NIHR Biomedical Research Centre, Moorfields Eye Hospital and the UCL Institute of Ophthalmology, London, UK.
UCL Institute of Ophthalmology, University College London, London, UK.
Clin Genet. 2024 Oct;106(4):505-511. doi: 10.1111/cge.14573. Epub 2024 Jun 11.
Biallelic variants in SUMF1 are associated with multiple sulfatase deficiency (MSD), a rare lysosomal storage disorder typically diagnosed in early infancy or childhood, marked by severe neurodegeneration and early mortality. We present clinical and molecular characterisation of three unrelated patients aged 13 to 58 years with milder clinical manifestations due to SUMF1 disease variants, including two adult patients presenting with apparent non-syndromic retinal dystrophy. Whole genome sequencing identified biallelic SUMF1 variants in all three patients; Patient 1 homozygous for a complex allele c.[290G>T;293T>A]; p.[(Gly97Val);(Val98Glu)], Patient 2 homozygous for c.866A>G; p.(Tyr289Cys), and Patient 3 compound heterozygous for c.726-1G>C and p.(Tyr289Cys). Electroretinography indicated a rod-cone dystrophy with additional possible inner retinal dysfunction in all three patients. Biochemical studies confirmed reduced, but not absent, sulfatase enzyme activity in the absence of extra-ocular disease (Patient 1) or only mild systemic disease (Patients 2, 3). These cases are suggestive that non-null SUMF1 genotypes can cause an attenuated clinical phenotype, including retinal dystrophy without systemic complications, in adulthood.
SUMF1 的双等位基因突变与多种硫酸酯酶缺乏症(MSD)有关,这是一种罕见的溶酶体贮积症,通常在婴儿期或儿童期早期诊断,其特征为严重的神经退行性变和早期死亡。我们介绍了 3 名无关联的患者的临床和分子特征,他们的年龄在 13 岁至 58 岁之间,由于 SUMF1 疾病变异,临床表现较轻,包括 2 名成年患者表现出明显的非综合征性视网膜营养不良。全基因组测序在所有 3 名患者中均发现了双等位基因 SUMF1 变异;患者 1 为杂合子,携带复杂等位基因 c.[290G>T;293T>A];p.[(Gly97Val);(Val98Glu)],患者 2 为纯合子,携带 c.866A>G;p.(Tyr289Cys),患者 3 为复合杂合子,携带 c.726-1G>C 和 p.(Tyr289Cys)。视网膜电图显示 3 名患者均存在杆状和锥状视网膜营养不良,可能伴有额外的内层视网膜功能障碍。生化研究证实,在没有眼外疾病(患者 1)或仅有轻度全身疾病(患者 2、3)的情况下,硫酸酯酶活性降低,但并未完全缺失。这些病例表明,非无效 SUMF1 基因型可能导致成人出现症状较轻的临床表型,包括无全身并发症的视网膜营养不良。