Adénome à prolactine : du désir de grossesse à l’accouchement

Fatfouta, I.; Delotte, J.; Mialon, O.; Isnard, V.; Bongain, A.

doi:10.1016/j.jgyn.2012.08.001

Cited by 5 publications

(2 citation statements)

References 36 publications

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“…The prolactin-secreting pituitary adenoma (prolactinoma) is the most common pituitary tumor, with an incidence of approximately 27 cases per million annually [1]. Although it has low incidence rate, prolactinoma is the most common pathologic reason for irregular menses, galactorrhea and infertility especially in young women [2]. Therefore, it is urgent to comprehensively inquire the mechanism underlying prolactinoma.…”

Section: Introductionmentioning

confidence: 99%

17β-estradiol binding to ERα promotes the progression of prolactinoma through estrogen-response element-induced CaBP-9k up-regulation

et al. 2020

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17β-estradiol (E2) is considered to be an important instigator of prolactinoma, and can positively regulate the expression of calbindin-D9k (CaBP-9k) which contains an estrogen responsive element (ERE) via estrogen receptors (ERs). However, the detailed mechanism of E2 in promoting CaBP-9k expression and their roles in prolactinoma progression remain unclear. Here, we aimed to characterize it. The luciferase gene reporter assay with luc-ERE transfection showed that E2 treatment significantly enhanced the transcriptional level of CaBP-9k, whereas CaBP-9k activity was reduced when GH3 and MMQ cells were treated with AZD9496, an antagonist of ERα. E2 treatment increased the protein expressions of CaBP-9k and ERα but not ERβ, whereas this effect was also abolished when cells were treated with AZD9496. Besides, immunoprecipitation (IP) and immunofluorescence assays demonstrated that CaBP-9k could directly interact with ERα not ERβ, and Chromatin IP (ChIP) assay showed that ERα could bind to ERE of the CaBP-9k promoter. Moreover, cell counting kit-8 (CCK-8) and flow cytometry assays showed that E2 treatment significantly enhanced cell viability and inhibited cell apoptosis, but these effects were all abolished when ERα was down-regulated by short hairpin RNA (shRNA) or inhibited by AZD9496, as well as CaBP-9K suppression in both GH3 and MMQ cell lines. Taken together, these findings indicated that E2 stimulation promoted prolactin cell proliferation and inhibited cell apoptosis through ERα-induced CaBP-9k up-regulation, which then accelerated the advanced progression of prolactinoma.

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Section: Introductionmentioning

confidence: 99%

17β-estradiol binding to ERα promotes the progression of prolactinoma through estrogen-response element-induced CaBP-9k up-regulation

et al. 2020

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“…A confirmed volumetric evolution and functional consequences will lead to the introduction of a dopaminergic agonist during pregnancy. Bromocriptine should be introduced as first-line therapy; the choice of other molecules is only justified in case of documented resistance or intolerance to it [8].…”

Section: Discussionmentioning

confidence: 99%

Spontaneous reduction in macroprolactinoma volume during pregnancy and after birth: A case report

Gharroudi¹,

Rafi²,

Mghari³

et al. 2023

World J. Adv. Res. Rev.

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Prolactinoma, the most common secretory pituitary tumor, is found in 100 patients per million. It is responsible for impaired reproductive function in both sexes. Its treatment in the context of fertility restoration gives very satisfactory results. The natural history of these tumors in the gestational period is variable depending on their size with a clinically signiﬁcative risk ranging from 5 to 30%. Their management is complex, requiring evaluation of the effects of pregnancy on tumor growth and the effects of therapy on embryonic and fetal development. We report the case of 23years patient with a macroprolactinoma and the successful outcome of this tumor during the pregnancy.

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