RESEARCH COMMUNICATIONS OF THE 28th ECVIM-CA CONGRESS

Ten dogs met the inclusion criteria (5 males and 5 females) with an age ranging from 6.5 to 13 years. Nine dogs had a suspected pituitary‐dependent hyperadrenocorticism. Clinical signs at the time of hypoadrenocorticism diagnosis were: lethargy (10/10), anorexia (10/10), vomiting (7/10), diarrhea (3/10), tremors (3/10) and polyuria‐polydipsia (1/10). Time between beginning of trilostane treatment and hypoadrenocorticism occurrence ranged from 4 days to 13 months; trilostane dose ranged from 1 to 12 mg/kg/day. Five dogs had a suspicion of concurrent infectious disease at the time of hypoadrenocortism diagnosis. Sodium/potassium ratio was under 24 in 5 dogs and under 28 in 8 dogs. All 8 dogs having an ACTH stimulation test performed had pre‐ and post‐stimulation cortisol concentration <55nmol/L. Trilostane dosage was decreased in 2 cases; trilostane was withdrawn in 1 case without further relapse of clinical signs of hyperadrenocorticism; 1 dog died at the time of diagnosis; glucocorticoids +/‐ mineralocorticoids supplementation was prescribed in 6 cases. Three out of these 6 dogs were lost to follow‐up, the other 3 had a diagnosis of permanent hypoadrenocorticism. Adrenal gland ultrasonogaphy in these 3 dogs showed a progressive reduction in glands size with a heterogeneous echogenicity.