Wallace Stephanie E, Lachman Ralph S, Mekikian Pertchoui B, Bui Kathy K, Wilcox William R
Medical Genetics Institute, Steven Spielberg Pediatric Research Center, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA.
Am J Med Genet A. 2004 Sep 1;129A(3):235-47. doi: 10.1002/ajmg.a.30148.
Progressive diaphyseal dysplasia (PDD) (Camurati-Engelmann disease) is an autosomal dominant craniotubular dysplasia characterized by hyperostosis and sclerosis of the diaphyses of the long bones and the skull. Mutations in transforming growth factor beta-1 (TGFB1) were recently found in patients with PDD. We report on a four-generation pedigree with seven individuals affected by PDD, linkage and mutational analysis results, and review the literature. This pedigree demonstrates the autosomal dominant inheritance pattern, remarkable variation in expressivity, and reduced penetrance. The most severely affected individual had progression of mild skull hyperostosis to severe skull thickening and cranial nerve compression over 30 years. His carrier father remained asymptomatic into his ninth decade and had no radiographic hyperostosis or sclerosis of the bones. Symptomatic relatives presented with lower limb pain and weakness. They were initially diagnosed with a variety of other conditions. Two of the symptomatic individuals were treated successfully with prednisone. We genotyped 7 markers from chromosome region 19q13.1-13.3 in 15 relatives and confirmed linkage to this region in this family. We screened the TGFB1 gene for mutations and identified a missense mutation resulting in an R218H substitution in the affected individuals, the asymptomatic obligate carrier, and another unaffected relative. We genotyped the family for seven known TGFB1 polymorphisms and a novel TAAA tetranucleotide repeat in intron 1. These polymorphisms did not appear to account for the variability in disease severity in this family. Our review illustrates how the disorder can significantly compromise health. Cranial involvement, which occurs in 61% of patients, can be severe, entrapping cranial nerves or causing increased intracranial pressure. Therapy with corticosteroids should be attempted in all symptomatic patients.
进行性骨干发育异常(PDD)(卡穆拉蒂 - 恩格尔曼病)是一种常染色体显性遗传的颅骨管状发育异常疾病,其特征为长骨骨干和颅骨的骨质增生和硬化。最近在PDD患者中发现了转化生长因子β-1(TGFB1)的突变。我们报告了一个四代家系,其中有7名个体患有PDD,给出了连锁分析和突变分析结果,并对相关文献进行了综述。这个家系显示出常染色体显性遗传模式、显著的表达变异性和降低的外显率。最严重受累的个体在30年中,从轻度颅骨骨质增生发展为严重的颅骨增厚和颅神经受压。他的携带者父亲在九十多岁时仍无症状,骨骼X线检查无骨质增生或硬化表现。有症状的亲属表现为下肢疼痛和无力。他们最初被诊断为多种其他疾病。两名有症状的个体用泼尼松治疗成功。我们对15名亲属的19号染色体区域19q13.1 - 13.3的7个标记进行了基因分型,证实该家系与该区域连锁。我们对TGFB1基因进行突变筛查,在受累个体、无症状的必然携带者和另一名未受累亲属中鉴定出一个导致R218H替代的错义突变。我们对该家系的7个已知TGFB1多态性位点和内含子1中的一个新的TAAA四核苷酸重复序列进行了基因分型。这些多态性似乎不能解释该家系疾病严重程度的差异。我们的综述表明该疾病如何能显著损害健康。61%的患者会出现颅骨受累,可能很严重,会压迫颅神经或导致颅内压升高。所有有症状的患者都应尝试使用皮质类固醇进行治疗。