Hyperadrenocorticism offers obstacles in diagnosis, treatment
The clinical signs associated with most cases of canine hyperadrenocorticism are the result of high circulating concentrations of glucocorticoids. Clinical signs include polydipsia, polyuria, polyphagia, abdominal enlargement, hepatomegaly, cutaneous changes (alopecia, cutaneous atrophy, calcinosis cutis, hyperpigmentation, pruritus), muscle weakness, decreased exercise tolerance, excessive panting, truncal obesity, lethargy, weight gain, insulin resistance and decreased sexual function.
About 15 percent of dogs with hyperadrenocorticism have adrenocortical tumors, either the right or left adrenal gland is affected with equal frequency. About 50 percent of adrenocortical tumors are adenomas, whereas 50 percent are carcinomas. Bilateral adrenal neoplasia does uncommonly occur in dogs; concurrent pituitary and adrenal tumors may also occur. Adrenocortical tumors occur most often in middle-aged to older dogs and in those dogs larger than 20 kg in body weight. Dog breeds most commonly affected include Poodles, German Shepherd, Dachshunds, Labrador Retrievers and various Terriers.Adrenocortical tumors Adrenocortical tumors arise spontaneously and are not associated with long-term ACTH stimulation as in pituitary-dependent hyperadrenocorticism. Adrenocortical tumors are usually unilateral and may be adenomas or carcinomas. Most adrenocortical tumors secrete excessive amounts of cortisol that suppresses ACTH concentrations by negative feedback on the pituitary gland and hypothalamus. The unaffected adrenal gland and normal cells in the affected adrenal gland are atrophic from the insufficient stimulation by ACTH. Cortisol secretion from adrenocortical tumors is not a continuous activity but is episodic. In most cases, ACTH receptors are preserved and adrenocortical tumors respond to exogenous administration of ACTH. Cortisol secretion from adrenocortical tumors is not affected by administration of exogenous dexamethasone.
Identifying markers Diagnosis of hyperadrenocorticism in dogs is based on historical and physical examination findings, blood and urine test results (CBC, serum chemistry profile, urinalysis, and urine cortisol-to-creatinine ratio), and specific endocrine function test results (ACTH stimulation test, low-dose dexamethasone suppression test, and possibly high-dose dexamethasone suppression test). The ACTH stimulation test is less sensitive for the diagnosis of adrenocortical tumors and pituitary-dependent hyperadrenocorticism. I prefer the urine cortisol-to-creatinine ratio as an effective screening test and the low-dose dexamethasone suppression test to confirm hyperadrenocorticism. The low-dose dexamethasone suppression test and urine cortisol-to-creatinine ratio are also not able to differentiate between adrenocortical tumors and pituitary-dependent hyperadrenocorticism.
The dog's history, physical examination findings and laboratory test results are not useful in differentiating malignant adrenal tumors from benign adrenal tumors. In general, large adrenocortical tumors that are greater than 50 percent of the size of the adjacent kidney are most likely to be malignant tumors and evidence of vascular or capsular invasion, local extension, or metastasis are also positive predictors of malignancy. Adrenocortical carcinomas usually invade local structures such as kidney, liver, vena cava, aorta, and retroperitoneum and metastasize to the liver and lung.
Ultrasonography of the abdomen serves three useful purposes in suspected cases of hyperadrenocorticism. First, ultrasonography is a part of the complete evaluation of the abdomen for any unexpected abnormalities in older dogs. Second, if an adrenocortical mass (tumor) is identified, ultrasonography is helpful in screening for liver and/or other organ metastasis, tumor invasion of the vena cava or other structures, and compression of adjacent tissues by a tumor. Third, ultrasonography evaluates the size and shape of the adrenal glands. If both adrenal glands are visualized and are relatively equal in size, this is considered strong evidence of adrenal hyperplasia due to pituitary-dependent hyperadrenocorticism. A unilateral abnormally enlarged adrenal mass with an abnormally small to nonvisible contralateral adrenal gland is supportive evidence of an adrenocortical tumor.