Veterinary Medicine - February 2008 - (Page 115) Hyperadrenocorticism and trilostane PEER-REVIEWED No adverse effects were noted, and it was concluded that the hair growth was related to downregulation of adrenal steroid synthesis or inhibition of estrogen receptors within the hair follicles themselves.24 Three affected Alaskan malamutes showed similar positive re- sponses when given 3 mg/kg trilostane twice daily.25 Treating atypical hyperadrenocorticism Atypical hyperadrenocorticism is a recently described disorder in which pa- tients manifest clinical signs suggesting hyperadrenocorticism, but the diagnosis is not supported by the results of standard screening tests (an ACTH stimulation test and a low-dose dexamethasone suppression test).26 If detailed steroid pro les are performed (e.g. University A case example of trilostane treatment for canine PDH Lady, a spayed female Old English sheepdog, received a diagnosis of PDH at the age of 9 and was initially treated with mitotane at a private referral practice in Virginia. However, her response to therapy was poor, with persistent signs of hyperadrenocorticism. Despite repeated periods of induction therapy, her post-ACTH cortisol concentration stayed over 15 µg/dl. A deliberate attempt to destroy the adrenal cortices using high doses of mitotane for a prolonged period (nonselective adrenocorticolysis treatment protocol) was unsuccessful. After six months of treatment, she was profoundly cushingoid (Figure A), and her owners were considering euthanasia. Trilostane therapy was discussed, and the FDA granted approval for a three-month supply. Lady began receiving trilostane at a dose of 120 mg orally once a day. At a check-up on day 10, she was doing well, and her post-ACTH stimulation cortisol concentration was 5.3 µg/dl. Within four weeks, she had dramatically improved; her thirst was normal, and her energy level increased. New hair growth was evident on her trunk, and she was able to get up onto the sofa at home. At the six-month evaluation, Lady was clinically normal (Figure B). Her coat was thick, and she was active and energetic. Her post-ACTH stimulation cortisol concentration remained between 3 and 6 µg/dl, and trilostane was continued. At a 12-month recheck, Lady’s post-ACTH stimulation cortisol concentration was 1.5 µg/dl. Although she was clinically well, the decision was made to decrease her dose by 50%. ACTH stimulation tests were performed every six months, and the post-stimulation cortisol concentration remained between 3 and 5 µg/dl. Lady was successfully maintained on 60 mg of trilostane once a day for the next four years with no recurrence of clinical signs. A. Lady after six months of failed mitotane therapy. B. Lady after six months of trilostane therapy.
For optimal viewing of this digital publication, please enable JavaScript and then refresh the page. If you would like to try to load the digital publication without using Flash Player detection, please click here.