Al-Hassnan Zuhair N, Al Dhalaan Hesham, Patay Zoltan, Faqeih Eissa, Al-Owain Mohammed, Al-Duraihem Adel, Faiyaz-Ul-Haque Mohammed
Department of Medical Genetics, King Faisal Specialist Hospital and Research Centre (KFSH&RC), Riyadh, Saudi Arabia.
J Child Neurol. 2009 Dec;24(12):1513-9. doi: 10.1177/0883073809341269.
Mutated PSAP gene resulting in sphingolipid activator protein B deficiency is known to cause metachromatic leukodystrophy variant in which arylsulfatase A is normal. Of 16 patients with metachromatic leukodystrophy that were evaluated in our center, 7 patients were diagnosed with arylsulfatase A-deficient metachromatic leukodystrophy, whereas 9 children from 4 unrelated Saudi families were found to have sphingolipid activator protein B deficiency. PSAP analysis found that the 4 families segregate the same homozygous mutation that was a g.722G>C transversion resulting in C241S change, which was previously reported in an Arab patient. Our work, which reports the largest series of patients with sphingolipid activator protein B deficiency, suggests that this variant is likely to be more common than arylsulfatase A-deficient metachromatic leukodystrophy in Arabs, a notion that has potential diagnostic and preventive implications.
已知导致鞘脂激活蛋白B缺乏的PSAP基因突变会引起异染性脑白质营养不良变异型,其中芳基硫酸酯酶A正常。在我们中心评估的16例异染性脑白质营养不良患者中,7例被诊断为芳基硫酸酯酶A缺乏型异染性脑白质营养不良,而在4个不相关的沙特家庭的9名儿童中发现有鞘脂激活蛋白B缺乏。PSAP分析发现,这4个家庭存在相同的纯合突变,即g.722G>C颠换,导致C241S改变,此前在一名阿拉伯患者中曾有报道。我们的研究报告了最大系列的鞘脂激活蛋白B缺乏患者,表明这种变异型在阿拉伯人中可能比芳基硫酸酯酶A缺乏型异染性脑白质营养不良更常见,这一观点具有潜在的诊断和预防意义。