Testing for Addison's disease - DVM
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Testing for Addison's disease
Gender, age and breed are key determining factors in diagnosing hypoadrenocorticism


DVM360 MAGAZINE


Na:K ratio

The Na:K ratio usually is low in dogs with hypoadrenocorticism. This ratio may be useful to determine the likelihood of hypoadrenocorticism and plan emergency diagnosis and treatment while waiting for definitive test results.

Use of an Na:K ratio cut-off of <27 or 28 for predicting a diagnosis of hypoadrenocorticism resulted in correct classification of disease state 95 percent of the time in a retrospective study of 76 dogs with hypoadrenocorticism and 200 dogs with other disorders.

It is important to remember, however, that this ratio is useful only in dogs that have electrolyte changes. As discussed above, electrolyte concentrations and therefore the Na:K ratio may be completely normal in dogs with both primary and secondary hypoadrenocorticism.

Imaging studies

Most untreated dogs with hypoadrenocorticism have one or more radiographic abnormalities on thoracic and abdominal radiographs, including microcardia, small cranial lobar pulmonary artery, narrow posterior vena cava or microhepatica. These changes reflect the degree of hypovolemia; therefore, they are more likely to be present in dogs with electrolyte abnormalities.

Some dogs may have evidence of megaesophagus. Most with hypoadrenocorticism have a measurable reduction in size of the adrenal glands, and sometimes the adrenal glands cannot be identified on ultrasound study. There is overlap, however, with the adrenal size of normal dogs. The presence of small adrenal glands on ultrasound study, although supportive of a diagnosis of hypoadrenocorticism, is not adequate for confirmation.

Electrocardiogram

In dogs with hyperkalemia, abnormalities may be present on the electrocardiogram. These include a peaked T-wave and shortening of the QT interval in mild hyperkalemia, widening of the QRS complex, decreased QRS amplitude, increased duration of the P wave, increased P-R interval in moderate hyperkalemia and loss of P waves and ventricular fibrillation or asystole in severe hyperkalemia.

Basal cortisol

Measurement of a basal cortisol concentration is not adequate for confirmation of a diagnosis of hypoadrenocorticism, because some normal dogs have a low basal cortisol concentration but have an appropriate response to ACTH administration.

Measurement of a basal cortisol of >2 mcg/dl had a negative predictive value of 100 percent in a study of 123 dogs evaluated for hypoadrenocorticism. Thus, a basal cortisol of >2 mcg/dl is a useful test to exclude a diagnosis of hypoadrenocorticism.

ACTH stimulation test

An ACTH stimulation test is necessary to confirm a diagnosis of hypoadrenocorticism because not all dogs with hypoadrenocorticism have the expected electrolyte changes, and because many other disorders may mimic the characteristic findings of Addison's disease.

It is acceptable to base emergency treatment upon a tentative diagnosis (based on electrolyte abnormalities); however, an ACTH stimulation test always should be performed prior to initiating long-term treatment.

For an ACTH stimulation test, synthetic ACTH (cosyntropin) at a dose of either 250 mcg per dog or 5 mcg per kg IV is recommended, with the second sample for measurement of cortisol collected one hour after administration of ACTH. The lower-dose 5 mcg/kg has been evaluated in both normal dogs and in dogs with suspected hypoadrenocorticism. Studies have confirmed that these two doses result in an equivalent increase in cortisol concentration.

Equivalent responses to cosyntropin have been reported with the IV and IM administration routes. One dose of dexamethasone can be administered before an ACTH stimulation test if clinically indicated. Cosyntropin can be reconstituted and frozen at-20 C in plastic syringes for six months with no adverse effects on bioavailability.

Use of compounded ACTH is an acceptable choice for performing the ACTH stimulation if cosyntropin is unavailable; however, potential variability between compounding pharmacies makes this a less-than-ideal choice.

In dogs with hypoadrenocorticism, both the pre-and post-ACTH cortisol concentrations usually are less than 1 mcg/dl, and both values should be less than the reference range for basal cortisol (usually 2 mcg/dl) to confirm the diagnosis. It is important to use the protocol and reference range established by the laboratory being used for cortisol testing.

Although there usually is a clear distinction between the response to ACTH in a dog with hypoadrenocorticism and that of a dog with adequate adrenal reserve, sometimes borderline results can occur (post-ACTH cortisol concentrations between 2 and 6 mcg/dl).

Other causes of inadequate response to ACTH stimulation include prior glucocorticoid administration (other than recent use of IV dexamethasone), mitotane, trilostane or ketoconazole administration, loss of activity of the ACTH product administered and errors in administration of ACTH.

Rarely, dogs with sex-hormone-secreting adrenal tumors will have a flat-line response to ACTH stimulation; however, these dogs usually have overt signs of hyperadrenocorticism. Interpretation of such test results is difficult if no other underlying cause of adrenal suppression can be identified.

It is possible that dogs with progressive loss of adrenal function initially may have borderline results, but this currently is poorly documented. Whether inadequate adrenal reserve in a dog with another underlying disease can contribute to clinical signs also is not established.

Recommendations for further evaluation in this situation include repetition of the ACTH stimulation test and measurement of concurrent ACTH concentration. Measurement of aldosterone and renin activity also might be useful in dogs with electrolyte abnormalities.

Whether dogs with apparent inade-quate adrenal reserve benefit from administration of glucocorticoids is unknown.


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