Transsphenoidal hypophysectomy for the treatment of hypersomatotropism secondary to a pituitary somatotroph adenoma in a dog

Abstract

Pituitary‐dependent hypersomatotropism is rarely diagnosed in dogs and surgical treatment is not reported. A 6‐year‐10‐month male neutered Patterdale Terrier presented with polyuria, polydipsia, progressive pharyngeal stertor, excessive hair growth and widened facial features and paws. Serum insulin‐like growth factor‐1 concentration via radioimmunoassay was consistent with hypersomatotropism (1783 ng/mL). A pituitary mass was identified on magnetic resonance and computed tomography imaging. Six weeks later, glucosuria, starved hyperglycemia and serum fructosamine above the reference range (467.6 μmol/L, RI 177‐314) were documented, consistent with diabetes mellitus. Transsphenoidal hypophysectomy was performed under general anesthesia without complications. Pituitary histopathology identified an acidophil neoplasm, with positive immunostaining for growth hormone. Postoperatively, there was rapid resolution of clinical, biochemical and morphologic changes of hypersomatotropism with persistence of diabetes mellitus. This case demonstrates successful resolution of hypersomatotropism with ongoing diabetes mellitus in a dog after surgical treatment by transsphenoidal hypophysectomy.

Progesterone-Related Diabetes Mellitus in the Bitch: Current Knowledge, the Role of Pyometra, and Relevance in Practice

“…The recognition of acromegalic features [ 78 ] in intact bitches should represent a stronger recommendation for spaying since the acromegalic phenotype can be considered a biomarker of the GH influence [ 178 ] ( Figure 7 ). However, it is important to note that the acromegaly phenotype in dogs may rarely occur due to pituitary somatotrophs [ 179 , 180 ] or due to primary hypothyroidism [ 181 , 182 , 183 ]. Despite P4-controlled GH’s negative influence on insulin sensitivity being documented only during diestrus, continued intermittent GH exposure over the next estrus cycles can predict increased cumulative risk for DM, especially due to aging effects on beta-cell function [ 10 ].…”