Chiarello Paola, Gualtieri Gianmarco, Bossio Sabrina, Seminara Giuseppe, Molinaro Marianna, Antonucci Gemma, Perri Anna, Rocca Valentina, Cannarella Rossella, La Vignera Sandro, Calogero Aldo E, Greco Emanuela A, Iuliano Rodolfo, Alcaro Stefano, Aversa Antonio
Department of Pediatrics, Dulbecco Azienda Ospedaliero-Universitaria of Catanzaro, 88100 Catanzaro, Italy.
Department of Experimental and Clinical Medicine, Università degli Studi Magna Græcia di Catanzaro, 88100 Catanzaro, Italy.
Int J Mol Sci. 2025 May 28;26(11):5207. doi: 10.3390/ijms26115207.
Congenital hypogonadotropic hypogonadism (CHH) is a rare and heterogeneous genetic disorder with variable penetrance caused by GnRH deficiency, leading to delayed puberty and infertility. In 50-60% of cases, CHH is associated with non-reproductive abnormalities, most commonly anosmia/hyposmia (Kallmann syndrome, KS). Over 60 genes have been implicated in CHH pathogenesis. We aimed to perform genetic screening in a cohort of 14 patients (10 males, 4 females; mean age 22 ± 7.72 years) with suspected or diagnosed HH/KS. Genetic analysis was conducted using next-generation sequencing (NGS) with a custom panel of 46 candidate genes. Variant interpretation followed ACMG standards and guidelines. Multiple tools were used to predict the structural effects of variants on tertiary protein structure, assessing their pathogenicity. Novel variants were functionally characterized by qRT-PCR on mRNA extracted from peripheral leukocytes. NGS identified nine rare variants and four novel variants in genes previously associated with normosmic isolated HH (nHH) and/or KS (, , , , , , , , , and ). The variant in (p.Trp275Ter) was pathogenic; variants in (c.541+1G>A), (c.1303_1304dup, p.Lys436ThrfsTer58), and (p.Lys361Ter) were likely pathogenic. Nine variants were classified as variants of uncertain significance (VUS). Our study identified a possible genetic cause in 71% of the CHH/KS cohort, emphasizing the importance of genetic screening and functional characterization of genetic variants in patients with a phenotypically and genetically heterogeneous disorder like CHH.
先天性低促性腺激素性性腺功能减退(CHH)是一种罕见的、具有遗传异质性的疾病,由促性腺激素释放激素(GnRH)缺乏导致,其外显率可变,可引起青春期延迟和不孕不育。在50% - 60%的病例中,CHH与非生殖系统异常有关,最常见的是嗅觉缺失/嗅觉减退(卡尔曼综合征,KS)。超过60个基因与CHH的发病机制有关。我们旨在对14例疑似或确诊为HH/KS的患者(10例男性,4例女性;平均年龄22±7.72岁)进行基因筛查。使用包含46个候选基因的定制面板,通过二代测序(NGS)进行基因分析。变异解读遵循美国医学遗传学与基因组学学会(ACMG)的标准和指南。使用多种工具预测变异对三级蛋白质结构的结构影响,评估其致病性。通过对从外周血白细胞中提取的mRNA进行定量逆转录聚合酶链反应(qRT-PCR),对新变异进行功能表征。NGS在先前与嗅觉正常的孤立性HH(nHH)和/或KS相关的基因中鉴定出9个罕见变异和4个新变异(、、、、、、、、和)。(p.Trp275Ter)中的变异是致病性的;(c.541 + 1G>A)、(c.1303_1304dup,p.Lys436ThrfsTer58)和(p.Lys361Ter)中的变异可能是致病性的。9个变异被分类为意义未明的变异(VUS)。我们的研究在71%的CHH/KS队列中确定了可能的遗传原因,强调了在像CHH这样具有表型和遗传异质性疾病的患者中进行基因筛查和基因变异功能表征的重要性。