Department of Pediatrics, Columbia University, New York, NY 10032, USA.
J Inherit Metab Dis. 2011 Oct;34(5):1013-22. doi: 10.1007/s10545-011-9343-3. Epub 2011 May 11.
We describe a single consanguineous family with three affected children exhibiting knee and/or hip pain associated with swelling. Detailed clinical evaluation demonstrated diffuse joint involvement with an unusual proliferative synovitis on MRI. Synovial biopsies were notable for an infiltration of macrophages with abundant cytoplasm filled with faintly basophilic vacuoles. We used homozygosity mapping with a panel of 262,000 single nucleotide polymorphism markers to identify a homozygous stretch of 40.52 Mb on chromosome 3p22.3 - 3p13 that segregated with the arthropathy in the family. Of the 378 genes in the interval, the three hyaluronoglucosaminidase genes were considered good candidates based on the phenotype. Dideoxy sequencing identified a homozygous deletion in HYAL1, c.104delT, resulting in a premature termination codon, p.Val35AlafsX25, found in all three affected children. Enzymatic analysis confirmed total HYAL1 deficiency in the three affected children. This confirms the diagnosis of Mucopolysaccharidosis IX (MPS IX) which has only been described in a single patient to date. In contrast to the previously described MPS IX patient, our three patients display a phenotype limited to the joints, suggesting that this is the primary manifestation of HYAL1 deficiency.
我们描述了一个单合子近亲家族,其中三个受影响的孩子表现为膝关节和/或髋关节疼痛伴肿胀。详细的临床评估显示弥漫性关节受累,MRI 显示不寻常的增生性滑膜炎。滑膜活检显示大量富含淡嗜碱性空泡的细胞质的巨噬细胞浸润。我们使用包含 262,000 个单核苷酸多态性标记物的面板进行纯合子作图,在 3p22.3-3p13 染色体上鉴定出与家族性关节炎共分离的纯合 40.52 Mb 片段。在该区间的 378 个基因中,基于表型,三个透明质酸葡糖胺糖苷酶基因被认为是候选基因。双脱氧测序确定 HYAL1 基因中存在纯合缺失,c.104delT,导致提前终止密码子,p.Val35AlafsX25,在所有三个受影响的孩子中均发现。酶分析证实三个受影响的孩子均存在 HYAL1 完全缺乏。这证实了黏多糖贮积症 IX(MPS IX)的诊断,迄今为止仅在一名患者中描述过。与之前描述的 MPS IX 患者不同,我们的三个患者表现为仅局限于关节的表型,提示这是 HYAL1 缺乏的主要表现。