Multihormonal Pituitary Adenomas

Heitz, Ph. U.

doi:10.1159/000178983

Cited by 75 publications

(19 citation statements)

References 22 publications

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“…The same circumstances may apply also to 6 of the 19 'inactive' adenomas in which a few scattered cells were found con taining one or several hormones. Similar findings have been described by Kovacs et al [15] for the group o f'null cell adenomas' and also 'unclassified adenomas' according to their classification [11].…”

Section: Discussionsupporting

confidence: 90%

Immunohistochemical Examination of Pituitary Adenomas

et al. 1985

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A comparison was made with the data of 62 cases of pituitary adenoma, evaluated pre- and postoperatively, including as well the results of immunohistochemical hormone examination (also for calcitonin). Prolactin was found in 18 of the 21 adenomas carrying the preoperative diagnosis of prolactinoma, whereas cells containing other hormones (growth hormone, LH, FSH, TSH, ACTH, β-endorphin), were only occasionally present. The growth hormone was strongly positive in the adenoma tissue in 16 of the 17 cases of acromegaly. 5 of these adenomas were accompanied by a marked hyperprolactinemia and also contained many prolactin cells. 6 of the 19 adenomas diagnosed as being ‘inactive’ contained hormone-positive cells, but only a very small number of cells. ACTH was found in 3 of the 4 pituitary adenomas of patients with Cushing’s disease. 2 of these were also positive for β-endorphin. The tissue of 1 gonadotrophic adenoma (with elevated FSH in serum) gave positive results with an anti-LH antiserum. Calcitonin was not found in any adenoma. The preoperative serum prolactin levels did not quantitatively correlate with the percentage of prolactin-positive cells.

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Section: Discussionsupporting

confidence: 90%

Immunohistochemical Examination of Pituitary Adenomas

et al. 1985

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“…Even though, only 11 such tumors has been reported in patients with Cushing disease. 28,34 However, double adenomas are not at all rare in autopsy pituitary in human 21 and in rat. 44 A MEN1 germline mutation was found in only 55% of our patients.…”

Section: Discussionmentioning

confidence: 99%

Pituitary Tumors and Hyperplasia in Multiple Endocrine Neoplasia Type 1 Syndrome (MEN1): A Case-Control Study in a Series of 77 Patients Versus 2509 Non-MEN1 Patients

Trouillas¹,

Labat-Moleur

Stürm

et al. 2008

American Journal of Surgical Pathology

204

132

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Patients affected by the multiple endocrine neoplasia type I syndrome (MEN1) display a high incidence of pituitary adenomas, though it is still unknown whether these pituitary tumors have specific pathologic features that would distinguish them from sporadic pituitary adenomas. Pituitary tissue specimens of 77 MEN1 patients from the GTE (Groupe d'étude des Tumeurs Endocrines) register were compared with unselected 2509 non-MEN1 sporadic pituitary tumors and also to a control subgroup of 296 cases, where 1 MEN1 tumor was matched with 4 sporadic tumors of the same hormonal immunoprofile. Sex, age, size, and invasiveness of tumors, and menin gene mutations were documented. Histologic analysis took into account 33 items, including immunocytochemical data, the proliferative marker Ki-67, and an examination of the juxtatumoral pituitary. MEN1 tumors were significantly larger and more often invasive by histology. MEN1 patients with large pituitary tumors (grade IV) were younger than non-MEN1 patients. MEN1 tumors had no other characteristic histologic features and no predominance of any one hormone producing subtype. However, plurihormonal adenomas versus monohormonal and nonimmunoreactive adenomas were more frequent in MEN1 tumors (39%) than in the control non-MEN1 group (P = 0.001). Especially, the growth hormone and prolactin plurihormonality with unusual association with follicle-stimulating hormone, luteinizing hormone, or adrenocorticotropic hormone was more frequent in MEN1 tumors. In addition, multiple adenomas were significantly more frequent (4% vs. 0.1%; P < 0.0001), especially prolactin-adrenocorticotropic hormone. Somatotroph hyperplasia, with or without a microadenoma was found in only 3 MEN1 patients, with growth hormone-releasing hormone hypersecretion by a pancreatic tumor in 2 of them. All types of mutation were observed, including frameshifts, nonsenses, missenses, and 1 case of germline MEN1 encompassing large deletion, strongly suggesting the absence of any phenotype-genotype correlation.

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“…A multihormonal pituitary adenoma is found when more than two pituitary hormones are elevated. Apparent pituitary adenomas are clinically multihormonal in 10-15% of cases [19]. Multihormonal adenomas may consist of one cell type secreting multiple hormones (monomorphous) or of several cell types each secreting one hormone (plurimorphous) [20].…”

Section: Discussionmentioning

confidence: 99%

Expression of Adrenocorticotropic Hormone, Prolactin and Transcriptional Factors in Clinically Nonfunctioning Pituitary Adenoma

et al. 2007

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Abstract. We describe here a case of a clinically nonfunctioning pituitary adenoma, but with expression of ACTH and PRL. A 42-year-old woman was referred to our department for further evaluation of pituitary tumor. She had no acromegaloid features, and no typical Cushingoid features. She had no galactorrhea, and had regular menses. GH, IGF-I, LH, FSH, TSH, ACTH and cortisol levels in blood were all within the normal ranges, while PRL levels were mildly elevated. Both ACTH and cortisol levels were adequately increased in response to CRH, and both were suppressed by a small dose of dexamethasone. Plasma ACTH and cortisol levels were decreased at night, suggesting the circadian rhythms for plasma ACTH levels were undisturbed. Based on these findings we did not clinically suspect ACTH-producing tumor, however immunohistochemistry revealed ACTH immunoreactivity in the pituitary adenoma. Therefore, the tumor was considered a silent corticotroph adenoma. PRL was co-expressed in a significant subpopulation of ACTH-immunoreactive tumor cells. Ptx1, Neuro D1, and T pit were densely expressed and Pit-1 was sparsely expressed in the nuclei of adenoma cells. It is therefore possible that a tumor originating in an immature or uncommited adenohypophysial stem cell may later differentiate into different cell types due to a combination of certain specific transcriptional factors.

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Multihormonal Pituitary Adenomas

Cited by 75 publications

References 22 publications

Immunohistochemical Examination of Pituitary Adenomas

Immunohistochemical Examination of Pituitary Adenomas

Pituitary Tumors and Hyperplasia in Multiple Endocrine Neoplasia Type 1 Syndrome (MEN1): A Case-Control Study in a Series of 77 Patients Versus 2509 Non-MEN1 Patients

Expression of Adrenocorticotropic Hormone, Prolactin and Transcriptional Factors in Clinically Nonfunctioning Pituitary Adenoma

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