Nowaczyk M J, Farrell S A, Sirkin W L, Velsher L, Krakowiak P A, Waye J S, Porter F D
Department of Pathology and Molecular Medicine, McMaster University, Canada.
Am J Med Genet. 2001 Sep 15;103(1):75-80. doi: 10.1002/1096-8628(20010915)103:1<75::aid-ajmg1502>3.0.co;2-r.
Smith-Lemli-Opitz syndrome (RHS) (SLOS, OMIM 270400) is an autosomal recessive disorder of cholesterol biosynthesis caused by mutations of the 3beta-hydroxysterol Delta(7)-Delta(8)-reductase gene, DHCR7. We report a fetus with holoprosencephaly and multiple congenital anomalies who was homozygous for the IVS8-1G-->C mutation. Following termination of pregnancy, both the elevated amniotic fluid 7-dehydrocholesterol level and the DHCR7 mutations were demonstrated. Two other newborn infants with IVS8-1G-->C/IVS8-1G-->C genotype are described. This report illustrates a severe phenotypic extreme of SLOS associated with a null genotype, underscores the complex relationship between SLOS and holoprosencephaly, and discusses the possible pathogenetic mechanisms of the development of holoprosencephaly in SLOS.
史密斯-勒米-奥皮茨综合征(RHS)(SLOS,OMIM 270400)是一种常染色体隐性胆固醇生物合成障碍疾病,由3β-羟基甾醇Δ(7)-Δ(8)-还原酶基因(DHCR7)突变引起。我们报告了一名患有前脑无裂畸形和多种先天性异常的胎儿,其IVS8-1G→C突变呈纯合状态。终止妊娠后,羊水7-脱氢胆固醇水平升高以及DHCR7突变均得到证实。还描述了另外两名具有IVS8-1G→C/IVS8-1G→C基因型的新生儿。本报告阐述了与无效基因型相关的SLOS的一种严重表型极端情况,强调了SLOS与前脑无裂畸形之间的复杂关系,并探讨了SLOS中前脑无裂畸形发生发展的可能致病机制。