Modification of hormonal secretion in clinically silent pituitary adenomas

Daems, Tania; Verhelst, Johan; Michotte, Alex; Abrams, Pascale; Ridder, Dirk De; Abs, Roger

doi:10.1007/s11102-008-0085-7

Cited by 36 publications

(30 citation statements)

References 25 publications

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“…An unusual case of STA was reported who presented 20 years after the initial surgery with evidence of hyperthyroidism [11]. As shown in the present study, STAs and FTSHomas shared common histological features, immunohistochemical profiles, and ultrastructural features.…”

Section: Discussionsupporting

confidence: 74%

“…"Silent" corticotroph adenoma is a classical example of this category, and "silent" somatotroph adenomas have been also documented [6][7][8]. TSH-producing adenomas that lack clinical symptoms due to TSH excess ("silent" TSH-producing adenomas (STAs)) are extremely rare [9][10][11], although the definition and diagnostic criteria of STA have not been ruled or widely accepted [11]. Patients with STA are usually found by symptoms of a mass lesion.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Clinicopathological Characterization of TSH-Producing Adenomas: Special Reference to TSH-immunoreactive but Clinically Non-functioning Adenomas

et al. 2009

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Thyrotropin (thyroid-stimulating hormone (TSH))-producing pituitary adenomas have been known to be quite variable in clinical features covering from typical functioning TSH-producing adenomas (FTSHomas) associated with hyperthyroidism to clinically silent TSH cell adenomas (STAs) that are apparently unassociated with hyperthyroidism. It is important to distinguish STAs from other types of clinically non-functioning adenomas for adequate postoperative managements. However, because of rareness of TSH-producing adenomas, their histopathological features linking to the clinical manifestations have not been well characterized. Herein, we investigated clinical and histopathological findings to characterize 29 TSH-producing adenomas including 20 FTSHomas and nine STAs. Clinical symptoms of the patients with STAs included headache, visual defect, vertigo, and nausea. All STAs and 19 FTSHomas were macroadenoma. The average tumor size of STAs was significantly larger than that of FTSHomas (P < 0.05). The invasiveness was detected in 33% STAs and in 20% FTSHomas. Both STAs and FTSHomas showed a variety of morphological features and immunohistochemical profiles. Chromophobic polygonal or short-spindled tumor cells usually proliferated in a diffuse pattern, while they exhibited globoid or whorl-like appearance with intertwined cytoplasmic processes in both subgroups. Stromal fibrosis and calcification were often noted. Their nuclei were somehow pleomorphic. Ultrastructural features of all four STAs examined were similar to those of normal thyrotrophs. Thus, STAs and FTSHomas were indistinguishable by histology alone. Immunohistochemically, the number of TSH-positive cells in individual FTSHomas was highly various. Six tumors showed only a few TSH-positive cells (1-5%), and three were negative for TSH by conventional method without antigen retrieval. After proteinase K treatment, these tumors turned out TSH positive. As defined, STAs were TSH positive in more than 20% of tumor cells and three of them in more than 50%. Growth hormone- and/or prolactin-positive cells were detected in 55% STAs and 63% FTSHomas. Both pituitary-specific transcription factor 1 and GATA-binding protein 2 were expressed in all STAs and 20 FTSHomas. Membranous somatostatin receptor (SSTR)-2A immunoreactivity was found in 89% STAs and 94% FTSHomas, whereas SSTR5 was positive in 78% of both STAs and FTSHomas. MIB-1 labeling index was related to tumor invasiveness and tumor size (P < 0.05, P = 0.09, respectively). Thus, although both STAs and FTSHomas showed unique histopathological features distinct from other type adenomas, these two subgroups were indistinguishable by histopathology. Immunohistochemistry for TSH by use of antigen retrieval, transcription factors, and SSTRs may be useful to confirm STAs and to determine the postoperative therapy among various kinds of clinically non-functioning adenomas.

