BACKGROUND: Trilostane is the treatment of choice for pituitary-dependent hypercortisolism (PDH) in dogs, but predictors of a poor response are unclear. HYPOTHESIS/OBJECTIVES: To identify variables associated with a poor response to trilostane in dogs with PDH. ANIMALS: Twenty-three dogs with PDH treated with trilostane. METHODS: Retrospective cohort study. Clinical, clinicopathological, endocrine, ultrasonographic, and treatment data were reviewed. Dogs were classified as good responders (GRs) or nonresponders (NRs) based on clinical outcomes after 4-8 months of trilostane treatment. The primary outcome was treatment response. RESULTS: Fifteen dogs were GRs and 8 were NRs. At diagnosis, GRs had lower alanine aminotransferase (ALT) (median IQR 182 70-251 vs 330 224-578 U/L; P = .004), eACTH (14.4 9.25-29.13 vs 49.2 34.35-62.35 pg/mL; P = .007), and pre-ACTH cortisol (4.28 3.07-6.52 vs 9.0 6.57-19.40 μg/dL; P = .019) than NRs. Bilateral adrenomegaly was more frequent in NRs (8/8) than in GRs (9/15; P = .007). At T1, NRs required more rechecks (median IQR 7 6-7 vs 3 3-5; P < .001) and higher trilostane doses (3.25 3-5.75 vs 1.22 0.66-1.60 mg/kg q12h; P < .001). After false discovery rate adjustment, ALT, eACTH, alopecia, and bilateral adrenomegaly remained significant (q = 0.047 for each). All GRs achieved complete clinical resolution within 4 months of treatment initiation. CONCLUSIONS AND CLINICAL IMPORTANCE: Higher baseline ALT, eACTH, and pre-ACTH cortisol, as well as bilateral adrenomegaly, were associated with a poor response to trilostane. A lack of improvement by 4-8 months and the need for higher doses or more rechecks supports early therapeutic reassessment.
Golinelli et al. (Fri,) studied this question.