Akahoshi Keiko, Spritz Richard A, Fukai Kazuyoshi, Mitsui Norimasa, Matsushima Kazushige, Ohashi Hirofumi
Department of Medical Genetics, Tokyo Children's Rehabilitation Hospital, Tokyo, Japan.
Am J Med Genet A. 2004 Apr 30;126A(3):290-2. doi: 10.1002/ajmg.a.20580.
Association of the pink-eye-dilution gene (P) with hypopigmentation is seen in patients who have oculocutaneous albinism type 2 (OCA2) and Prader-Willi syndrome (PWS) or Angelman syndrome (AS). However, it remains unknown whether duplication or amplification of the P gene causes hyperpigmentation. We previously reported a woman who had hyperpigmentation with a duplication of the proximal part of 15q, including the P gene. Here, we describe an additional patient with mosaicism of inv dup(15) and clinical manifestations of severe psychmoter retardation, epilepsy, and pigmentary dysplasia showing mottled and linear patterns of hyperpigmentation. His karyotype was 47,XY,+idic(15)(pter-->q14::q14-->pter)[38]/46,XY[12] de novo. Chromosomal fluorescence in situ hybridization (FISH) showed six copies of the P gene. Therefore, his cutaneous mosaicism might be caused by the presence of both normal and hyperpigmented skin due to multicopies of the P gene.
在患有2型眼皮肤白化病(OCA2)以及普拉德-威利综合征(PWS)或安吉尔曼综合征(AS)的患者中,可见红眼稀释基因(P)与色素减退有关。然而,P基因的重复或扩增是否会导致色素沉着过度仍不清楚。我们之前报道过一名女性,她因15q近端部分(包括P基因)的重复而出现色素沉着过度。在此,我们描述了另一名患有inv dup(15)嵌合体的患者,其临床表现为严重精神运动发育迟缓、癫痫和色素发育异常,色素沉着呈现斑驳和线状模式。他的核型为47,XY,+idic(15)(pter→q14::q14→pter)[38]/46,XY[12],为新发突变。染色体荧光原位杂交(FISH)显示有6个P基因拷贝。因此,他的皮肤嵌合体可能是由于P基因多拷贝导致正常皮肤和色素沉着过度皮肤同时存在所致。