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Section: Discussionsupporting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Clinicopathological Characterization of TSH-Producing Adenomas: Special Reference to TSH-immunoreactive but Clinically Non-functioning Adenomas

et al. 2009

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“…Rarely, initially silent corticotroph tumours may evolve to secrete ACTH after many years of follow-up, and this transformation may also herald more aggressive tumour behaviour (42,43,44,45). Silent subtype III or plurihormonal silent tumours (40) also may exhibit a more aggressive clinical course compared with silent gonadotroph tumours (46).…”

Section: Reasoningmentioning

confidence: 99%

European Society of Endocrinology Clinical Practice Guidelines for the management of aggressive pituitary tumours and carcinomas

Raverot

Burman

McCormack

et al. 2018

European Journal of Endocrinology

463

583

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Background: Pituitary tumours are common and easily treated by surgery or medical treatment in most cases. However, a small subset of pituitary tumours does not respond to standard medical treatment and presents with multiple local recurrences (aggressive pituitary tumours) and in rare occasion with metastases (pituitary carcinoma). The present European Society of Endocrinology (ESE) guideline aims to provide clinical guidance on diagnosis, treatment and follow-up in aggressive pituitary tumours and carcinomas. Methods: We decided upfront, while acknowledging that literature on aggressive pituitary tumours and carcinomas is scarce, to systematically review the literature according to the GRADE (Grading of Recommendations Assessment, Development and Evaluation) system. The review focused primarily on first-and second-line treatment in aggressive pituitary tumours and carcinomas. We included 14 single-arm cohort studies (total number of patients = 116) most on temozolomide treatment (n = 11 studies, total number of patients = 106). A positive treatment effect was seen in 47% (95% CI: 36-58%) of temozolomide treated. Data from the recently performed ESE survey on aggressive pituitary tumours and carcinomas (165 patients) were also used as backbone for the guideline. In patients responding to first-line temozolomide, we suggest continuing treatment for at least 6 months in total. Furthermore, the guideline offers recommendations for patients who recurred after temozolomide treatment, for those who did not respond to temozolomide and for patients with systemic metastasis.

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“…Alternatively, secretion of ACTH by these tumours may be intermittent and/or serum ACTH levels so subtly elevated as to escape recording. It should be related to the failure exocytosis and increased intracellular disposal, by lysosomes or a defective packing into secretory granules due to inadequately developed Golgi apparatus [12].…”

Section: Discussionmentioning

confidence: 99%

Type II muscle fibers atrophy associated with silent corticotroph adenoma in a dog.

Trapani

De²,

Insabato³

et al. 2010

Folia Histochem Cytobiol.

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Abstract:The Silent Corticotroph Adenoma (SCA) is a pituitary adenoma variant characterized by the immunoreactivity for adrenocorticotropic hormone (ACTH) and related peptides, without the clinical signs of Cushing's disease. SCA has been postulated to either secrete structurally abnormal ACTH that is inactive but detectable by immunohistochemistry or radioimmunoassay, or to secrete ACTH intermittently or at low levels continuously. Excess of ACTH has been associated to type II muscle atrophy. We describe a case of type II muscle fibers atrophy associated with silent corticotroph adenoma in a dog. The dog showed moderate to severe proximal muscle wasting and weakness with normal levels of muscle-associated enzymes. In the limb muscle biopsies, type II fibers were uniformly smaller than type I fibers. In temporalis muscles, there were few atrophic fibers, and several irregular areas of loss of enzymatic activity observed in NADH, SDH and COX stains. The tumour showed a trabecular growth pattern and immunohistochemical analysis demonstrated the presence of cytoplasmic immunoreactivity for ACTH. The muscle atrophy was considered to be related to an excess of inactive ACTH. Studying spontaneous occurring rare diseases in animals could help to understand the mechanism of similar diseases in human has well.

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Modification of hormonal secretion in clinically silent pituitary adenomas

Abstract: These two cases, one somatotroph and one thyrotroph adenoma, are an illustration that clinically silent pituitary adenomas may in rare circumstances evolve over time and become active, as previously demonstrated in silent corticotroph adenomas.

Cited by 36 publications

References 25 publications

Clinicopathological Characterization of TSH-Producing Adenomas: Special Reference to TSH-immunoreactive but Clinically Non-functioning Adenomas

Clinicopathological Characterization of TSH-Producing Adenomas: Special Reference to TSH-immunoreactive but Clinically Non-functioning Adenomas

European Society of Endocrinology Clinical Practice Guidelines for the management of aggressive pituitary tumours and carcinomas

Type II muscle fibers atrophy associated with silent corticotroph adenoma in a dog.

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