Abstract

A number of methods have been proposed for monitoring trilostane therapy for canine hyperadrenocorticism. Lack of consensus on timing and targets for adrenocorticotropic hormone (ACTH) stimulation testing, coupled with the fact that post-ACTH cortisol levels may not correlate well with clinical control, suggest that stimulation testing may not be as reliable a monitoring tool as initially thought. This article reviews developments in our understanding of the action, dosage, and monitoring of trilostane therapy of canine hyperadrenocorticism. Trilostane pharmacodynamics should be considered both in monitoring therapy and in tailoring dosage and frequency of administration.

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