Abstract

Pituitary adenomas comprise a heterogenous group of adenohypophyseal tumours with distinct clinicopathological features across both the clinically functioning and silent groups. Although, predicting a clinically aggressive course remains challenging, accurate subtyping of pituitary adenomas offers valuable prognostic information that together with other clinical and radiological information serves as a platform for tailored treatment and follow-up. For instance, silent subtype 3 pituitary adenomas, silent corticotroph adenomas, acidophil stem cell adenomas, Crooke cell adenomas, and sparsely granulated somatotroph adenomas show more invasive growth. This review has been formulated as a set of practical questions that address the distinct clinical behaviour of a selected group of pituitary adenoma subtypes.

Highlights

  • As members of the multidisciplinary endocrine oncology team providing care for patients with pituitary disease we have often been intrigued by the relative scarcity of studies in the field that describe the clinical relevance of accurate pituitary adenoma subtyping

  • Modern approaches to the classification of pituitary adenomas use a panel approach by integrating adenohypophyseal celllineage specific transcription factors (Pit-1, Tpit, SF-1, and ER), monoclonal antibodies against adenohypophyseal hormones (Growth hormone: GH, Prolactin: PRL, betathyroid stimulating hormone: beta-TSH, beta-follicle stimulating hormone: beta-FSH, beta-luteinizing hormone: beta-LH, Adrenocorticotropic hormone: ACTH, and alpha-subunit), low molecular weight keratin (CAM5.2 or cytokeratin 18), and Ki-67 (MIB-1) [1,2,3,5,6]. p53 immunohistochemistry is a part of this panel in some practices [5]

  • This approach identifies tumours that are more frequently associated with invasive growth (Hardys’ grade III/IV and Knosp’s grade III/IV), higher recurrent rates, and a distinct response to therapy (Table 1). This morphologic categorization into aggressive subtypes has been suggested to be complementary and in some instances perhaps even superior to the designation of atypical pituitary adenomas, which are invasive adenomas showing p53 positivity and/or a MIB-1 labeling index >3%. In this brief review that has been formulated as a set of questions we will address the distinct behaviour of a selected group of pituitary adenoma subtypes in selected clinical settings

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Summary

Introduction

As members of the multidisciplinary endocrine oncology team providing care for patients with pituitary disease we have often been intrigued by the relative scarcity of studies in the field that describe the clinical relevance of accurate pituitary adenoma subtyping. P53 immunohistochemistry is a part of this panel in some practices [5] This approach identifies tumours that are more frequently associated with invasive growth (Hardys’ grade III/IV and Knosp’s grade III/IV), higher recurrent rates, and a distinct response to therapy (Table 1). This morphologic categorization into aggressive subtypes has been suggested to be complementary and in some instances perhaps even superior to the designation of atypical pituitary adenomas, which are invasive adenomas showing p53 positivity and/or a MIB-1 labeling index >3%.

Clinically non-functioning pituitary adenomas
Adenomas causing prolactin excess
Question for the Pathologist
Questions for the Pathologist
Adenomas causing ACTH excess
Adenomas causing TSH excess
Thyrotroph hyperplasia mimicking a pituitary adenoma
Pituitary Carcinoma
Findings
Conclusion
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