There are several manifestations of adrenal disease in cats, ranging from hypoadrenocorticsm to several forms of hyperadrenal activity. All are considered relatively rare, but it is possible that we may discover some more frequently if we have a higher index of suspicion.

Hypoadrenocorticism

Primary hypoadrenocorticism has been reported in few cats, but does occur spontaneously. It has been seen as idiopathic atrophy of the adrenal glands, similar to that of dogs. It has also been diagnosed in association with other illness such as trauma and lymphoma. It is also possible to see iatrogenic hypoadrenocorticism with rapid withdrawal of glucocorticoids although cats are considered to be relatively resistant to this. Relative adrenal insufficiency associated with sepsis is controversial, but has been reported recently in cats.

Routine laboratory testing has revealed anemia, lymphocytosis, eosinophilia, hyperkalemia, hyponatremia, evidence of renal dysfunction with dilute urine. On thoracic radiographs, changes associated with dehydration may be noted (microcardia). EKG changes may be reflective of the presence of hyperkalemia.

Diagnosis is by ACTH stimulation test. Results showing lack of stimulation would be consistent with the diseases.

Therapy for hypoadrenocorticism is similar to that in dogs, including therapy for shock and supplementation of glucocorticoids and mineralocorticoids. Spontaneous atypical hypoadrenocorticism (hypocortisolism alone) has not been reported in cats. Long-term survival is considered to be excellent, with dedicated owners.

Hyperadrenocorticism (HAC)

Hypercortisolemia

Feline hyperadrenocorticism is a rare disease of excessive cortisol secretion by the adrenal glands. Most often this is caused by a pituitary adenoma (80%), but also may be adrenal dependent (20%). It is usually seen in middle aged to older cats with females slightly more likely to develop the disease. The disease usually involves concurrent diabetes mellitus. The most common clinical signs are insulin resistant diabetes mellitus, cutaneous atrophy, polydipsia, polyuria, abdominal enlargement, muscle weakness, recurrent infections. On physical exam the most common abnormalities include abdominal enlargement, alopecia, and thin skin with wounds.

Routine diagnostic testing reveals elevated alanine aminotransferase (ALT), hyperglycemia, hypercholesterolemia and low blood urea nitrogen. A hemogram may reveal erythrocytosis and stress leukogram. A urinalysis may appear to be concentrated due to the concurrent glycosuria.

Screening tests that can be used are the Urinary cortisol to creatinine ratio (UCCR), ACTH stimulation test, and Low dose dexamethasone suppression test. A normal UCCR has value in ruling out the disease, but an elevated result must be confirmed by further testing. ACTH stimulation tests have a low sensitivity, with only 50-60% of cats with HAC having exaggerated responses. Many cats will have a low response. There is some controversy amongst veterinary endocrinologists, but low dose dexamethasone testing is considered to be the test of choice, by some, for diagnosis of HAC in cats.

Differentiation tests include High dose dexamethasone suppression test, endogenous ACTH concentration and abdominal ultrasonography. Magnetic resonance imaging or computed tomography can be used to image either the adrenal or pituitary glands.

Medical therapy has generally been considered to be unsuccessful. Mitotane, which is cytotoxic to adrenocortical cells, has generally been ineffective in cats. Trilostane has been reported in several cats, and has had moderate effectiveness. It inhibits 3B-hydroxysteroid dehydrogenase, and can actually increase levels of some of the intermediary hormones. The significance of this is unknown at this time. The dose generally initiated in cats is 30 mg by mouth once per day, and adjusted from there. Other therapeutic options include pituitary radiation, hypophysectomy, or bilateral adrenalectomy. The prognosis is guarded to grave.