Adrenal disease in cats (Proceedings)
Although only recently discovered, feline adrenal disorders are becoming increasingly more recognized. Feline adrenal disorders include diseases such as hyperadrenocorticism (Cushing's syndrome) and hyperaldosteronism (Conn's syndrome). The clinical signs of feline hyperadrenocorticism, which include unregulated diabetes mellitus and severe skin atrophy, are unique to the cat. Other signs of feline hyperadrenocorticism, such as potbellied appearance, polydipsia, polyuria, and susceptibility to infections are also seen in dogs with hyperadrenocorticism. Conn's syndrome has only recently been described in the cat and is in fact more common in cats than in dogs. Characterized by severe hypokalemia, hypertension, and muscle weakness, Conn's syndrome may be misdiagnosed as renal failure. The clinician should become familiar with the clinical signs of adrenal disorders in cats and the common diagnostic tests used to diagnose and treat these syndromes.
Feline Cushing's syndrome (FCS) is a disorder of excessive cortisol secretion by the adrenal glands. FCS is most often caused by a pituitary adenoma with subsequent corticotrophic hyperplasia and excess adrenocortical cortisol secretion. Also found in cats with FCS are autonomously functioning benign adenomas or malignant adrenal carcinomas. Iatrogenic FCS due to glucocorticoid administration is rare in cats. Differential diagnoses include diabetes mellitus, insulin resistance, acromegaly, hepatopathy, renal disease, sex hormone-secreting adrenal tumors, and yperthyroidism.
Pituitary-dependent hyperadrenocorticism (HAC) is usually a disease of the middle-aged to older cat. There is a slight difference in sex distribution in feline HAC; female cats are slightly more likely to develop the disease than males. No breed predilection has been found.Feline HAC is usually (80%) accompanied by diabetes mellitus (DM). The most common clinical signs associated with HAC in cats are insulin-resistant DM, cutaneous atrophy, polydipsia, polyuria, polyphagia, lethargy, abdominal enlargement or potbelly, panting, obesity, muscle weakness, and recurrent upper respiratory and urinary tract infections. On physical examination, the most commonly noted abnormalities include abdominal enlargement, hepatomegaly, bilaterally symmetric alopecia, cutaneous atrophy with open sores, and seborrhea. Lethargy (dullness) has been reported due to muscle weakness or the effects of a pituitary mass. Excess sex hormones, such progesterone, have also been identified in cats with FCS.
In the dog, the most common serum chemistry abnormality observed in association with HAC is an increased serum alkaline phosphatase activity (ALP), which is high in most dogs. However, in the cat serum ALP is not elevated because of hypercortisolemia but rather is a result of poorly regulated concomitant DM. This occurs because cats lack the glucocorticoid-induced isoenzyme for ALP. High serum alanine transferase activity (ALT), hypercholesterolemia, hyperglycemia, and low blood urea nitrogen (BUN) are also common findings. The hemogram may reveal a mild erythrocytosis as well as a classic "stress leukogram" (i.e., eosinopenia, lymphopenia, and mature leukocytosis).
Although in dogs with HAC, the urine specific gravity is usually less than 1.015, cats often show concentrated urine specific gravity (>1.030) despite profound polydipsia and polyuria resulting from the concurrent DM. Finally, many cats with HAC have evidence of urinary tract infection without pyuria (positive culture), bacteriuria, and proteinuria resulting from glomerulosclerosis.
The urine cortisol: creatinine ratio (UCCR) is a simple and valuable screening test for HAC in cats. To perform this test, the owner is instructed to collect morning urine samples from an empty litter box at the same time of day on two to three consecutive days. Special precautions are needed for the urine collection itself (no contamination with litter) and the urine samples should be kept refrigerated. This home-collection protocol avoids the "stress" of a visit to the veterinary clinic.
The low-dose dexamethasone suppression test is considered by many to be the test of choice for the diagnosis of HAC in cats. It requires 10 times the dose used in dogs or 0.1 mg/kg IV. Plasma is obtained for cortisol concentrations before, 4 hours after, and 8 hours after dexamethasone administration. If the low dose of dexamethasone (0.1 mg/kg) fails to adequately suppress circulating cortisol concentrations in a cat with compatible clinical signs, this is consistent with a diagnosis of HAC. Normal cats and cats with nonadrenal illness will show adequate suppression of serum or plasma cortisol at 4 and 8 hours post dexamethasone administration. However, in contrast to dogs with pituitary dependent hyperadrenocorticism (PDH), many cats with PDH will not suppress at 4 hours and a few cats will suppress at 8 hours after dexamethasone administration.
The corticotropin ACTH stimulation test, mainly a test of adrenal reserve, requires little time, is easy to interpret, and can be used to document iatrogenic HAC. Only 50 to 60% of cats with HAC have an exaggerated response to ACTH administration. The preferred method for ACTH stimulation testing in cats is to determine serum cortisol concentrations 30 minutes before and 1 hour after the intravenous or intramuscular injection of cosyntropin.