Veterinary Medicine - February 2008 - (Page 108) Hyperadrenocorticism and trilostane PEER-REVIEWED ways to differentiate between PDH and an adrenocortical tumor include measuring endogenous ACTH concentrations (normal or elevated in patients with PDH, low in patients with hyperadrenocorticism due to an adrenocortical tumor) and performing a high-dose dexamethasone suppression test (suppression supports a diagnosis of PDH). Abdominal radiography may reveal calci cation associated with an adrenal mass but is not a sensitive test for this purpose. TABLE 4 Low-dose Dexamethasone Suppression Testing Methodology and Interpretation Test methodology • The patient should be fasted before testing. • Check all samples carefully for hemolysis and lipemia. • Promptly spin and separate serum or plasma before refrigeration. • Obtain a baseline blood sample. • Inject 0.01 mg/kg of dexamethasone intravenously (dilute in 0.9% sodium chloride solution for dosing accuracy). • Collect a second blood sample four hours later. • Collect a third blood sample eight hours later. Test interpretation • An eight-hour cortisol concentration > 1.4 µg/dl is consistent with hyperadrenocorticism. • A four-hour cortisol concentration 1.4 µg/dl supports PDH. Note: • Failure to suppress at four hours does not differentiate adrenocortical tumors from PDH. • Nonadrenal disease can affect the test results. • The results of the low-dose dexamethasone suppression test must be reviewed in light of other findings. Treatment Surgical removal of the affected adrenal gland is the treatment of choice for patients with hyperadrenocorticism caused by an adrenocortical tumor. If the tumor is inoperable, distant metastases are detected, or the patient is an unsuitable anesthetic candidate, medical therapy can be used to control clinical signs. In the United States, medical therapy is the mainstay of treatment of dogs with PDH. But in people, endoscopic removal of the underlying pituitary tumor is the standard of care and is curative. A successful method for hypophysectomy (rather than tumor removal) has been reported in dogs with hyperadrenocorticism, but it requires substantial expertise and is unlikely to be routinely performed.4 Medical therapy controls the signs of hyperadrenocorticism; it does not cure the disease. Lifelong treatment will be necessary, and owners need to commit to regular follow-up examinations. All of the options have side effects or limitations (Table 5), so provide clients with detailed information before initiating treatment.5 Because of negative experiences or poor responses, some veterinarians are reluctant to recommend treatment in dogs with hyperadrenocorticism. Although studies have not documented improved longevity with therapy, the quality of life for both patients and clients appears to be substantially improved if the disease is successfully controlled. Complications from untreated hyperadrenocorticism include hypertension, diabetes mellitus, glomerulopathy, and thromboembolism; effective regulation of cortisol secre- Cholesterol Pregnenolone Progesterone 17 alpha-Hydroxypregnenolone 11-Deoxycorticosterone Dehydroepiandrosterone (DHEA) 17 alpha-Hydroxyprogesterone Corticosterone 11-Deoxycortisol Androstenedione ESTROGENS ANDROGENS ALDOSTERONE CORTISOL 1. The synthesis of steroid hormones. The brown arrows show the site of action of 3-beta-hydroxysteroid dehydrogenase. 108 February 2008 VETERINARY MEDICINE
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