Identification of Somatotrophs, Mammosomatotrophs, and Mammotrophs by Sandwich Cell Immunoblot Assay in GH-Secreting Adenomas and Prolactinomas. Correlations between the Proportions of Hormone Secreting Cells and Tumor Size.

Kojima, Yasuhiro; Suzuki, Shinichi; Yamamura, Koji; Kawasaki, Takashi; Yamamoto, Isao

doi:10.1507/endocrj.47.143

Cited by 6 publications

(3 citation statements)

References 36 publications

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“…It has been reported that there is no correlation between serum PRL levels and the number of PRL-positive cells [10]. Furthermore, normoprolactinemia was observed in 60% patients with GH-producing pituitary adenoma even with positive immunostaining for PRL [11]. Accordingly, positive immunostaining for PRL in GHproducing pituitary adenomas may not always reflect hyperprolactinemia as in the present case.…”

Section: Discussioncontrasting

confidence: 49%

A Case of Acromegaly Associated with Subclinical Cushing's Disease

et al. 2006

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Abstract.A 54-year-old man with type 2 diabetes was referred to our hospital for endocrine evaluation of acromegaly. Physical examination showed typical acromegalic features without Cushingoid features. Magnetic resonance imaging of the brain revealed the presence of a pituitary macroadenoma. Basal plasma levels of GH and insulin-like growth factor-I under fasting hyperglycemia (202 mg/dl) were markedly elevated. Plasma GH levels paradoxically increased after stimulation with TRH and LH-RH, and decreased after bromocriptine and octreotide administration. Endocrine examination of the hypothalamo-pituitary-adrenal (HPA) axis showed a lack of circadian rhythm of ACTH and cortisol, non-suppressibility to low-dose (1 mg), but suppressibility to high-dose (8 mg) dexamethasone, and normal response to CRH stimulation. The tumor resected by transsphenoidal surgery was histopathologically consistent with the diagnosis of eosinophilic adenoma: positive immunoreactivities of GH, PRL and ACTH were demonstrated, but negative immunoreactivities of prohormone convertase (PC) 1/3 by immunohistochemical method. After surgery, plasma GH and IGF-I levels decreased along with normalization of HPA axis. Metabolic co-morbidities such as diabetes and hypertension disappeared after removal of the pituitary tumor. This is a very rare case of GH-producing pituitary adenoma causing typical acromegaly with concomitant production of ACTH causing subclinical Cushing's disease.

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Section: Discussioncontrasting

confidence: 49%

A Case of Acromegaly Associated with Subclinical Cushing's Disease

et al. 2006

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“…Generally, PRL levels are elevated in pituitary adenomas, mostly due to two possible mechanisms: 1) hypothalamic-pituitary disconnection, resulting in attenuation of PRL inhibitory factor, or 2) PRL-producing tumors [17,18]. Most PRL-producing tumors are diagnosed from very high PRL levels in blood.…”

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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“…We studied differentiated pituitary somatotrophs, which synthesize and secrete growth hormone. Like in the other pituitary cells, the amount of growth hormone discharged from somatotrophs is regulated by numerous cellular signalling mechanisms [11] and also by the number of secretory cells available by apoptosis [12–14].…”

Section: Introductionmentioning

confidence: 99%

Apoptosis triggered redistribution of caspase‐9 from cytoplasm to mitochondria

et al. 2003

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Caspase-9 is an apoptosis initiator protease activated as a response to the mitochondrial damage in the cytoplasmic complex apoptosome. By £uorescence labelling of proteins, confocal microscopy and subcellular fractionations we demonstrate that caspase-9 is in the cytoplasm of non-apoptotic pituitary cells. The activation of apoptosis with rotenone triggers the redistribution of caspase-9 to mitochondria. Experiments using the general caspase inhibitor z-VAD.fmk and the speci¢c caspase-9 inhibitor z-LEHD.fmk show that the caspase-9 redistribution is a regulated process and requires the activity of a caspase other than the caspase-9. We propose that this spatial regulation is required to control the activity of caspase-9. ß

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Identification of Somatotrophs, Mammosomatotrophs, and Mammotrophs by Sandwich Cell Immunoblot Assay in GH-Secreting Adenomas and Prolactinomas. Correlations between the Proportions of Hormone Secreting Cells and Tumor Size.

Cited by 6 publications

References 36 publications

A Case of Acromegaly Associated with Subclinical Cushing's Disease

A Case of Acromegaly Associated with Subclinical Cushing's Disease

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

Apoptosis triggered redistribution of caspase‐9 from cytoplasm to mitochondria

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