Crooke Cell Adenoma, an Aggressive Corticotroph Pituitary Adenoma: Case Report

Document Type

Conference Proceeding

Publication Date

10-22-2025

Publication Title

J Endocr Soc

Keywords

cytokeratin, hyalin, hydrocortisone, prolactin, synaptophysin, ACTH secreting adenoma, ACTH secreting cell, adenoma, adrenal insufficiency, adult, case report, cerebellum, clinical article, conference abstract, cousin, Cushing disease, dexamethasone suppression test, diagnosis, diplopia, dizziness, female, follow up, headache, hemisphere, histopathology, human, human tissue, hydrocortisone urine level, hypercortisolism, hypophysis, hypophysis adenoma, male, middle aged, MRI scanner, nuclear magnetic resonance imaging, optic chiasm, pons, recurrence risk, surgery

Abstract

Background: Crooke Cell Adenoma (CCA) is an aggressive yet rare subtype of pituitary adenoma. The first case was reported in 1981, while the first description of the characteristic Crooke's hyaline changes in corticotroph cells was made in 1935. Specifically, CCA is a variant of T-PIT-driving corticotroph adenomas characterized by the deposition of cytoplasmic, perinuclear cytokeratin (CK) filaments, leading to hyaline changes in the neoplastic cells. It can present as a functioning corticotroph adenoma, leading to Cushing's disease, or rarely it can be clinically silent. Patients with CCA often have poorer endocrinologic outcomes compared to those with more typical corticotroph adenomas, with less frequent post-operative hormone normalization and a higher likelihood of persistent hypercortisolism. In addition to being clinically aggressive, there is a high rate of recurrence following surgical resection. Clinical Case: A 58-year-old female presented with a new onset headache, double vision, and dizziness. CT head incidentally noted an enlarged pituitary (up to 11mm), with mild suprasellar extension and contact with optic chiasm. MRI showed an acute infarct in the paramedian pons and cerebellar hemisphere and confirmed a cystic pituitary lesion, measuring 8 x 12 mm, projecting slightly into the suprasellar cistern and abutting the inferior surface of the optic chiasm without significant displacement. The hormonal evaluation was significant for an elevated ACTH at 70 pg/ml (normal: 7-63 pg/ml) and a nonsuppressed dexamethasone suppression test. The rest of the studies including prolactin, thyroid studies, random cortisol, 24-hour urine cortisol, and IGF-1 were within normal limits. The patient underwent resection of the pituitary tumor four months later due to worsening vision changes. Histopathology showed a densely granulated corticotroph PitNET with focal Crooke cell change, with strongly positive synaptophysin and ACTH in the neoplastic cell population. Post-operatively, the patient experienced adrenal insufficiency requiring hydrocortisone replacement. The two-month follow-up MRI was stable with no residual enhancing tissue. of note, the patient reports a similar history of pituitary adenoma and Cushing's disease in her first-degree cousin, who underwent surgery but had recurrence of the disease 6 years later. Conclusion: Given the higher likelihood of recurrence of CCA and poorer endocrinologic outcomes when compared to other typical pituitary corticotroph adenomas, close monitoring of hormonal levels and imaging at regular intervals is imperative. Unfortunately, due to the rarity of the condition, no specific guidelines are available. Although there is no clear genetic component to CCA, there is a potential hereditary factor if it occurs in the context of familial syndromes.

Volume

9

First Page

A751

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