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在印度尼西亚一组46,XY男性化不足男孩队列中鉴定出的先天性低促性腺激素性性腺功能减退基因变异。

Variants in congenital hypogonadotrophic hypogonadism genes identified in an Indonesian cohort of 46,XY under-virilised boys.

作者信息

Ayers Katie L, Bouty Aurore, Robevska Gorjana, van den Bergen Jocelyn A, Juniarto Achmad Zulfa, Listyasari Nurin Aisyiyah, Sinclair Andrew H, Faradz Sultana M H

机构信息

Murdoch Childrens Research Institute, Melbourne, Victoria, Australia.

Department of Paediatrics, University of Melbourne, Melbourne, Victoria, Australia.

出版信息

Hum Genomics. 2017 Feb 16;11(1):1. doi: 10.1186/s40246-017-0098-2.

Abstract

BACKGROUND

Congenital hypogonadotrophic hypogonadism (CHH) and Kallmann syndrome (KS) are caused by disruption to the hypothalamic-pituitary-gonadal (H-P-G) axis. In particular, reduced production, secretion or action of gonadotrophin-releasing hormone (GnRH) is often responsible. Various genes, many of which play a role in the development and function of the GnRH neurons, have been implicated in these disorders. Clinically, CHH and KS are heterogeneous; however, in 46,XY patients, they can be characterised by under-virilisation phenotypes such as cryptorchidism and micropenis or delayed puberty. In rare cases, hypospadias may also be present.

RESULTS

Here, we describe genetic mutational analysis of CHH genes in Indonesian 46,XY disorder of sex development patients with under-virilisation. We present 11 male patients with varying degrees of under-virilisation who have rare variants in known CHH genes. Interestingly, many of these patients had hypospadias.

CONCLUSIONS

We postulate that variants in CHH genes, in particular PROKR2, PROK2, WDR11 and FGFR1 with CHD7, may contribute to under-virilisation phenotypes including hypospadias in Indonesia.

摘要

背景

先天性低促性腺激素性性腺功能减退(CHH)和卡尔曼综合征(KS)是由下丘脑 - 垂体 - 性腺(H - P - G)轴功能紊乱引起的。特别是,促性腺激素释放激素(GnRH)的产生、分泌或作用减少通常是其病因。多种基因与这些疾病有关,其中许多基因在GnRH神经元的发育和功能中发挥作用。临床上,CHH和KS具有异质性;然而,在46,XY患者中,它们可表现为男性化不足的表型,如隐睾症和小阴茎或青春期延迟。在罕见情况下,也可能出现尿道下裂。

结果

在此,我们描述了对印度尼西亚患有男性化不足的46,XY性发育障碍患者的CHH基因进行的遗传突变分析。我们呈现了11例具有不同程度男性化不足且在已知CHH基因中存在罕见变异的男性患者。有趣的是,这些患者中有许多患有尿道下裂。

结论

我们推测,CHH基因的变异,特别是与CHD7相关的PROKR2、PROK2、WDR11和FGFR1基因的变异,可能导致印度尼西亚男性化不足的表型,包括尿道下裂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/876d/5314676/128d26ef9d0a/40246_2017_98_Fig1_HTML.jpg

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