Deconinck Nicolas, Messaaoui Anissa, Ziereisen France, Kadhim Hazim, Sznajer Yves, Pelc Karine, Nassogne Marie Cécile, Vanier Marie T, Dan Bernard
Department of Neurology, Hôpital Universitaire des Enfants Reine Fabiola, Université Libre de Bruxelles, Av. J.J. Crocq 15, 1020 Brussels, Belgium.
Eur J Paediatr Neurol. 2008 Jan;12(1):46-50. doi: 10.1016/j.ejpn.2007.05.004. Epub 2007 Jul 5.
Metachromatic leukodystrophy (MLD) is an autosomal recessive neurodegenerative lysosomal disease characterized by accumulation of sulfatides, extensive white matter damage and loss of both cognitive and motor functions. In vivo, the catabolism of sulfatide requires both the enzyme arylsulfatase A and a specific sphingolipid activator protein, saposin-B, encoded by the PSAP gene. Arylsulfatase A activity is deficient in the classical forms of MLD, but exceedingly rare cases of MLD are due to saposin-B deficiency. We report here a detailed clinical, radiological and histological description of a new case in a 2-year-old Italian girl, who presented as a late infantile case of MLD with normal arylsulfatase A activity, urinary excretion of sulfatides and mutations in the PSAP gene.
异染性脑白质营养不良(MLD)是一种常染色体隐性神经退行性溶酶体疾病,其特征为硫脂蓄积、广泛的白质损伤以及认知和运动功能丧失。在体内,硫脂的分解代谢需要芳基硫酸酯酶A和由PSAP基因编码的特定鞘脂激活蛋白——鞘磷脂激活蛋白B。在经典型MLD中,芳基硫酸酯酶A活性缺乏,但极为罕见的MLD病例是由鞘磷脂激活蛋白B缺乏所致。我们在此报告一名2岁意大利女童的新病例的详细临床、放射学和组织学描述,该女童表现为具有正常芳基硫酸酯酶A活性、硫脂尿排泄及PSAP基因突变的晚发性婴儿型MLD。