Division of Nephrology and Endocrinology, The University of Tokyo Hospital, Tokyo, Japan.
Osteoporosis Center, The University of Tokyo Hospital, Tokyo, Japan.
J Bone Miner Res. 2022 Jun;37(6):1125-1135. doi: 10.1002/jbmr.4550. Epub 2022 Apr 11.
Homozygous ENPP1 mutations are associated with autosomal recessive hypophosphatemic rickets type 2 (ARHR2), severe ossification of the spinal ligaments, and generalized arterial calcification of infancy type 1. There are a limited number of reports on phenotypes associated with heterozygous ENPP1 mutations. Here, we report a series of three probands and their families with heterozygous and compound heterozygous ENPP1 mutations. The first case (case 1) was a 47-year-old male, diagnosed with early-onset osteoporosis and low-normal serum phosphate levels, which invoked suspicion for hypophosphatemic rickets. The second and third cases were 77- and 54-year-old females who both presented with severe spinal ligament ossification and the presumptive diagnosis of diffuse idiopathic skeletal hyperostosis (DISH). Upon workup, fibroblast growth factor 23 (FGF23) was noted to be relatively high in case 2 and serum phosphorous was low-normal in case 3, and the diagnoses of X-linked hypophosphatemic rickets (XLH) and ARHR2 were considered. Genetic testing for genes related to congenital hypophosphatemic rickets was therefore performed, revealing heterozygous ENPP1 variants in cases 1 and 2 (case 1, c.536A>G, p.Asn179Ser; case 2, c.1352A>G, p.Tyr451Cys) and compound heterozygous ENPP1 variants in case 3 constituting the same variants present in cases 1 and 2 (c.536A>G, p.Asn179Ser and c.1352A>G, p.Tyr451Cys). Several in silico tools predicted the two variants to be pathogeneic, a finding confirmed by in vitro biochemical analysis demonstrating that the p.Asn179Ser and p.Tyr451Cys ENPP1 variants possessed a catalytic velocity of 45% and 30% compared with that of wild-type ENPP1, respectively. Both variants were therefore categorized as pathogenic loss-of-function mutations. Our findings suggest that ENPP1 mutational status should be evaluated in patients presenting with the diagnosis of idiopathic DISH, ossification of the posterior longitudinal ligament (OPLL), and early-onset osteoporosis. © 2022 American Society for Bone and Mineral Research (ASBMR).
纯合性 ENPP1 突变与常染色体隐性低磷血症性佝偻病 2 型(ARHR2)、严重的脊柱韧带骨化以及婴儿型 1 型全身性动脉钙化有关。关于杂合性 ENPP1 突变相关表型的报道数量有限。在此,我们报告了一系列携带杂合和复合杂合性 ENPP1 突变的三个先证者及其家系。第一个病例(病例 1)为 47 岁男性,诊断为早发性骨质疏松症和血清磷酸盐水平正常低值,提示低磷血症性佝偻病。第二和第三个病例为 77 岁和 54 岁女性,均表现为严重的脊柱韧带骨化和弥漫性特发性骨肥厚(DISH)的拟诊。在检查过程中,发现第 2 例的成纤维细胞生长因子 23(FGF23)相对较高,第 3 例的血清磷正常低值,考虑 X 连锁低磷血症性佝偻病(XLH)和 ARHR2 的诊断。因此,对与先天性低磷血症性佝偻病相关的基因进行了基因检测,发现病例 1 和 2 存在杂合性 ENPP1 变异(病例 1,c.536A>G,p.Asn179Ser;病例 2,c.1352A>G,p.Tyr451Cys),病例 3 为复合杂合性 ENPP1 变异,包含病例 1 和 2 中存在的相同变异(c.536A>G,p.Asn179Ser 和 c.1352A>G,p.Tyr451Cys)。几种计算工具预测这两种变异是致病性的,体外生化分析证实,p.Asn179Ser 和 p.Tyr451Cys ENPP1 变异的催化速度分别比野生型 ENPP1 低 45%和 30%。因此,这两种变异都被归类为致病性失功能突变。我们的研究结果表明,在诊断为特发性 DISH、后纵韧带骨化(OPLL)和早发性骨质疏松症的患者中,应评估 ENPP1 突变状态。© 2022 美国骨矿研究协会(ASBMR)。