Knops Noël B B, Bos Krista K, Kerstjens Mieke, van Dael Karin, Vos Yvonne J
Department of Pediatric Nephrology, Wilhelmina Children's Hospital, University Medical Center Utrecht, Utrecht, The Netherlands.
Am J Med Genet A. 2008 Jul 15;146A(14):1853-8. doi: 10.1002/ajmg.a.32386.
We report on an infant boy with congenital hydrocephalus due to L1 syndrome and polyuria due to diabetes insipidus. We initially believed his excessive urine loss was from central diabetes insipidus and that the cerebral malformation caused a secondary insufficient pituitary vasopressin release. However, he failed to respond to treatment with a vasopressin analogue, which pointed to nephrogenic diabetes insipidus (NDI). L1 syndrome and X-linked NDI are distinct clinical disorders caused by mutations in the L1CAM and AVPR2 genes, respectively, located in adjacent positions in Xq28. In this boy we found a deletion of 61,577 basepairs encompassing the entire L1CAM and AVPR2 genes and extending into intron 7 of the ARHGAP4 gene. To our knowledge this is the first description of a patient with a deletion of these three genes. He is the second patient to be described with L1 syndrome and NDI. During follow-up he manifested complications from the hydrocephalus and NDI including global developmental delay and growth failure with low IGF-1 and hypothyroidism.
我们报告了一名患有因L1综合征导致的先天性脑积水及因尿崩症导致的多尿症的男婴。我们最初认为他的大量尿液流失是中枢性尿崩症所致,且脑部畸形导致垂体抗利尿激素释放继发性不足。然而,他对使用抗利尿激素类似物治疗无反应,这表明是肾性尿崩症(NDI)。L1综合征和X连锁NDI是分别由位于Xq28相邻位置的L1CAM和AVPR2基因突变引起的不同临床病症。在这个男孩中,我们发现一个61,577个碱基对的缺失,该缺失涵盖整个L1CAM和AVPR2基因,并延伸至ARHGAP4基因的第7内含子。据我们所知,这是首例这三个基因均缺失的患者的描述。他是第二例被描述为患有L1综合征和NDI的患者。在随访期间他出现了脑积水和NDI的并发症,包括全面发育迟缓、生长发育不良伴胰岛素样生长因子-1水平低及甲状腺功能减退。