients recover with time if the drug is withdrawn, but in others the damage to the adrenals is permanent. The other form can occur in Cushing disease patients overtreated with drugs used to control cortisol overproduction. In this form of Addison disease, damage to the adrenals is permanent.
More than 85% of adrenal gland reserve must be lost before clinical signs of hypoadrenocorticism are manifested.2 An important clinical sign of Addison disease is that the symptoms come and go. Depression is often the first sign. The dog becomes weak, loses his appetite, vomits, and looks malnurished. Some dogs with this disease drink and urinate a lot. Decreased production of glucocorticoids and increased sensitivity to insulin contribute to the development of moderate hypoglycemia. In some dogs, hyperpigmentation of the skin occurs.1
Addison disease has been referred to as "the great pretender" due to its ability to mimic other common canine diseases, and thereby represents a diagnostic challenge. 3 Diagnosis of hypoadrenocorticism involves blood tests. Dogs with gastrointestinal signs and abnormally low level of albumin in the blood, or, abnormally small amounts of cholesterol in the circulating blood should be evaluated for atypical hypoadrenocorticism. Follow-up electrolyte monitoring is recommended because some will develop electrolyte abnormalities.5
Because this disease is potentially life-threatening, treatment may begin before test results confirm the diagnosis. Affected dogs may have very low blood pressure and abnormal electrolyte levels. These are serious signs that can cause shock and death. Both these problems can be helped by increasing fluid intake and re-hydration therapy is started immediately, even before beginning to treat the adrenal problem. If profound electrolyte abnormalities are present, rapid treatment is vital. Hyperkalemia (excessive levels of potassium) in particular can be life threatening, if not treated expeditiously. Aims of emergency treatment include correction of low blood pressure and hypovolemia (abnormally low volume of blood circulating through), correction of electrolyte imbalances, acidosis, hypoglycemia, anemia, and hormonal deficiency.2 Cortisone is the easiest to replace; low doses of the drug prednisone are used for this. The adrenally produced mineralocorticoids are more difficult to replace. These hormones normally regulate production of electrolytes, without which the body is unable to function. The medication for this can be given orally on a daily basis, injected monthly or implanted under the skin in pellet form every ten months. A dog must be retested periodically to assure proper dosage.
- Hypoadrenocorticism. Merck Manuals
- Stephen J. Ettinger, DVM, DACVIM and Edward C. Feldman, DVM, DACVIM. Textbook of Veterinary Internal Medicine
- Canine hypoadrenocorticism: Part I
Susan C. Klein and Mark E. Peterson
- Steven R. Lindsay. Handbook of Applied Dog Behavior and Training: Procedures and protocols
- A retrospective study of dogs with atypical hypoadrenocorticism: a diagnostic cut-off or continuum? J Small Anim Pract. Author manuscript; available in PMC 2017 Jul 4.