A Comprehensive Long-term Retrospective Analysis of Silent Corticotrophic Adenomas vs Hormone-Negative Adenomas

Abstract

In the largest series to date, SCAs exhibited comparable size, but increased cavernous sinus invasion and progression/recurrence vs HNAs. SCAs exhibit deficient pro-opiomelanocortin to ACTH conversion. Close follow-up is warranted for SCAs.

Silent corticotroph adenomas

“…Up to 60% of SCAs manifest with preoperative hypopituitarism, similar to rates observed in nonfunctioning adenomas [9,10,20,50,61] though one series reported rates as high as 76% in SCAs (n=33) compared to 50% in NFAs (n=126) [19]. Radiologic features are generally similar between SCAs and NFAs [9,10,19,43] though cavernous sinus invasion may be more prevalent in SCAs than in nonfunctioning adenomas [4,20,49,50,63]. One group identified multiple microcysts (<3 mm) of high intensity signal on T2 weighted images in 77% of SCAs compared 21% in CD and 5% of NFAs, and macrocysts in 23% of SCAs [7].…”

“…SCAs potentially derive from POMC producing cells in the vestigial pars intermedia of the human pituitary [17], and the clinical silence may be due to dysregulated POMC processing [37]. Prohormone convertase (PC) 1/3 transcripts, which cleave POMC to ACTH, indeed are downregulated in SCAs [51], with CD having 30-fold higher levels than SCAs, and 10-fold higher levels observed in type I compared to type II SCAs which further suggest a defect in conversion of POMC to ACTH in SCAs [20].…”

Hypophysitis: a single-center case series

“…Specifically, there were several cases where pre-treatment clinical context or radiographic appearance could not differentiate between inflammatory lesions, sarcoidosis, Langerhans cell histiocytosis, or lymphoma, each of which would necessitate a different treatment approach (e.g., glucocorticoids, focused radiotherapy or chemoradiotherapy, respectively). Given the safety of transsphenoidal surgery [59][60][61], we felt it was in the patients' best interest to achieve a definitive diagnosis.…”

A review on the diagnosis and treatment of patients with clinically nonfunctioning pituitary adenoma by the Neuroendocrinology Department of the Brazilian Society of Endocrinology and Metabolism

“…In general, RT is reserved for cases of tumors not completely resected by surgery and that present progressive tumor growth during follow-up. Adjuvant RT should also be considered for patients who, at diagnosis, already present aggressive tumors (large adenomas with invasion and compromise to structures adjacent to sellar region) and/or tumors with pathologic characteristics that demonstrate aggressiveness, such as high mitotic index, Ki-67 > 3% and extensive immunostaining for p53 (atypical adenomas according to the classification of the 2004 World Health Organization) (49), and possibly silent corticotropinoma (77,78). Additionally, RT should be indicated in cases of persistent residual tumor after second surgery performed due to tumor recurrence.…”

“…Similarly, extensive immunostaining for p53 suggests a more aggressive tumor, whereas tumors that are IHC-negative for p53 may or may not exhibit aggressive behavior (125). Finally, pluri-hormone adenomas also appear to present a higher chance of recurrence or relapse (133), and silent corticotroph adenomas may also have more aggressive behavior (77,78).…”