Shimizu Reiko, Mitsui Norimasa, Mori Yasuhiro, Cho Shogen, Yamamori Shunji, Osawa Makiko, Ohashi Hirofumi
Department of Pediatrics, School of Medicine, Tokyo Women's Medical University, Tokyo, Japan.
Am J Med Genet A. 2008 Jun 1;146A(11):1458-61. doi: 10.1002/ajmg.a.32319.
We report on a boy who had multiple synostosis syndrome 1, an autosomal dominant disorder characterized by progressive symphalangism, multiple joint fusions, conductive deafness, and mild facial dysmorphism. In addition the boy developed delay of puberty, bone age, and closure of the epiphyseal lines of long bones with tall stature. These findings and decreased plasma LH and FSH levels at age 19 years were compatible with hypogonadotropic hypogonadism. G-banded chromosomes showed a balanced translocation t(10;17)(p15.3;q22). Chromosomal FISH analysis, using a series of BAC clones surrounding the translocation breakpoints, detected a 2.2-3.9 Mb deletion at 17q22. The deletion encompassed NOG, a gene responsible for multiple synostosis syndrome 1. It was assumed that a gene for pituitary secretion of gonoadotropic hormones was deleted at the 17q22 segment.
我们报告了一名患有多指(趾)关节融合综合征1型的男孩,这是一种常染色体显性疾病,其特征为进行性指(趾)间关节融合、多关节融合、传导性耳聋以及轻度面部畸形。此外,该男孩还出现了青春期延迟、骨龄延迟以及长骨干骺端闭合延迟并伴有身材高大。这些发现以及19岁时血浆促黄体生成素(LH)和促卵泡生成素(FSH)水平降低与低促性腺激素性性腺功能减退相符。G显带染色体显示存在平衡易位t(10;17)(p15.3;q22)。使用一系列围绕易位断点的细菌人工染色体(BAC)克隆进行染色体荧光原位杂交(FISH)分析,在17q22处检测到2.2 - 3.9 Mb的缺失。该缺失包含了与多指(趾)关节融合综合征1型相关的NOG基因。据推测,17q22区段存在一个负责垂体促性腺激素分泌的基因缺失。