Hoyme H E, Higginbottom M C, Jones K L
Pediatrics. 1981 Feb;67(2):288-91.
Two infants with structural defects previously undescribed in the survivor of a monozygotic twin pair are reported. One infant had hydranencephaly and a spinal cord transection, with an associated dead monozygotic co-twin of 24 weeks gestation; the other child had complete atresia of the colon and a horseshoe kidney, with a deceased co-twin of approximately six weeks gestation. These defects are presumed to be the result of in utero disruption of previously normally formed structures. They occur secondary to vascular exchange from a dead to a living monozygotic twin through placental vascular anastomoses. As illustrated by the two children described, the nature of the vascular defects seen in the survivor of a monozygotic twin pair depends on the time during gestation at which the co-twin dies. Recognition of the disruptive vascular etiology of the structural defects outlined in this report will allow for appropriate counseling with respect to the negligible recurrence risk for similar vascular accidents.
本文报告了一对单卵双胞胎中,存活婴儿出现了此前未被描述过的结构缺陷。一名婴儿患有积水性无脑畸形和脊髓横断,与之相关的是一名孕24周的单卵双胎死胎;另一名儿童患有结肠完全闭锁和马蹄肾,与之相关的是一名孕约6周的双胎死胎。这些缺陷被推测是由于子宫内先前正常形成的结构受到破坏所致。它们是通过胎盘血管吻合从死胎单卵双胞胎向存活单卵双胞胎进行血管交换的继发结果。如所描述的两名儿童所示,单卵双胞胎中存活婴儿出现的血管缺陷的性质取决于双胎死亡时的孕周。认识到本报告中概述的结构缺陷的破坏性血管病因,将有助于就类似血管意外的可忽略不计的复发风险进行适当的咨询。