Today's Veterinary Practice

JAN-FEB 2016

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tvpjournal.com | January/February 2016 | Today's VeTerinary PracTice canine PiTuiTary dePendenT HyPeradrenocorTicism series Peer reviewed 39 » Does not appropriately suppress ACTH secretion (therefore does not suppress cortisol) when a low dose (0.01 mg/kg) is administered » In 75% of dogs with PDH, ACTH and cortisol concentrations decrease when a high dose (0.1 mg/kg) is administered » In 25% of dogs with PDH, suppression of ACTH and cortisol does not occur even after administration of higher dosages; in these patients, a large pituitary tumor or a tumor developing from the pars intermedia is more likely. A description of how to perform dexamethasone suppression tests is outlined in Table 4. The largest study evaluating both suppression tests—LDDS and high-dose dexamethasone suppression (HDDS)— included dogs with PDH (n = 181) and ATs (n = 35). 2 With LDDS, criteria for identifying dogs with PDH included: • 4-hour post LDDS cortisol concentrations below laboratory cutoff or < 50% of basal cortisol concentration • 8-hour post LDDS cortisol concentrations < 50% of the basal cortisol concentration and greater than the laboratory cutoff. With HDDS, criteria for cortisol suppression were a 4- and/or 8-hour cortisol concentration below the laboratory cutoff or < 50% of the basal cortisol concentration. Approximately 75% of dogs with PDH met at least one criterion for suppression on either LDDS (88%) or HDDS (12%). 2 Dexamethasone resistance (ie, no criteria were met) occurred in all dogs with AT and the remainder (25%) of the dogs with PDH. 2 In another study of 41 dogs with ATs, 28 LDDS and 30 HDDS tests were performed, with no suppression seen on any test. 2,30 In dogs demonstrating lack of suppression with LDDS, use of endogenous ACTH rather than HDDS is recommended to differentiate PDH from ADH. Since suppression in response to dexamethasone supports a diagnosis of PDH, a dog with dexamethasone resistance can have either AT or PDH. Table 4. Diagnostic Tests That Differentiate Between PDH and ADH TEST COMPONENTS PROCEDURES RESULTS Low-Dose Dexamethasone Suppression a Dexamethasone sodium phosphate or polyethylene glycol: 0.01–0.015 mg/kg IV b Obtain blood samples: 1. Before administration 2. 4 H after administration 3. 8 H after administration • With LDDS, suppression to < 50% baseline in a dog with HAC confrms PDH. • If no suppression with LDDS, cACTH measurement or abdominal ultrasound is recommended. • With LDDS or HDDS, lack of suppression does not confrm AT (approximately 25% of dogs with PDH fail to suppress). High-Dose Dexamethasone Suppression a Dexamethasone sodium phosphate: 0.1 mg/kg IV c Endogenous ACTH cACTH 1. Collect blood into chilled, silicone- coated glass or plastic EDTA tubes. 2. Centrifuge within 15 min (ideally cooled centrifuge). 3. Transfer plasma to plastic tubes and freeze immediately; samples must stay frozen until analysis. d Normal or elevated concentrations are consistent with PDH, while suppressed values are consistent with AT. a. LDDS and HDDS results cannot be considered 100% absolute; when imaging and endocrine test results confict, the latter should be given preference. b. Calculate dose using parent compound. c. For HDDS, avoid the free alcohol form. d. Addition of the protease inhibitor aprotinin prevents ACTH degradation by plasma proteases and greatly facilitates sample handling. Check with your laboratory regarding suitability because, with some assays (ie, Immulite), aprotinin introduces an artifactual decrease in results. Evaluation of the pituitary-adrenal axis is indicated in the following circumstances: ` Patients with clinical signs and laboratory findings consistent with PDH and in which nonadrenal illness has been ruled out or is well controlled. ` Patients in which an adrenal/pituitary mass or bilateral adrenal hyperplasia has been discovered in conjunction with compatible clinical signs. ` Patients with an incidentally discovered adrenal mass, with adrenalectomy being considered. ` Diabetic dogs with insulin resistance. Evaluation of the Pituitary– Adrenal Axis

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