Ectopic Adrenocorticotropin Syndrome Exhibiting Paradoxical Adrenocorticotropin Responsiveness to Gonadotropin-Releasing Hormone.

Ujihara, Makoto; Yoshimoto, Takanobu; Cho, Reika; Totsuka, Yasuo; Imaki, Toshihiro; Nomura, Kazuhiro; Nishikawa, Toshio; Takano, Kazue

doi:10.1507/endocrj.48.19

Cited by 3 publications

(3 citation statements)

References 12 publications

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“…In addition, plasma ACTH did not respond to TRH in two of the examined patients. Ujihara et al reported that in a patient who had Cushing's syndrome, TRH and CRH had no effect on the secretion of ACTH, whereas GnRH increased plasma ACTH levels [14]. Including this report, it is therefore possible to speculate that no response of ACTH to TRH may be due to the lack of TRH receptors in ACTH cell adenoma.…”

Section: Discussionmentioning

confidence: 68%

“…Reverse transcription was performed by incubating 1 mg total RNA with 1 ml of PowerScript reverse transcriptase (Clontech, USA) and 1 ml of 0.5 mg/ml oligo(dT) [12][13][14][15][16][17][18] primer (Life Technologies, USA) at 42°C for 70 minutes in 20 ml reaction buffer. RT products were diluted ten times with 10 mM Tricine-KOH (pH 9.2)/0.1 mM EDTA, and stored at -20°C until used for PCR.…”

Section: Histological Studiesmentioning

confidence: 99%

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Gene Expression Study of Thyrotropin Releasing Hormone (TRH) Receptor Using RT-PCR: Relationship to Clinical and Immunohistochemical Phenotypes in a Series of Human Pituitary Adenomas

et al. 2003

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Abstract. Thyrotropin releasing hormone receptor 1 (TRHR1) and 2 (TRHR2) mRNAs were examined using reverse transcription polymerase chain reaction (RT-PCR). These data were then correlated with endocrinological and histological characteristics in 65 human pituitary adenomas including one non tumorous pituitary gland, to clarify the role of TRHR1 and 2 gene expression in human pituitary adenomas, especially as it relates to the paradoxical stimulatory effects of TRH found in pituitary adenomas. TRHR mRNA was not identified in four ACTH cell adenomas, whereas TRHR mRNA expression was found in 12/23 acromegaly specimens, 7/8 prolactinomas, 3/3 TSH cell adenomas, and 22/27 clinically nonfunctioning adenomas. Specimens obtained from patients expressing the TRHR gene were found to express TRHR1 and TRHR2 or TRHR1 alone, whereas no cases were identified in which TRHR2 alone was expressed. In examining the relationship between GH, PRL, TSH, or gonadotropin subunit response to TRH administration and TRHR gene expression, TRHR mRNA was found to be absent in 9 out of 10 GH cell adenomas without paradoxical GH response to TRH (non-responder), whereas TRHR genes were shown to be expressed in 10 out of 12 GH cell adenomas with paradoxical GH response to TRH (responders) (c 2 = 11.73, p = 0.0009). However, there was no significant correlation between TRHR gene expression and responsiveness to PRL or gonadotropins to TRH administration in PRL cell adenomas (c 2 = 0.16, p = 0.87) or gonadotroph cell adenomas (c 2 = 0.0006, p = 1), respectively. We concluded that the existence of the TRH receptor in adenoma cells plays an important role in the paradoxical GH response to TRH administration in GH cell adenomas. It should be noted that the PRL response to TRH in prolactinoma or an abnormal response of gonadotropin and/or its subunits to TRH in gonadotroph cell adenomas is considered to be due to a mechanism other than direct TRH action in adenoma cells. However, further studies are required to elucidate the role of TRHR2 in pituitary adenomas.

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Section: Discussionmentioning

confidence: 68%

Section: Histological Studiesmentioning

confidence: 99%

Gene Expression Study of Thyrotropin Releasing Hormone (TRH) Receptor Using RT-PCR: Relationship to Clinical and Immunohistochemical Phenotypes in a Series of Human Pituitary Adenomas

et al. 2003

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“…The underlying mechanism of ACTH response by desmopressin could be accounted for by the amount of V1bR expressed by ACTH-producing tumors irrespective of pituitary or non-pituitary origin [6,23,25]. There have been only two cases of desmopressin-responsive EAS associated with thymic NET thus far reported in the English literature [26,27].…”

Section: Discussionmentioning

confidence: 99%

Ectopic ACTH syndrome caused by desmopressin-responsive thymic neuroendocrine tumor

et al. 2015

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Role of Glucocorticoids in Fasting-induced Changes in Hypothalamic and Pituitary Components of the Growth Hormone (GH)-axis

Kim

Seo

Chung

et al. 2008

Korean J Physiol Pharmacol

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To directly test if elevated glucocorticoids are required for fasting-induced regulation of growth hormone (GH)-releasing hormone (GHRH), GHRH receptors (GHRH-R) and ghrelin receptors (GHS-R) expression, male rats were bilaterally adrenalectomized or sham operated. After 7 days, animals were fed ad libitum or fasted for 48 h. Bilateral adrenalectomy increased hypothalamic GHRH to 146% and decreased neuropeptide Y (NPY) mRNA to 54% of SHAM controls. Pituitary GHRH-R and GHS-R mRNA levels were decreased by adrenalectomy to 30% and 80% of sham-operated controls. In shamoperated rats, fasting suppressed hypothalamic GHRH (49%) and stimulated NPY (166%) mRNA levels, while fasting increased pituitary GHRH-R (391% ) and GHS-R (218% ) mRNA levels. However, in adrenalectomized rats, fasting failed to alter pituitary GHRH-R mRNA levels, while the fasting-induced suppression of GHRH and elevation of NPY and GHS-R mRNA levels remained intact. In fasted adrenalectomized rats, corticosterone replacement increased GHRH-R mRNA levels and intensified the fasting-induced decrease in GHRH, but did not alter NPY or GHS-R response. These data suggest that elevated glucocorticoids mediate the effects of fasting on hypothalamic GHRH and pituitary GHRH-R expression, while glucocorticoids are likely not the major determinant in fasting-induced increases in hypothalamic NPY and pituitary GHS-R expression.

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Ectopic Adrenocorticotropin Syndrome Exhibiting Paradoxical Adrenocorticotropin Responsiveness to Gonadotropin-Releasing Hormone.

Cited by 3 publications

References 12 publications

Gene Expression Study of Thyrotropin Releasing Hormone (TRH) Receptor Using RT-PCR: Relationship to Clinical and Immunohistochemical Phenotypes in a Series of Human Pituitary Adenomas

Gene Expression Study of Thyrotropin Releasing Hormone (TRH) Receptor Using RT-PCR: Relationship to Clinical and Immunohistochemical Phenotypes in a Series of Human Pituitary Adenomas

Ectopic ACTH syndrome caused by desmopressin-responsive thymic neuroendocrine tumor

Role of Glucocorticoids in Fasting-induced Changes in Hypothalamic and Pituitary Components of the Growth Hormone (GH)-axis

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