Garin Intza, Mantovani Giovanna, Aguirre Urko, Barlier Anne, Brix Bettina, Elli Francesca M, Freson Kathleen, Grybek Virginie, Izzi Benedetta, Linglart Agnès, Perez de Nanclares Guiomar, Silve Caroline, Thiele Susanne, Werner Ralf
Molecular (Epi)Genetics Laboratory, BioAraba National Health Institute, Hospital Universitario Araba-Txagorritxu, Vitoria-Gasteiz, Spain.
Endocrinology and Diabetology Unit, Department of Clinical Sciences and Community Health, University of Milan, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Eur J Hum Genet. 2015 Apr;23(4):438-44. doi: 10.1038/ejhg.2014.127. Epub 2014 Jul 9.
Pseudohypoparathyroidism is a rare endocrine disorder that can be caused by genetic (mainly maternally inherited inactivating point mutations, although intragenic and gross deletions have rarely been reported) or epigenetic alterations at GNAS locus. Clinical and molecular characterization of this disease is not that easy because of phenotypic, biochemical and molecular overlapping features between both subtypes of the disease. The European Consortium for the study of PHP (EuroPHP) designed the present work with the intention of generating the standards of diagnostic clinical molecular (epi)genetic testing in PHP patients. With this aim, DNA samples of eight independent PHP patients carrying GNAS genetic and/or epigenetic defects (three patients with GNAS deletions, two with 20q uniparental disomy and three with a methylation defect of unknown origin) without GNAS point mutations were anonymized and sent to the five participant laboratories for their routine genetic analysis (methylation-specific (MS)-MLPA, pyrosequencing and EpiTYPER) and interpretations. All laboratories were able to detect methylation defects and, after the data analysis, the Consortium compared the results to define technical advantages and disadvantages of different techniques. To conclude, we propose as first-level investigation in PHP patients copy number and methylation analysis by MS-MLPA. Then, in patients with partial methylation defect, the result should be confirmed by single CpG bisulphite-based methods (ie pyrosequencing), whereas in case of a complete methylation defect without detectable deletion, microsatellites or SNP genotyping should be performed to exclude uniparental disomy 20.
假性甲状旁腺功能减退症是一种罕见的内分泌疾病,可由GNAS基因座的遗传(主要是母系遗传的失活点突变,尽管基因内和大片段缺失很少见报道)或表观遗传改变引起。由于该疾病两种亚型之间存在表型、生化和分子重叠特征,因此对这种疾病进行临床和分子特征分析并非易事。欧洲假性甲状旁腺功能减退症研究联盟(EuroPHP)开展了本研究,旨在制定假性甲状旁腺功能减退症患者诊断性临床分子(表观)遗传学检测的标准。为此,将8例携带GNAS基因和/或表观遗传缺陷(3例有GNAS缺失,2例有20号染色体单亲二倍体,3例有不明来源的甲基化缺陷)且无GNAS点突变的独立假性甲状旁腺功能减退症患者的DNA样本进行匿名处理,并送至5个参与实验室进行常规遗传分析(甲基化特异性(MS)-MLPA、焦磷酸测序和EpiTYPER)及解读。所有实验室均能检测到甲基化缺陷,数据分析后,联盟比较结果以确定不同技术的技术优缺点。总之,我们建议对假性甲状旁腺功能减退症患者进行一级检查时采用MS-MLPA进行拷贝数和甲基化分析。然后,对于部分甲基化缺陷的患者,结果应通过基于单CpG亚硫酸氢盐的方法(即焦磷酸测序)进行确认,而对于无可检测到的缺失的完全甲基化缺陷的情况,应进行微卫星或SNP基因分型以排除20号染色体单亲二倍体。