Hasegawa Kosei, Tanaka Hiroyuki, Futagawa Natsuko, Miyahara Hiroyuki, Tsukahara Hirokazu
Department of Pediatrics, Okayama University Hospital, 2-5-1 Shikata-Cho, Kita-Ku, Okayama 700-8558, Japan.
Department of Pediatrics, Okayama Saiseikai General Hospital, 1-7-18 Ifuku-Cho, Kita-Ku, Okayama 700-8511, Japan.
Case Rep Genet. 2022 Aug 25;2022:5021758. doi: 10.1155/2022/5021758. eCollection 2022.
Fibrodysplasia ossificans progressiva (FOP) is a rare skeletal disorder characterized by congenital malformation of the great toes and progressive heterotopic ossification. Malformation of the great toes appears at birth, while heterotopic ossification generally occurs during childhood and rarely occurs during infancy. Classical FOP results from the heterozygous p.Arg206His variant of the ACVR1 gene, which encodes Activin A receptor type 1. Recently, some atypical FOP patients with other ACVR1 gene variants and clinical features that are not observed in classical FOP patients have been reported. Herein, we describe a girl with severe FOP and multiple anomalies, including syndactyly of the hands and feet, nail agenesis, mandibular hypoplasia, heterotopic ossification occurring from infancy, and congenital cardiac malformation. In our patient, we identified de novo occurrence of the heterozygous p.Arg258Gly variant of ACVR1, which has previously been reported in only two severe FOP patients. Heterotopic ossification occurred earlier and more frequently compared with classical FOP patients. We present the time-series changes in heterotopic ossification in our patient and compare her clinical features with those of the previously reported patients with p.Arg258Gly. Our report deepens understanding of the clinical features in severe FOP with p.Arg258Gly and of FOP as a systemic disorder.
进行性骨化性纤维发育不良(FOP)是一种罕见的骨骼疾病,其特征为大脚趾先天性畸形和进行性异位骨化。大脚趾畸形在出生时就出现,而异位骨化通常发生在儿童期,在婴儿期很少发生。典型的FOP是由ACVR1基因的杂合p.Arg206His变体引起的,该基因编码激活素A受体1型。最近,已经报道了一些具有其他ACVR1基因变体且具有典型FOP患者未观察到的临床特征的非典型FOP患者。在此,我们描述了一名患有严重FOP和多种异常的女孩,包括手足并指、指甲发育不全、下颌发育不全、婴儿期就出现的异位骨化以及先天性心脏畸形。在我们的患者中,我们鉴定出ACVR1基因杂合p.Arg258Gly变体的新发情况,此前仅在两名严重FOP患者中报道过该变体。与典型FOP患者相比,异位骨化出现得更早且更频繁。我们展示了我们患者异位骨化的时间序列变化,并将她的临床特征与先前报道的携带p.Arg258Gly变体的患者进行了比较。我们的报告加深了对携带p.Arg258Gly变体的严重FOP临床特征以及FOP作为一种全身性疾病的理解。