| Literature DB >> 31218168 |
Naixiang Zhai1,2, Yanqin Lu1,2, Yanzhou Wang3, Shie Zhang1,2, Chuanming Peng1,2, Shanshan Zhang1,2, Tianyou Li3, Mei Chen4, Junlong Liu4, Fengling Fang4, Xiuzhi Ren4, Jinxiang Han1,2.
Abstract
Osteogenesis imperfecta (OI) is a genetic disorder characterized by bone fragility and blue sclerae, which are mainly caused by a mutation of the COL1A1 or COL1A2 genes that encode type I procollagen. Mutations in the splice site of type I collagen genes are one of the mutations that cause OI and usually lead to a mild or moderate OI phenotype. A heterozygous A to G point mutation in intron 9 at the -2 position of the splice receptor site of COL1A1 was identified in a family with type I or IV OI. Three affected individuals in four generations of one family all presented with several clinical symptoms. They all had pectus carinatum, flat feet, gray-blue sclerae, and normal stature, teeth, hearing, and vision. Forearm fractures, small joint dislocations, and muscle weakness were all present in the patient's father and grandmother, who presented with a moderate type IV phenotype. The 10-year-old proband with type I OI had suffered a fracture twice, but had no history of joint dislocation or skin hyperextensibility. Charting the family helped to identify clinical symptoms in patients with mutations at the N-terminal of type I collagen genes.Entities:
Keywords: COL1A1; N-terminal of type I collagen; Osteogenesis imperfecta; splice receptor-site mutation
Year: 2019 PMID: 31218168 PMCID: PMC6557241 DOI: 10.5582/irdr.2019.01046
Source DB: PubMed Journal: Intractable Rare Dis Res ISSN: 2186-3644