Alcántara-Ortigoza M A, García-de Teresa B, González-Del Angel A, Berumen J, Guardado-Estrada M, Fernández-Hernández L, Navarrete-Martínez J I, Maza-Morales M, Rius-Domínguez R
Laboratorio de Biología Molecular, Departamento de Genética Humana, Instituto Nacional de Pediatría, Distrito Federal, México.
Departamento de Medicina Experimental, Facultad de Medicina, Universidad Nacional Autónoma de México, Distrito Federal, México.
Clin Genet. 2016 May;89(5):574-83. doi: 10.1111/cge.12738. Epub 2016 Feb 9.
Hunter syndrome or mucopolysaccharidosis type II (MPSII) is caused by pathogenic variants in the IDS gene. This is the first study that examines the mutational spectrum in 25 unrelated Mexican MPSII families. The responsible genotype was identified in 96% of the families (24/25) with 10 novel pathogenic variants: c.133G>C, c.1003C>T, c.1025A>C, c.463_464delinsCCGTATAGCTGG, c.754_767del, c.1132_1133del, c.1463del, c.508-1G>C, c.1006+1G>T and c.(-217_103del). Extensive IDS gene deletions were identified in four patients; using DNA microarray analysis two patients showed the loss of the entire AFF2 gene, and epilepsy developed in only one of them. Wide allelic heterogeneity was noted, with large gene alterations (e.g. IDS/IDSP1 gene inversions, partial to extensive IDS deletions, and one chimeric IDS-IDSP1 allele) that occurred at higher frequencies than previously reported (36% vs 18.9-29%). The frequency of carrier mothers (80%) is consistent with previous descriptions (>70%). Carrier assignment allowed molecular prenatal diagnoses. Notably, somatic and germline mosaicism was identified in one family, and two patients presented thrombocytopenic purpura and pancytopenia after idursulfase enzyme replacement treatment. Our findings suggest a wide allelic heterogeneity in Mexican MPSII patients; DNA microarray analysis contributes to further delineation of the resulting phenotype for IDS and neighboring loci deletions.
亨特综合征或II型黏多糖贮积症(MPSII)由IDS基因突变所致。这是首项对25个无亲缘关系的墨西哥MPSII家庭的突变谱进行研究的报告。在96%(24/25)的家庭中确定了致病基因型,发现了10种新的致病变异:c.133G>C、c.1003C>T、c.1025A>C、c.463_464delinsCCGTATAGCTGG、c.754_767del、c.1132_1133del、c.1463del、c.508-1G>C、c.1006+1G>T和c.(-217_103del)。在4例患者中发现了广泛的IDS基因缺失;通过DNA微阵列分析,2例患者显示整个AFF2基因缺失,其中仅1例发生癫痫。发现了广泛的等位基因异质性,大的基因改变(如IDS/IDSP1基因倒位、部分至广泛的IDS缺失以及1个嵌合的IDS-IDSP1等位基因)的发生频率高于先前报道(36%对18.9 - 29%)。携带致病基因母亲的频率(80%)与先前描述一致(>70%)。致病基因携带者的确定有助于进行分子产前诊断。值得注意的是,在1个家庭中发现了体细胞和生殖细胞嵌合现象,2例患者在接受艾杜糖醛酸酶替代治疗后出现血小板减少性紫癜和全血细胞减少。我们的研究结果表明,墨西哥MPSII患者存在广泛的等位基因异质性;DNA微阵列分析有助于进一步明确IDS及邻近基因座缺失所导致的表型。