The ABCs of Addison's

ArticleLast Updated January 20093 min read
Print/View PDF

Hypoadrenocorticism (Addison's disease) most commonly results from primary adrenal failure resulting in a deficiency of both cortisol and aldosterone from the adrenal cortex. Secondary hypoadrenocorticism is less common, is the result of failure of adrenocorticotropic hormone (ACTH) secretion, and results in pure glucocorticoid deficiency. Mineralocorticoid secretion is expected to be normal. Primary disease is suspected to be immune-mediated; other causes include granulomatous destruction, infarction of the adrenal gland, adrenalitis, neoplasia, amyloidosis, and necrosis. Immune-mediated destruction can occur with other immune-mediated diseases and other endocrine disorders. Primary adrenal failure can be caused by drugs (mitotane, ketoconazole, trilostane, or glucocorticoids). Approximately 70% of affected dogs are female, and most are young to middle-aged. A heritable form of the disease is found in standard poodles, bearded collies, Portuguese water dogs, and Nova Scotia duck tolling retrievers (NSDTRs). Clinical signs vary and wax and wane; 85% to 90% of the adrenal gland must be affected before clinical signs are seen. These signs most commonly include anorexia, vomiting, lethargy/depression, weakness, weight loss, diarrhea, shaking/shivering, polyuria, polydipsia, and abdominal pain. Signs can be severe, and animals can present in shock, with seizures, and with gastrointestinal hemorrhage. Most but not all dogs with hypoadrenocorticism have classic electrolyte changes. In one study of NSDTRs, 32% had normal values. The Na-K ratio is usually low and a cut-off less than 27 or 28 has been shown to have a predictive value of 95%. This ratio is only helpful in dogs with electrolyte abnormalities. Measurement of basal cortisol alone is not adequate; a basal cortisol level more than 2 mcg/dL usually rules out the disease. ACTH-stimulation testing is still the most useful test for diagnosis. Synthetic cosyntropin at a dose of 250 mcg/dog or 5 mcg/kg yields similar results, and the drug can be given intravenously or intramuscularly. In dogs with hypoadrenocorticism, the pre- and post-ACTH cortisol concentrations tend to be less than 1 mcg/dL. Endogenous ACTH concentrations may be helpful in diagnosing dogs with electrolyte levels within the normal range to determine whether the cause is primary or secondary. Measurement of plasma aldosterone levels has limited utility; aldosterone-to-renin and cortisol-to-ACTH ratios may be potentially useful but are difficult to measure in the clinical setting.**COMMENTARY:** This article provides a nice overview of the inherent challenges in diagnosing canine hypoadrenocorticism. While most of us are familiar with the ACTH-stimulation test, this review also covers the use of basal cortisol levels and new information on aldosterone-to-renin and cortisol-to-ACTH ratios. An important topic covered in this review is the syndrome of isolated glucocorticoid-deficient hypoadrenocorticism, which serves to remind practitioners that normal electrolyte levels do not rule out hypoadrenocorticism.Update on the diagnosis of Addison's disease. Scott-Moncrieff C. NAVC Proc 2009,pp 409-412.