Diagnosis: Tentative diagnosis is hyperadrenocorticism (cushing disease) based on the typical presenting signs. Click here to see image of the case from merck vet manual site.
DDx: Hypothyroidism, diabetes mellitus, renal diseases and other causes of PU/PD.
Low Dose Dexamethasone Suppression Test (LDDS):
Basal cortisol: 5.1 µg/dL
4-hour post test: 2.2 µg/dL
8-hour post test: 6.5 µg/dL [<1.0>
These values indicate the hyperadrenocorticism, but to differentiate the adrenal tumor from pituitary dependent hyperadrenocorticism (PDH) we need to perform HDDS test.
High Dose Dexamethasone Suppression Test (HDDS):
Basal cortisol: 4.8 µg/dL
8-hours post test: 0.8 µg/dL [<1.0>
(The ACTH stimulation test is a screening test for diagnosis of hyperadrenocorticism, but was not done in this case.)
Definitive diagnosis: Pituitary dependent hypheradrenocorticism.
Mitotane is a commonly used drug in hyperadrenocorticism. Ketoconazole can be used in dogs which are unable to tolerate mitotane at the required dose.
This patient was started on 60 mg of Trilostane (Vetoryl®) once daily and his status will be monitored with an ACTH stimulation test in 1-2 weeks time. If he has still not achieved a hypoadrenal response at this time or has achieved a response but is still exhibiting clinical signs, we can consider increasing his dose or increasing to a BID regime. After achieving therapeutic stability, the patient should have an ACTH stimulation test every 3-4 months to monitor cortisol response to therapy.
Trilostane tends to be better tolerated by dogs. Trilostane is a competitive inhibitor of 3-β-hydroxysteroid dehydrogenase. This enzyme mediates the conversion of pregnenolone to progesterone in the adrenal gland, with the net effect being inhibition of cortisol production.
With PDH treatment, it is important to achieve a hypoadrenal response but avoid the complete adrenal suppression to a point that glucocorticoids and mineralocorticoids are deficient. Specifically, mineralocorticoid deficieny and hypoaldosteronism have the deleterious effects of cardiac disturbances (due to hyperkalemia and hyponatremia), hypovolemia and hypotension.
Labels: cushing disease, Hyperadernocoticism, PDH