Reference Centre for Inborn Errors of Metabolism, Robert Debré University Hospital, APHP, Paris, France.
Department of Haematology, Robert Debré University Hospital, APHP, Paris, France.
Eur J Paediatr Neurol. 2017 Nov;21(6):907-911. doi: 10.1016/j.ejpn.2017.07.015. Epub 2017 Jul 29.
Acid sphingomyelinase (ASM) deficient Niemann-Pick disease is a lysosomal storage disorder resulting from mutations in the SMPD1 gene. The clinical spectrum distinguishes a severe infantile neurological form (type A), a non-neurological visceral form (type B) and a rare intermediate neurovisceral form. We report the first case of presymptomatic cord blood transplantation in a child with the intermediate type of ASM deficiency due to a homozygous Tyr369Cys mutation, whose affected elder brother had developed neurodevelopmental delay from 19 months of age, and had died from severe visceral complications at the age of 3. In the transplanted propositus, neurological deterioration became evident by 4 years of age; the child was alive at age 8, although severely disabled. Whereas the transplant prevented visceral progression and early death, it could only delay neurocognitive deterioration.
酸性鞘磷脂酶 (ASM) 缺乏型尼曼-匹克病是一种溶酶体贮积症,由 SMPD1 基因突变引起。临床表型可区分严重的婴儿神经型(A型)、非神经内脏型(B 型)和罕见的中间神经内脏型。我们报告了首例中间型 ASM 缺乏症患者的脐带血移植病例,该患者因 Tyr369Cys 突变纯合子导致疾病,其受影响的哥哥在 19 个月时出现神经发育迟缓,3 岁时因严重内脏并发症死亡。在接受移植的先证者中,4 岁时神经功能恶化变得明显;患儿在 8 岁时仍然存活,但已严重残疾。尽管移植可以预防内脏进展和早期死亡,但只能延迟神经认知恶化。