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Diagnosis of Hyperadrenocorticism

David Bruyette United States

A.   History and clinical signs

B.   R/O iatrogenic disease with questions concerning current or past medications

These medications can include oral medications, ophthalmic and otic preparations, and topical medications. Steroids are everywhere and in everything! Make sure the owner tells you about everything and anything that went on or in their pet.

C. Laboratory data

1. Hemogram

A.   Polycythemia (PCV 45-55%)

B.   Stress leukogram

1. Lymphopenia

2. Eosinopenia

3. Neutrophilia (mature)

2. Biochemistry profile

A.   Elevations in:

1. Serum alkaline phosphatase (SAP)

2. Cholesterol

3. Serum alanine aminotransferase (ALT)

4. Fasting blood glucose: diabetes in 5-10%

3. Thyroid function tests

A.   T3 and T4 basal levels are generally decreased

B.   Response to TSH parallels normal

C.   Secondary to negative feedback of cortisol on pituitary

D.   Does not require thyroid supplementation

4. Blood pressure: Many are hypertensive, cause unknown

A.   Recent study demonstrated normal or decreased levels of atrial natriuretic factor (ANF) in dogs with hyperadrenocorticism. Argues against hypervolemia as the etiology of the hypertension.

5. Urinalysis

A.   Decreased urine specific gravity

B.   Proteinuria

D. Radiographic abnormalities

1. Thoracic films

A.   Bronchial calcification

B.   Metastases from adrenal adenocarcinoma

2. Abdominal films

A.   Hepatomegaly

B.   Osteopenia

C.   50% of adrenal tumors are calcified

D.   Subcutaneous calcification

E. Adrenal function tests

1. Three tests used to diagnose hyperadrenocorticism. They may not differentiate between pituitary vs. adrenal disease.

A.   ACTH stimulation test

1. Look for exaggerated cortisol response in response to ACTH

2. See protocols at the end of this discussion

3. Diagnostic in 85% of pituitary-dependent cases (PDH)

4. Diagnostic in 69% of adrenal tumors (AT)

5. Overall accuracy 80-85 %

6. A suppressed response to ACTH in animals with clinical signs of hyperadrenocorticism indicates iatrogenic disease

B.   Low-dose dexamethasone suppression test

1. Low doses of steroids inhibit ACTH release from the pituitary via negative feedback and decrease plasma cortisol concentrations in normal dogs

2. Dogs with Cushing's are more resistant to steroid suppression. Therefore, lack of suppression following dexamethasone = hyperadrenocorticism.

3. Diagnostic in 95% of PDH

4. Diagnostic in 100% of AT

5. Overall 90-95%

6. See protocols

C.   Urine cortisol/creatinine ratio

1. Assessment of cortisolproduction and excretion rate

2. Sensitivity of this test is greater than that of the LDDS (I.e. some animals with clinical signs of hyperadrenocorticism may have normal LDDS XE "Dexamethasone: low dose suppression test"  response tests but elevated urine cortisolto creatinine ratios). Used as a screening test.

3. Test is easy to perform

4. As with all adrenal function tests, elevated results may occur in animals with non-adrenal disease

5. Positive tests confirmed with a LDDS

2. Tests to differentiate PDH from AT (performed after confirming diagnosis of hyperadrenocorticism).

A.   High-dose dexamethasone suppression test

1. With PDH, a high dose of steroids results in a decrease in ACTH release from the pituitary and a decrease in plasma cortisol

2. With AT, the tumor secretes cortisol autonomously thereby suppressing ACTH production. With low ACTH concentrations already present, dexamethasone has no effect on plasma cortisol.

3. 70% of patients with PDH suppress plasma cortisol to less than 50% of the pre-treatment value

4. 100% of patients with AT do not suppress

5. Therefore: Suppression = PDH Lack of suppression = Inconclusive

6. See protocol

B.   Endogenous ACTH concentration

1. PDH: Levels normal or high

2. AT: Levels low to undetectable

3. Contact lab regarding sample handling and collection. Available at only a few labs. Use of a preservative (Aprotinin XE "Aprotinin" ) may allow for greater utilization of this test.

4. Excellent method to differentiate PDH from AT

Testing Protocols

These suggested protocols are used in the evaluation of patients with hyperadrenocorticism. You must use the protocol and normal values from the laboratory to which you are submitting samples to properly evaluate endocrine tests.

1. ACTH Stimulation Test

A.   Synthetic ACTH (Cortrosyn) 0.25 mg IM; collect serum at zero and one hour, or

B.   ACTH gel (Cortigel) 2.2 U/kg IM; collect serum at zero and two hours.

C.   Hyperadrenocorticism if post-cortisol > 20 ug/dl (530 nmol/L)

2. Low-Dose Dexamethasone Suppression Test

A.   8 am: Baseline serum cortisol. Administer 0.01 mg/kg dexamethasone sodium phosphate IV

B.   12 p.m: Collect 4 hour post-dexamethasone cortisol

C.   4 p.m: Collect 8 hour post-dexamethasone cortisol

D.   In normal animals cortisol suppresses to less than 1.0 ug/dl (27.5 mmol/L) at 8 hours

E.   50% or greater suppression at either four or eight hours together with lack of suppression at eight hours is diagnostic for PDH and a HDDS test is not necessary

3. Urine Cortisol/Creatinine Ratio

A.   Submit urine sample (free catch, cysto, etc.)

B.   First morning urine sample is preferred

C.   Stable at room temperature or refrigerated for three days

D.   Normal range 2.8–4.8. A normal result effectively rules-out hyperadrenocorticism an abnormal result should be confirmed with a LDDS

4. Differentiating PDH From AT

A.   Low-Dose Dexamethasone Suppression Test

1. See above.

B.   High-Dose Dexamethasone Suppression Test

1. 8 a.m: Obtain serum cortisol. Administer 0.1 mg/kg dexamethasone sodium phosphate IV

2. 4 p.m: Collect post-dexamethasone cortisol.

3. Suppression defined as greater than a 50% reduction of cortisol

4. Suppression = PDH, non-suppression = Inconclusive

C.   Endogenous ACTH Concentration

1. Check with lab on sample collection and handling

2. Normal: 20-100 pg/ml (4.4-22.0 pmol/L)

3. PDH: 40-500 pg /ml (8.8-110 pmol/L)

4. AT: < 20 pg/ml (<4.4 pmol/L)

5. Many labs now offer ACTH testing using EDTA tubes containing aprotonin (Trasylol). This eliminates the complicated sample handling requirements that previously existed.

Diagnostic imaging can facilitate differentiation of PDH from AT when screening tests and clinical findings suggest hyperadrenocorticism. Approximately half of canine adrenal tumors are mineralized and can be recognized radiographically. Abdominal radiographic findings in dogs with hyperadrenocorticism included hepatomegaly and obesity. Ultrasonographic evaluation of adrenal size and morphology has been described for dogs and cats. Nonfunctional adrenal tumors can be incidental findings in humans undergoing abdominal imaging. The incidence of “silent” adrenal masses in the dog is unknown. The presence of unilateral adrenomegaly or distortion of adrenal architecture in an animal suspected of hyperadrenocorticism is strong evidence of AT. In addition, imaging can very helpful when contemplating surgical removal or an adrenal mass or pituitary. Abdominal computerized tomography (CT) and magnetic resonance imaging (MRI) are available at several veterinary institutions, and may offer improved resolution for the detection of adrenal and pituitary tumors or hyperplasia. It is best to use imaging in conjunction with endocrine testing to arrive at the most accurate diagnosis.

Notes


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