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7 Pituitary-Dependent Hyperadrenocorticism in Dogs and Cats 53

polyuria and polydipsia or alopecia), absent clinical signs, Baseline Diagnostics
VetBooks.ir or unusual isolated manifestations of the disease. In all patients being screened for PDH, the following ini­

tial diagnostics should be performed prior to endocrine
Diagnosis diagnostics.
Thorough history including prior treatment with sys­
●
Diagnosis of PDH requires incorporating information temic or topical glucocorticoids.
from the history, physical examination, and routine labo­ Physical examination.
ratory tests. Specific endocrine tests and imaging modal­ ● Complete routine database, including complete blood
ities are available to diagnose hyperadrenocorticism ● count, serum biochemical profile, urinalysis, urine
(HAC) and distinguish between the various causes of culture, and blood pressure.
hypercortisolism. No single test is perfect and if the ini­
tial screening test is negative and high clinical suspicion These diagnostics are important as the clinical signs of
of HAC exists, additional tests should be performed. PDH are rarely pathognomonic, and patients are gener­
Endocrine evaluation of patients with HAC and nonad­ ally older and may have co‐morbidities, which affect
renal illness can be difficult, and it is important to elimi­ endocrine function tests and impact therapeutic options
nate or manage the concurrent illness before undertaking and prognosis.
adrenal function tests. If a patient has a concurrent serious illness, postpone
testing until the illness or injury has resolved or been
ACVIM Consensus Statement controlled to minimize false‐positive test results.
In 2012, the American College of Veterinary Internal Endocrine Diagnostics
Medicine (acvim.org) issued a consensus statement
addressing the diagnosis of spontaneous canine hyper­ Specific endocrine tests and imaging modalities are
adrenocorticism, which provides a thorough review of the available to both diagnose PDH and distinguish between
diagnostic approach to patients with PDH and addresses the various causes of HAC (Tables 7.1 and 7.2). No single
many common clinical concerns. Access this statement test is perfect and if the initial screening test is negative
at onlinelibrary.wiley.com/doi/10.1111/jvim.12192/epdf. and high clinical suspicion of PDH exists, additional

Table 7.1 Diagnostic tests to evaluate patients with suspected PDH

Test Components Procedures Results

Low‐dose Dexamethasone sodium Obtain blood samples: Consult with your reference
dexamethasone phosphate or 1) Before administration laboratory for specific
suppression polyethylene glycol: 2) 4 h after administration reference ranges
a
(LDDS) 0.01–0.015 mg/kg IV 3) 8 h after administration
(dog), 0.10 mg/kg IV (cat)
ACTH Cosyntropin or Obtain blood samples: Consult with your reference
stimulation tetracosactrin: 1) Before administration laboratory for specific
5 μg/kg IV or IM (dog), 2) 60 min after administration reference ranges
0.125 mg IV (cat)
Urine cortisol to Urine collected from dog Have owner collect urine at home for at Consult with your reference
creatinine ratio in the morning c least 2–3 consecutive mornings; submit laboratory for specific
(UCCR) b an aliquot of the pooled samples to reference ranges
diagnostic laboratory
a Calculate dose using parent compound.
b High UCCRs in dogs without a high degree of clinical suspicion of hyperadrenocorticism should be interpreted cautiously.
c Urine collected by the owner is less likely to be influenced by stress; in addition, morning urine is preferred because it usually represents several
hours of urine production.
Notes:
● The effect of feeding on LDDS or ACTH stimulation test results is unknown; however, feeding during these tests is not recommended. Fasting
before testing is not necessary unless lipemia affects the cortisol assay results (check with your laboratory for specific details).
● In veterinary medicine, the ability of glucocorticoids, progestagens, and ketoconazole to suppress cortisol secretion is known. However, no effect
on LDDS, ACTH stimulation, or UCCR has been documented in dogs treated with phenobarbital.
ACTH, adrenocorticotrophic hormone; IM, intramuscular; IV, intravenous.