Hypersomatotropism and Hypercortisolism Caused by a Plurihormonal Pituitary Adenoma in a Dog

Abstract

A 12-year-old, male Labrador Retriever was presented because of polyuria, polydipsia, polyphagia, joint pain, and physical features consistent with acromegaly. Circulating insulin-like growth factor-1 (IGF-1) concentration was increased (> 1000 ng/mL; reference interval [RI], 42-449), suggestive of hypersomatotropism. An abnormal low-dose dexamethasone suppression test and increased circulating adrenocorticotropic (ACTH) concentration indicated pituitary-dependent hypercortisolism. Computed tomography identified an enlarged pituitary gland. Treatment with cabergoline initially decreased circulating IGF-1 and ACTH concentrations and urinary cortisol-to-creatinine ratio (UCCR), with a notable reduction in acromegalic physical features. However, 7 months after the start of cabergoline treatment, IGF-1, ACTH, and UCCR had increased again, although pituitary gland size remained stable. Because of worsening joint pain, euthanasia was performed. On necropsy, double immunohistochemistry identified pituitary tumor cells with cytoplasmic co-expression of both growth hormone (GH) and ACTH, consistent with a monomorphic plurihormonal macroadenoma. This case shows that concurrent hypersomatotropism and hypercortisolism can occur in dogs caused by a plurihormonal pituitary adenoma.

Keywords: acromegaly; caber goline; corticotropinoma; cushing's syndrome; growth hormone; insulin‐like growth factor‐1; somatotropinoma.

FIGURE 1

Progressive facial changes in a Labrador Retriever with hypersomatotropism and hypercortisolism. (A) Normal appearance at 8 years of age. (B) Mild facial and interdental space widening at 9 years of age. (C) Pronounced facial enlargement with increased skin folds, excessive hair growth, and tongue enlargement at 11 years of age. (D) Severe soft tissue overgrowth in the head and neck, with marked facial and tongue enlargement at 12 years of age.

FIGURE 2

Physical changes in a Labrador Retriever with hypersomatotropism and hypercortisolism. (A) Lateral view showing generalized soft tissue overgrowth, thickened skin folds, and an enlarged protruding tongue. (B) Oral cavity with widened interdental spaces, thickened gums, and tongue enlargement.

FIGURE 3

Transversal post‐contrast computed tomography (CT) scans of a pituitary macroadenoma (yellow arrow) in a 12‐year‐old Labrador Retriever with hypersomatotropism and hypercortisolism. (A) At diagnosis. (B) After 7 months of cabergoline treatment, showing unchanged tumor size (P/B 0.6). Sagittal views are shown in the lower‐right insets.

FIGURE 4

Physical changes in a dog with hypersomatotropism and hypercortisolism before and during cabergoline treatment. (A) At diagnosis. (B) Three months after starting cabergoline, showing a marked reduction in soft tissue overgrowth in the face, head, neck, and paws.

FIGURE 5

Macroscopic (A) and microscopic (B–H) images of a plurihormonal pituitary adenoma in a dog with hypersomatotropism and hypercortisolism. (A) Pituitary adenoma on necropsy (asterisk). (B) Acidophilic pituitary adenoma stained with hematoxylin–eosin. (C) Panoramic view and (D) magnification showing cytoplasmic immunoreactivity for growth hormone (GH) in the pituitary adenoma (somatotropinoma). (E) Panoramic view and (F) magnification showing cytoplasmic immunoreactivity for adrenocorticotropic hormone (ACTH) within the pituitary adenoma (dashed box). (G) Double immunohistochemistry for adrenocorticotropic hormone (ACTH, red) and growth hormone (GH, brown) focusing on the dashed box from image E. (H) Magnification of image G, showing cytoplasmic co‐expression of both growth hormone (GH, brown) and adrenocorticotropic hormone (ACTH, red) within the same cell (arrows).