Watanabe A, Kawabata Y, Okada O, Tanabe N, Kimura H, Hatamochi A, Shinkai H, Sakai N, Shimada T, Hiroshima K, Kuriyama T
Dept of Respirology, Graduate School of Medicine, Chiba University, Chiba City, Japan.
Eur Respir J. 2002 Jan;19(1):195-8. doi: 10.1183/09031936.02.00219202.
Ehlers-Danlos syndrome type IV (EDS IV) is caused by mutation within the COL3AI gene, resulting in the disorder of type III procollagen. The diagnosis is confirmed by demonstrating the synthesis of abnormal type III procollagen molecules from cultured dermal fibroblasts or by identifying the mutation in the COL3A1 gene. The authors report a case of EDS IV caused by a novel point mutation in the COL3A1 gene in a 16-yr-old female. Recurrent haemoptysis and cavitary formation of the lung were evidence of pulmonary involvement. However, extrathoracic manifestations of EDS IV were mostly absent. To the best of the authors' knowledge, all previously reported Ehlers-Danlos syndrome IV patients with respiratory disease had the characteristic findings or histories of Ehlers-Danlos syndrome IV. In the present case, connective tissue friability was suspected due to tissue laceration observed in the biopsied lung specimen, and the diagnosis was made beginning from this pivotal finding.
IV型埃勒斯-当洛综合征(EDS IV)由COL3AI基因突变引起,导致III型前胶原紊乱。通过证明培养的皮肤成纤维细胞合成异常III型前胶原分子或通过鉴定COL3A1基因中的突变来确诊。作者报告了一例16岁女性因COL3A1基因新的点突变导致的EDS IV病例。反复咯血和肺部空洞形成是肺部受累的证据。然而,EDS IV的胸外表现大多不存在。据作者所知,所有先前报道的患有呼吸系统疾病的IV型埃勒斯-当洛综合征患者都有IV型埃勒斯-当洛综合征的特征性表现或病史。在本病例中,由于在活检的肺标本中观察到组织撕裂,怀疑存在结缔组织脆性,诊断由此关键发现开始。