Neuropathology of Pituitary Adenomas and Sellar Lesions

Abstract

The pituitary gland is the site of numerous neoplastic and inflammatory processes. The overwhelmingly most frequent tumors arise from cells of the anterior lobe, the pituitary neuroendocrine tumors (PitNETs). Immunohistochemistry assay staining for pituitary hormones is the core tool for classifying PitNETs, resulting in the diagnosis of somatotroph PitNETs, lactotroph PitNETs, and so on. For cases showing no hormonal expression, the updated WHO classification system now considers the assessment of several transcription factors: PIT-1 (pituitary-specific POU-class homeodomain transcription factor); T-PIT (T-box family member TBX19); and SF-1 (steroidogenic factor regulating gonadotroph cell differentiation) before rendering a diagnosis of null cell adenoma. Other tumors and disease processes of this site often mimic PitNETs radiographically and sometimes even clinically (ie, compression of the optic chiasm). These potpourri of processes include germ cell neoplasms (especially germinomas), tumors that originate from Rathke's pouch (craniopharyngiomas, Rathke's cleft cyst), tumors that originate from the posterior lobe of the pituitary (pituicytoma, spindle cell oncocytoma, granular cell tumor), and tumors that originate from the meninges (especially meningiomas). In addition to neoplasms, several described inflammatory and related conditions exist that need to be distinguished from PitNETs. These include lymphocytic hypophysitis and Langerhans cell histiocytosis, a neoplastic disorder of histiocytes. In this review, we aim to briefly describe the main pituitary and sellar lesions, with emphasis on the most common tumors, the PitNETs.

Commentary: Neuropathology of Pituitary Adenomas and Sellar Lesions

“…Invasion of the pituitary capsule, on the other hand, has been evaluated by microscopic examination and was found to correlate with the increasing adenoma size, highest in those PA with suprasellar extension, but was not an independent prognostic factor, 6,7 obviating the need for intraoperative or subsequent pathologic examination for this purpose. Two peculiar microscopic findings, also mentioned in this Review, 1 that should not be confused with invasion of the surrounding neuroglial tissues by PA are basophil invasion of the neurohypophysis, referring to the common presence of basophilic cells within the neurohypophysis, and gangliocytic differentiation within PA.…”

“…udos to Kobalka et al 1 for providing this comprehensive review on the pathology of pituitary adenomas (PA) and sellar lesions. Along with classical knowledge on PA and other lesions commonly seen in the sellar/suprasellar region, contemporary information such as the pituitary transcription factors and the concept of pituitary neuroendocrine tumors (PitNET) has been discussed.…”

“…Predicting biologic behavior based on classical cytohistomorphologic features, such as necrosis, cytologic atypia, and pleomorphism, has not proven to be accurate in PA, as is the case with many neuroendocrine tumors in other organs. As mentioned in Kobalka et al, 1 the diagnosis of pituitary carcinoma can only be made in retrospect, and not at the time of initial diagnosis of PA, after craniospinal spread and/or distant metastasis are eventually identified. The former should be in the form of discontinuous spread; direct invasion of the neuroglial parenchyma is not sufficient.…”

Hypophysitis, the Growing Spectrum of a Rare Pituitary Disease

“… Summary of hypophysitis types, features and treatment options (created with BioRender.com). Histopathology image sources: lymphocytic (author’s [MF] pathology department), granulomatous ( 17 ), xanthomatous ( 9 ), necrotizing ( 23 ), immunoglobulin G4-related ( 14 ), and immunotherapy-induced ( 96 ). Abbreviations: ACTH, adrenocorticotrophic hormone; AI, adrenal insufficiency; APS, autoimmune polyglandular syndrome; DI, diabetes insipidus; DM, diabetes mellitus; ECD, Erdheim-Chester disease; F, female; GC, glucocorticoids; GH, growth hormone; GPA, granulomatosis with polyangiitis; HPF, high power field; LCH, Langerhans cell histiocytosis; M, male; MRI, magnetic resonance imaging; NETs, neuroendocrine tumors; POMC, proopiomelanocortin; PRL, prolactin.…”

Magnetic resonance fingerprinting for preoperative differentiation between gonadotroph and non-gonadotroph pituitary macroadenomas

“…Gonadotroph adenomas are defined as tumors with the gonadotropic hormones including luteinizing hormone (β-LH) and follicle-stimulating hormone (β-FSH), secreted by the gonadotropic cells of the anterior pituitary gland [4]. For non-gonadotroph adenomas, somatotroph adenomas are defined as tumors that produce mainly growth hormones and arise from pituitary-specific POU-class homeodomain transcription factor (Pit-1) lineage adenohypophyseal cells; lactotroph adenomas are defined as tumors that produce mainly prolactin and arise from Pit-1 lineage adenohypophyseal cells; corticotroph adenomas are defined as tumors that prod u c e a d r e n o c o r t i c o t r o p i c h o r m o n e s a n d o t h e r proopiomelanocortin-derived peptides, which arise from adenohypophyseal cells of T-box family member TBX19 lineage; and null cell adenomas are defined as tumors that lack expression of pituitary hormonal markers and pituitary transcription factors [4,5]. Somatostatin receptor type 3 (SSTR3) is expressed in 94% of gonadotroph pituitary adenomas, which is a putative target for drug therapy as a replacement for commonly used surgical treatment [6,7].…”