Feline adrenal disease (Proceedings)
Hyperadrenocorticism develops most commonly in middle-aged to older cats (mean age = 10.4 years; range 6 - 15 years). Of the 26 reported cases of feline Cushing's syndrome and one previously unreported case, 21 (78%) have been females. This female sex predilection resembles the human syndrome and contrasts with canine hyperadrenocorticism, where no sex predilection occurs.
The most common historical and clinical signs associated with feline hyperadrenocorticism are polyuria, polydipsia, and polyphagia. These signs likely correspond to the high incidence of concurrent diabetes mellitus (76%) found in cats with hyperadrenocorticism, and are consistent with the lack of overt signs preceding marked glucose intolerance observed in experimentally-induced disease. The typical "Cushingoid" pot-bellied appearance with hepatomegaly, weight gain, and generalized muscle wasting is common in cats as in dogs. Dermatologic abnormalities frequently recognized include an unkempt haircoat with patchy alopecia, and very thin skin prone to traumatically-induced tears and secondary infections.Hyperglycemia is the most common laboratory abnormality found on serum biochemistries. Cats appear more sensitive to the diabetogenic effects of glucocorticoid excess than dogs. Cats with concurrent diabetes mellitus often exhibit cortisol-induced insulin resistance, requiring high daily doses of insulin to control their hyperglycemia and glucosuria. Hypercholesterolemia is also common, and may relate to insulin resistance and increased lipolysis. Cats lack the steroid-induced isoenzyme of alkaline phosphatase found in the canine, and the half-life of the enzyme appears to be significantly shorter in the cat. Elevation of serum alkaline phosphatase (SAP) is present in only approximately one-third of cats compared to nearly 90% of dogs with hyperadrenocorticism. Increases in SAP and the hepatocellular enzyme ALT appear to correspond with the regulation of the diabetic state, rather than representing direct indicators of glucocorticoid excess. These enzymes frequently normalize with adequate regulation of diabetes, even without therapy directed towards the hyperadrenocorticism. Hematologic findings associated with hypercortisolemia (lymphopenia, eosinopenia, and neutrophilic leukocytosis) occur inconsistently in feline hyperadrenocorticism. Despite clinical polyuria and polydipsia, cats appear to maintain urine specific gravities of greater than 1.020 more frequently than dogs, and only occasionally exhibit dilute urine and decreased blood urea nitrogen concentrations commonly seen in dogs with hyperadrenocorticism.
Endocrinologic evaluation of cats suspected of hyperadrenocorticism involves screening tests to confirm the diagnosis, and differentiating tests to distinguish pituitary-dependent disease (PDH) from adrenal tumors (AT). Adrenocorticotropin (ACTH) stimulation testing in adrenocortical hyperfunction is not as definitive as for hypoadrenocorticism. Fifteen to 30% of cats with confirmed hyperadrenocorticism have had normal cortisol response to ACTH administration (false negatives). In addition, stressed cats and those with non-adrenal illnesses may show an exaggerated response to ACTH in the absence of hyperadrenocorticism (false positives). A normal urine cortisol-to-creatinine ratio (UCCR) can be used to exclude the diagnosis of hyperadrenocorticism in cats as described in dogs. The UCCR is attractive due to the ease of sampling compared to other endocrine function tests, but is non-specific and will be elevated in a variety on non-adrenal illnesses. An exaggerated ACTH stimulation test or an elevated UCCR should be pursued with suppression testing prior to initiating any therapy.
Normal cats are more variable than dogs with respect to the degree and duration of adrenocortical suppression following dexamethasone administration. Intravenous doses of dexamethasone that have been evaluated in the cat range from 0.005 to 1.0 milligrams per kilogram. A dosage of 0.01 mg/kg of dexamethasone, commonly used in low-dose dexamethasone suppression testing in dogs, led to a significant drop in serum cortisol levels in ten normal cats, but 2 of the cats showed a slight escape from suppression by 8 hours after injection. Intravenous dexamethasone sodium phosphate (DSP), 0.01 and 0.1 mg/kg, produced equivalent reductions of plasma cortisol levels, but suppression was sustained below baseline longer with the higher dosage. Cats with various non-adrenal illnesses have also shown inadequate cortisol suppression after a low-dose (0.01 mg/kg) of DSP. The 0.1 mg/kg dosage of dexamethasone seems to more reliably suppress cortisol levels in normal cats and cats with non-adrenal illnesses. Elevated cortisol levels eight hours post-dexamethasone injection, using the 0.1 mg/kg dosage, appears to be as sensitive a diagnostic test for feline hyperadrenocorticism (8/9; 89%) as the low-dose (0.01 mg/kg) screening test in the dog.