Background: Feline Cushing’s syndrome (FCS) is a disorder of excessive cortisol secretion by the adrenal glands and is rare
in cats. The most frequently observed clinical signs are polyuria, polydipsia, and polyphagia which are also consistent with
diabetes mellitus. These diabetic cats are often insulin resistants. The dexamethasone suppression test is considered the test of
choice for the diagnosis of hyperadrenocorticism. The majority of cats with naturally occurring Cushing’s syndrome have
pituitary-dependent hyperadrenocorticism and it is caused by functional microadenoma or macroadenoma pituitary. Computed
tomography or magnetic resonance imaging is helpful in diagnosis of pituitary tumors. Treatments of pituitary-dependent
hyperadrenocorticism include surgery of the pituitary or adrenals, radiation of the pituitary, and medical therapies. Bilateral
adrenalectomy continues to represent the best long-term therapeutic strategy until hypophysectomy becomes more widely
available. This paper reports a cat with macroadenoma pituitary causing hiperadrenocorticism and insulin resistance.
Case: A 12-year-old female castrated Brazilian shorthair cat was referred to the veterinary due to polyuria, polydipsia, weight
loss and polyphagia. The presence of hyperglycemia (blood glucose >250 mg/dl), glucosuria and elevated fructosamine
concentration revealed diabetes mellitus. Insulin therapy was introduced but the glycemia was poorly controlled despite the
high dose of insulin. Concomitant disease was suspected. Abdominal ultrasonography revealed bilaterally enlarged adrenals.
The dexamethasone suppression test showed pituitary-dependent hyperadrenocorticism. Computed tomography or hypophysectomy
wasn‘t available. Medical therapy with mitotane was introduced but anorexia and vomiting developed. Bilateral
adrenalectomy was performed without complications and histological evaluation of adrenal revealed hyperplasia. After
surgery, treatment with mineralcorticoids and glucocorticoids was introduced. The cat had resolution of clinical signs and
insulin requirements were decreased. According to the owner, three weeks after surgery, the cat showed abnormal behavior,
compulsive walking and circling. The cat died eight months after bilateral adrenalectomy. A complete necropsy was performed
and histopathological examination confirmed the pituitary macroadenoma.
Discussion: Insulin resistance should be suspected in diabetic cat if control of glycemia is poor despite the high insulin
dosage. Clinical signs related to poorly controlled diabetes mellitus are common in cats with hyperadrenocorticism.
Hyperadrenocorticism can cause severe insulin resistance and it is often associated with a pituitary macrotumor. Pituitary
tumors may lead to hypercotisolism. Bilateral adrenalectomy is a viable alternative to transphenoidal hypophysectomy for
treatment of feline pituitary-dependent hyperadrenocorticism when hypophysectomy is not available. Neurological signs can
be a result of pituitary tumors and they can get worse after the adrenalectomy because of the enlargement of the tumor. Despite
of clinical signs, the cat had improved in response to the bilateral adrenalectomy and had a good quality of life during eight
months after surgery.
