Silent corticotroph adenomas

Abstract

Purpose-Silent corticotroph adenomas (SCAs) comprise 20% of all corticotroph adenomas and 3-19% of nonfunctioning adenomas (NFAs). As they do not manifest clinical or biochemical hypercortisolism, they are diagnosed after pathologic examination of resected tumor tissue demonstrates positive ACTH expression. While preoperative features are similar to those of NFAs, SCAs may have more cavernous sinus invasion. Further, patients with SCAs tend to have more frequent and earlier recurrences than those with NFAs, often necessitating multiple surgeries and other modalities of treatment. This article reviews the incidence, pathogenesis, and clinical behavior of SCAs.Methods-A systematic literature review was performed using PubMed for information regarding silent corticotroph adenomas.Results-Up to date findings regarding epidemiology, pathogenesis, pathology, clinical presentation, postoperative course, and management of patients with SCAs are presented.Conclusions-This review highlights the necessity of rigorous monitoring for recurrences and hypopituitarism in patients with SCAs.

MRI texture analysis as a predictor of tumor recurrence or progression in patients with clinically non-functioning pituitary adenomas

“…Furthermore, our clinical outcomes are consistent with other reports in the literature; our remission rate after surgery was 47%, and 8% of these tumors recurred, similar to the 47% and 10.6%, respectively, found in a recent meta-analysis (7). Both silent corticotroph and silent somatotroph adenomas have been reported to be more aggressive than other NFPAs (31,32). We did not find that ACTH or GH positivity on immunohistochemistry was associated with recurrence or progression, but we only had four patients in either category, limiting our power to detect any difference.…”

Recent advances in understanding corticotroph pituitary tumor initiation and progression

“…This tumor entity is immunopositive for Tpit and expresses different POMC precursor proteins but does not secrete ACTH; moreover, genes related to ACTH synthesis are differently expressed in comparison with ACTH-secreting CAs 2, 69 . Thus, silent CAs clinically represent a member of the group of non-functioning pituitary adenomas (NFPAs), and according to recent studies, up to 20% of all NFPAs are silent CAs 5 . There are several hypotheses and speculations about silent CAs and their inability to secrete ACTH.…”

“…Whereas silent CAs are immunopositive for adrenocorticotropic hormone (ACTH), but do not manifest biochemical or clinical hypercortisolism 5 , the majority of clinically active CAs secrete excessive amounts of ACTH, causing chronic hypercortisolism due to lack of hypothalamus–pituitary–adrenal (HPA) axis feedback regulation at the level of the CA, leading to manifestations of the clinical features of Cushing’s disease 1 . Normally, there is a delay of several years between the onset of the disease and its diagnosis because early symptoms of Cushing’s disease are rather unspecific.…”

An unsuspected complication with immune checkpoint blockade: a case report

“…PAs may be classified as functional or nonfunctional, although this classification has been augmented by a more comprehensive system based on IHC studies of transcription factors. The 2017 World Health Organization classification officially requires routine IHC testing of the anterior lobe hormones and additionally requires transcription factors, such as PIT1, SF-1, and TPIT [4]. According to this classification scheme, hormone-negative adenomas may be classified in four groups: SF1-positive gonadotroph adenoma, PIT1-positive adenoma, TPIT-positive corticotroph adenoma, and transcription factor-negative null cell adenoma.…”