Early Trilostane research study (Royal Vet College, University of London)
Below is an abstract for a study on Trilostane which was presented at the American College of Veterinary Internal Medicine Conference in the year 2000, but the study was done at the Royal Vet College, University of London prior to 2000.
Quote:
Abstract #195
LONG TERM EFFICACY AND SAFETY OF TRILOSTANE FOR TREATMENT OF CANINE HYPERDRENOCORTICISM Neiger R., Hurley K, Royal Vet College, Univ. of London, UK
Commonly used therapeutic agents for canine hyperadrenocorticism (HAC) may be only partially effective or have undesirable and potentially life-threatening side effects. The efficacy and long term safety of trilostane, a synthetic inhibitor of adrenal steroidogenesis, was evaluated in 30 dogs (age: mean 9.0 (SD ± 2.8 ) years; 14 male; weight: mean 20.5 (SD ± 13.8 ) kg) with confirmed HAC. Initial diagnoses was based on typical clinical signs, and biochemical abnormalities and an ACTH-stimulation test (n=28 ) and/or low-dose dexamethasone suppression test (n=15). Three dogs had an adrenal tumour confirmed by abdominal ultrasound; surgery was performed in one. Re-evaluation occurred after 10, 30-40, 60-90 days and thereafter at 3-4 monthly intervals and an ACTH-stimulation test was performed each time. Initial trilostane dose was based on body weight and was adjusted upon resolution of clinical signs and the ACTH-stimulation test.
Polydipsia (n=27) and polyphagia (n=14) abated within days starting trilostane in all dogs. Dermatological signs, pendulous abdomen or exercise intolerance improved over a longer period of time. 18 dogs are alive after a mean of 366 days (range: 70-730) while 12 dogs are dead after a mean of 287 days (range: 30-630) (adrenal tumour dogs after 630, 390 & 300 days). Mean initial trilostane dose was 6.1 (SD ± 3.3) mg/kg. Based on clinical signs and ACTH-stimulation test, trilostane dose was adjusted to 7.3 (SD ± 5.3) mg/kg. While initial ACTH-stimulation test was indicative of HAC in 19 dogs with a mean stimulated cortisol of 850 (SD ± 370) nmol/l (normal: <600 nmol/l), stimulated cortisol was in the normal range in all re-evaluations of all dogs except one ACTH-stimulation test of a dog with an adrenal tumour (mean ± SD stimulated cortisol: 10 days: 251 ± 157.5 nmol/l; 30-40 days: 214 ± 155.6 nmol/l; 60-90 days: 285 ± 244.4 nmol/l).
Trilostane was stopped altogether due to spontaneous resolution of HAC in 3 dogs and for a few days due to a flat response of the ACTH-stimulation test in one dog. Two dogs developed hyperkalemia which normalised without intervention after stopping trilostane. Of two dogs with a Na:K-ratios < 24, one developed severe arrhythmia and one had an uncontrollable urinary tract infection; trilostane was stopped in both but one was euthanised and one died shortly thereafter. In conclusion, trilostane seems to be an effective and safe treatment option in the long run for dogs with HAC.
