Leroy J G, Nuytinck L, De Paepe A, De Rammelaere M, Gillerot Y, Verloes A, Loeys B, De Groote W
Department of Pediatrics Ghent University School of Medicine 185, De Pintelaan, B-9000 Ghent, Belgium.
Pediatr Radiol. 1998 Oct;28(10):781-9. doi: 10.1007/s002470050465.
Three unrelated patients with congenital arthrogryposis and brittle bones, the main neonatal signs of Bruck syndrome, are presented. In infancy and early childhood recurrent fractures of ribs and long bones and persistent Wormian bones in the calvarium are reminiscent of osteogenesis imperfecta (OI) even with white sclerae, normal dental quality and normal hearing as important clinical negatives. The diagnosis was made before two years of age in two, and in adolescence in the third patient. The latter's radiologically documented long-term natural course reveals slow progressivity of osteopenia and growth deficiency, worsening tendon contractures and pterygia in addition to increasing spine and pelvis deformation. Mental development remains normal. Bruck syndrome is monogenic and probably due to homozygosity of an as yet unidentified gene. As no alteration in the collagens I and III is detected and molecular screening reveals no mutation in the COL1A1 and COL1A2 genes, the pathogenesis of this severe disorder of connective tissue remains largely unknown.
本文介绍了三名患有先天性关节挛缩和脆骨病的患者,这是布鲁克综合征的主要新生儿体征。在婴儿期和幼儿期,肋骨和长骨反复骨折以及颅盖骨持续存在缝间骨,即使巩膜呈白色、牙齿质量正常且听力正常(这些都是重要的临床阴性特征),也让人联想到成骨不全症(OI)。两名患者在两岁前确诊,第三名患者在青春期确诊。后者经放射学记录的长期自然病程显示,骨质减少和生长发育迟缓进展缓慢,除脊柱和骨盆变形加剧外,肌腱挛缩和翼状胬肉也在恶化。智力发育仍正常。布鲁克综合征是单基因疾病,可能是由于一个尚未确定的基因纯合所致。由于未检测到I型和III型胶原蛋白的改变,且分子筛查未发现COL1A1和COL1A2基因的突变,这种严重结缔组织疾病的发病机制在很大程度上仍不清楚。