A patient with Cushing's diease with restart of hair growth on Lysoderm therapy.
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Hyperadrenocorticism, increased functional activity of the adrenal cortex, is the primary endocrine disease of older dogs.
Hyperadrenocorticism may be caused by the presence of an adrenocortical tumor or from excessive production of adrenocorticotropic
hormone (ACTH) from the pituitary gland that results in bilateral adrenal gland hyperplasia. Exogenous administration of glucocorticoids
may also result in comparable clinical signs of hyperadrenocorticism. In most cases, adrenocortical tumors of dogs are associated
with excessive adrenal secretion of cortisol, but excessive secretion of other adrenal hormones may also occur.
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.
Truncal alopecia and hyperpigmentation in a Yorkshire Terrier with Cushing's disease.
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Diagnosis of most adrenocortical tumors is usually based on survey radiography, abdominal ultrasonography and/or computed
tomography. About 50 percent of adrenocortical tumors are mineralized and identifiable on survey abdominal radiography. In
those adrenocortical tumors in which mineralization is not seen, the tumors may be seen by abdominal ultrasonography. Computed
tomography may also be used to identify possible adrenal and pituitary masses. In addition, ultrasonography and computed tomography
may be useful to identify metastatic disease and indicate the extent of tumor invasion. Specific endocrine function tests
such as the high-dose and low-dose dexamethasone suppression tests are useful in distinguishing 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.
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