Cushing's syndrome is usually caused by the secretion of corticotropin or cortisol by a pituitary or adrenal tumor, respectively, or by ectopic secretion of corticotropin. It is possible to determine the specific abnormality in most patients, but it can sometimes be difficult to decide whether the patient has hypercortisolism and whether it is primary or due to major depressive disorder or to the stress of other diseases. Determining the cause of the hypercortisolism involves performing multiple tests in a logical sequence; the results should all be consistent with the same diagnosis. Treatment should aim to cure the hypercortisolism and to eliminate any tumor that threatens the patient's health, while minimizing the chance of an endocrine deficiency or long-term dependence on medications.

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Primary hypoadrenocorticism was diagnosed in ten young to middle-aged cats of mixed breeding. Five of the cats were male, and five were female. Historic signs included lethargy (n = lo), anorexia (n = lo), weight loss (n = 9), vomiting (n = 4), and polyuria (n = 3). Dehydration (n = 9), hypothermia (n = 8), prolonged capillary refill time (n = 5), weak pulse (n = 5), collapse (n = 3), and sinus bradycardia (n = 2) were found on physical examination. Results of initial laboratory tests revealed anemia (n = 3), absolute lymphocytosis (n = 2), absolute eosinophilia (n = l), and azotemia and hyperphosphatemia (n = 10). Serum electrolyte changes included hyponatremia (n = lo), hyperkalemia (n = 9), hypochloremia (n = 9), and hypercalcemia (n = 1). The diagnosis of primary adrenocortical insufficiency was established on the basis of results of adrenocorticotropic hormone (ACTH) stimulation tests (n = 10) and endogenous plasma ACTH determinations (n = 7). Initial therapy for hypoadrenocorticism included intravenous administration of 0.9% saline and dexamethasone and intramuscular administration of desoxycorticosterone acetate in oil. Three cats were euthanatized shortly after diagnosis because of poor clinical response. Results of necropsy examination were unremarkable except for complete destruction of both adrenal cortices. Seven cats were treated chronically with oral prednisone or intramuscular methylprednisolone acetate for glucocorticoid supplementation and with oral fludrocortisone acetate or intramuscular injections of repository desoxycorticosterone pivalate for mineralocorticoid replacement. One cat died after 47 days of therapy from unknown causes; the other six cats are still alive and well after 3 to 70 months of treatment. (Journal of Veterinary Internal Medicine 1989; 355-58) PRIMARY HYPOADRENOCORTICISM (Addison's disease) results from inadequate glucocorticoid and mineralocorticoid production by the adrenal cortex. Although recognized in both humans and dogs,'-4 only one case of naturally occumng feline primary hypoadrenocorticism has been reported previ~usly.~ Since that time, we studied an additional nine cases of primary hypoadrenocorticism in cats. Our purpose is to characterize further the feline disease by describing the clinical signs, laboratory findings, and results of treatment in all ten cats. Materials and MethodsFrom January 1981 to September 1988, we diagnosed naturally occurring primary hypoadrenocorticism in ten cats, based on the history, clinical signs, and results of hematologic and serum biochemical testing and urinalysis. Diagnosis was confirmed by showing low to lownormal basal serum cortisol concentrations that did not increase 1 and 2 hours after intramuscular administration of adrenocorticotropic hormone (ACTH) gel (2.2 U/kg). In seven cats, blood was also collected for a determination of plasma ACTH concentrations before replacement therapy or administration of ACTH for diagnostic testing. Results of these determinations confirmed that these cats had primary, not secondary, ...

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