Bigger Glands, Better Control? Trilostane Therapy Enlarges Adrenals in Dogs with PDH

Changes in Ultrasonographic Appearance of Adrenal Glands in Dogs with Pituitary-Dependent Hyperadrenocorticism Treated with Trilostane

Panagiotis Mantis, Christopher R. Lamb, Angela L. Witt, Reto Neiger

Background
Pituitary-dependent hyperadrenocorticism (PDH) in dogs is most commonly managed with mitotane, but alternatives like trilostane—a reversible 3β-hydroxysteroid dehydrogenase inhibitor—have gained popularity due to a more favorable safety profile. While mitotane is known to reduce adrenal gland size through cortical necrosis, limited data exist on the ultrasonographic effects of trilostane therapy. This study aimed to evaluate changes in adrenal gland dimensions and echogenicity on ultrasound in dogs with PDH receiving long-term trilostane treatment.

Methods
This prospective study included 19 dogs diagnosed with PDH based on endocrine testing and ultrasonography. Each underwent ultrasonographic assessment of both adrenal glands before and at least six months after initiating trilostane therapy. Adrenal length and caudal pole thickness were measured. Dosages of trilostane were weight-based and adjusted according to follow-up ACTH stimulation tests. Statistical analysis of pre- and post-treatment measurements was performed using Wilcoxon signed-rank tests.

Results
Adrenal enlargement occurred in 84% of glands. Right adrenal length and caudal pole thickness, as well as left adrenal thickness, increased significantly during treatment, while left adrenal length did not. The median percentage increases were +32% for right adrenal length and +25% for right thickness. In 37% of dogs, adrenal echogenicity changed, most commonly showing increased distinction between the hypoechoic outer zone and hyperechoic center. Two dogs showed adrenal shape distortion post-treatment, with one showing pre-existing irregularity. These changes may reflect nodular hyperplasia or early neoplastic transformation, though histologic confirmation was unavailable.

Limitations
The study lacked histopathological correlation and had a small sample size. Ultrasonographic interpretation was subjective for echogenicity and shape. Variability in trilostane pharmacokinetics and treatment duration may have influenced adrenal responses.

Conclusions
Trilostane therapy in dogs with PDH is associated with significant increases in adrenal gland size and changes in ultrasonographic appearance, likely due to elevated ACTH stimulating adrenal hypertrophy. These findings suggest adrenal enlargement is a common and potentially expected consequence of effective trilostane treatment and should not be mistaken for treatment failure or neoplasia without further evidence.

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