An Infant Case of Macroprolactinemia with Transient Idiopathic Central Precocious Puberty

Kubo, Toshio; Furujo, Mahoko; Mori, Shiro; Imai, Ken; Ueda, Yuko; Tsukahara, Kohei; Morita, Hirosuke; Ogura, Kunihiro; Fukuhara, Shinichi; Shimizu, Junya; Koyama, Teruhisa; Kanadani, Tomohisa; Saito, Hiroshi; Shinozuka, Masako; Terasaki, Tomoyuki; Hattori, Naoki

doi:10.1507/endocrj.k07-010

Cited by 3 publications

(2 citation statements)

References 15 publications

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“…Although subjects in this study may be too old to determine when macroprolactinaemia began, the current data suggest that macroprolactinaemia is likely to begin before middle age. This assumption is supported by a few reports that demonstrated the presence of macroprolactinaemia in childhood and adolescence (19,20,21).…”

Section: Discussionmentioning

confidence: 55%

The natural history of macroprolactinaemia

Hattori

Adachi

Ishihara

et al. 2012

European Journal of Endocrinology

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Objective: Macroprolactinaemia is a condition in which serum prolactin (PRL) consists mainly of large molecular weight PRL (macroPRL). The aim of this study was to examine the natural history of macroprolactinaemia. Design and participants: Six hundred and fifty-four hospital workers participated in this study, including 27 subjects with macroprolactinaemia and 627 controls. MacroPRL and serum PRL concentrations were evaluated over a 4-year period. The ratio of macroPRL was examined by the polyethylene glycol (PEG) method and gel filtration chromatography. IgG-bound PRL and anti-PRL autoantibodies were examined by protein G and 125 I-PRL binding studies respectively. Results: Over the 4 years of the study, all 27 macroprolactinaemic subjects had persistent macroprolactinaemia without the development of raised free PRL, while none of the 627 controls developed macroprolactinaemia. The ratios of PEG-precipitable PRL and IgG-bound PRL did not significantly change, but 125 I-PRL binding ratios significantly increased. As a whole, total and free serum PRL concentrations did not significantly change in subjects with macroprolactinaemia over the 4-year period. However, hyperprolactinaemia developed in five of the 18 macroprolactinaemic subjects who were initially normoprolactinaemic along with an increase in anti-PRL autoantibody titres. One of the remaining nine macroprolactinaemic subjects who were initially hyperprolactinaemic showed a decrease in serum PRL concentrations, which occurred concomitantly with a decrease in the anti-PRL autoantibody titre. Conclusions: Macroprolactinaemia may develop before middle age and is likely a chronic condition leading to hyperprolactinaemia.

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Section: Discussionmentioning

confidence: 55%

The natural history of macroprolactinaemia

Hattori

Adachi

Ishihara

et al. 2012

European Journal of Endocrinology

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“…The incidence of pituitary prolactinoma is reportedly 27 cases per million individuals per year (1,2). Abnormal levels of prolactin (PRL) and growth hormone (GH) in patients with prolactinoma can lead to dysregulation of the central gonadal axis (3,4) and central precocious puberty in children (5). Current treatments of pituitary tumors are mainly based on hormone therapy and surgery, with auxiliary chemotherapy and radiotherapy (6).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑29‑3p regulates the β‑catenin pathway by targeting IGF1 to inhibit the proliferation of prolactinoma cells

Xia

et al. 2021

Mol Med Rep

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The present study aimed to analyze the effects and underlying mechanisms of microRNA (miR)-29-3p on the proliferation and secretory abilities of prolactinoma cells by targeting insulin-like growth factor (IGF)-1/β-catenin. The relationship between miR-29a-3p and the survival of prolactinoma cells was analyzed with the Kaplan-Meier method in reference to The Cancer Genome Atlas. The expression levels of miR-29a-3p and IGF-1 in MMQ and GH3 cells were detected. A dual-luciferase reporter gene assay was performed to verify the combination of miR-29a-3p and IGF-1. Cells were transfected with a miR-29a-3p mimic and/or IGF-1 pcDNA3.1 to analyze the effects on the proliferation, apoptosis and secretion of prolactin (PRL) and growth hormone (GH) of prolactinoma cells. The effects on β-catenin in the cytoplasm and nucleus were investigated by western blot analysis. The results showed that miR-29a-3p expression was low in MMQ and GH3 cells. Overexpression miR-29a-3p inhibited IGF-1 mRNA and protein expression. miR-29a-3p inhibited cell proliferation and PRL and GH expression, and promoted apoptosis by inhibiting IGF-1. Increasing the expression of miR-29a-3p increased β-catenin levels in the cytoplasm, whereas IGF-1 promoted β-catenin activation and entry into the nucleus, and reversed the inhibitory effects of miR-29a-3p on β-catenin. To conclude, miR-29a-3p inhibited the proliferation and secretory abilities of prolactinoma cells by inhibiting nuclear translocation of β-catenin via a molecular mechanism that is inseparable from IGF-1.

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