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Part I
Cushing’s Disease Is Hard To Diagnose
(cushing’s disease is easy to treat)
Thomas Schermerhorn, VMD, DACVIM(SAIM) Kansas State University Manhattan, Kansas, USA
Overview
- Why test?
- When to test?
- How to test?
- • Will you treatWill you treat??
- How to treat?
CLINICAL SIGNS
- Polyuria
- Polydipsia
- Alopecia
- Pendulous abdomen
- HHepatomegaly t l
- Polyphagia
- Muscle weakness/atropy
- Panting
- Skin signs (comedones, hyperpigmentation, calcinosis cutis)
- Reproductive signs (anestrus, testicular atropy)
Picture at http://www.vetinfo.com/dpcush.html
CLINICAL SIGNS
- Polyuria
- Polydipsia
- Pendulous abdomen
- HHepatomegaly t l
- Panting
- Restlessness
- Suspicion based on incidental findings
Pituitary Dependent Hyperadrenocorticism (PDH)
- Most common form - 85% of cases
- Pituitary tumor overproduces ACTH
- Excess ACTH causes bilateral adrenal hyperplasia
Adrenal Dependent Hyperadrenocorticism (ADH)
- ADH - 15% of cases
- Autonomous production of cortisol (+/- other steroid hormones)
- Adenoma-~50%
- Carcinoma- ~50%
- Malignant
- local extension
- metastasis to liver and lungs
Why test for Cushing’s Disease
WHY
- Address a particular client complaint.
- Paraneoplastic syndrome.
- Prevent sequelae of hyperadrenocorticism.
WHY NOT
- No clinical signs/no client complaint
- Expensive to diagnose and treat.
- Undefined risk of complications - controversial
Diagnosis of HAC
Definitive diagnosis is difficult
- No one test is perfectNo one test is perfect.
- Hypercortisolemia occurs during non-adrenal illness.
- Clinical signs may be present but diagnostics do not support the diagnosis of HAC (aka Atypical Cushings Disease) Atypical Cushing's Syndrome in Dogs: Arguments For and Against Behrend EN , Vet Clin N Amer Small Anim Pract. 2010 Mar;40(2):285-296.
2-Step Diagnostic Approach
Screening Tests – confirm adrenal hypersecretion
- Urine cortisol:creatinine ratio (UCCR)
- Low dose dexamethasone suppression test (LDDST)
- ACTH stimulation test
- Combination of ACTH stim test + LDDS test
- • Baseline cortisol concentrationBaseline cortisol concentration – not recommendednot recommended.
- Determine GC-induced ALP isoform– not recommended.
Differentiating tests – distinguish PDH and ADH
- Adrenal US (other diagnostic imaging)
- Endogenous ACTH
- High dose dexamethasone suppression test (HDDST)
STEP 1 - Screening Tests
Screening Tests
Urine Cortisol:Creatinine Ratio (UCCR)
- Test principle – Excessive hormone secretion •Useful for identifying affected dogs (sensitive test)
- Normal result virtually rules out HAC
- Abnormal result requires additional screening test (e.g. LDDS).
Screening Tests
Low Dose Dexamethasone Suppression Test
- Test principle – impaired negative feedback
- Effective screening test.
- Can be a differentiating test
- Stress/Nonadrenal illness = false + (less sensitive)
Screening Tests
ACTH Stimulation Test
- Test principle – Adrenal secretory capacity
- Good choice if non-adrenal illness is suspected
- Generally considered more Specific than LDDS
- Cannot distinguish between PDH and AT
STEP 2 - Differentiation Tests
Only after HAC has been confirmed using a screening test
Abdominal Ultrasound
Doesn’t assess function – possible misdiagnosis
PDH
- Bilateral adrenal hypertrophy
- Normal and hypertrophied glands overlap in sizesize
ADH
- Unilateral adrenal enlargement
- Nodular change
- Atrophy of contra-lateral gland
Dia = 0.67 cm
High Dose Dexamethasone Suppression Test (HDDST)
Dexmethasone dose 10X LDDST
- Suppress – PDH
- No Suppression – AT
- Di ti i h PDH ADH (70%)
Misleading test if dog has not been properly screened Only dogs with HAC should be tested.
No PDH escape
- Distinguishes PDH vs.ADH (70%)
- 30% PDH – no suppression
- Only rare AT suppress (incomplete)
