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本文引用的文献

1
Case for Diagnosis.诊断病例
Proc R Soc Med. 1920;13(Sect Study Dis Child):132-6. doi: 10.1177/003591572001301935.
2
Progressive diaphyseal dysplasia.进行性骨干发育不良
Radiology. 1948 Jul;51(1):11-22. doi: 10.1148/51.1.11.
3
Camurati-Engelmann disease (progressive diaphyseal dysplasia) in a Moroccan family.一个摩洛哥家庭中的卡穆拉蒂-恩格尔曼病(进行性骨干发育异常)
Osteoporos Int. 2005 Sep;16(9):1167-70. doi: 10.1007/s00198-005-1896-2. Epub 2005 Jun 16.
4
Transforming growth factor-beta1 to the bone.转化生长因子-β1作用于骨骼。
Endocr Rev. 2005 Oct;26(6):743-74. doi: 10.1210/er.2004-0001. Epub 2005 May 18.
5
Marked phenotypic variability in progressive diaphyseal dysplasia (Camurati-Engelmann disease): report of a four-generation pedigree, identification of a mutation in TGFB1, and review.进行性骨干发育异常(卡穆拉蒂 - 恩格尔曼病)的显著表型变异性:四代家系报告、转化生长因子β1(TGFB1)突变鉴定及文献综述
Am J Med Genet A. 2004 Sep 1;129A(3):235-47. doi: 10.1002/ajmg.a.30148.
6
TGFB1 mutations in four new families with Camurati-Engelmann disease: confirmation of independently arising LAP-domain-specific mutations.四个患有卡穆拉蒂-恩格尔曼病的新家族中的TGFB1突变:独立出现的富含亮氨酸重复序列(LAP)结构域特异性突变的确认
Am J Med Genet A. 2004 May 15;127A(1):104-107. doi: 10.1002/ajmg.a.20671.
7
Transforming growth factor-beta-induced inhibition of myogenesis is mediated through Smad pathway and is modulated by microtubule dynamic stability.转化生长因子-β诱导的成肌抑制通过Smad信号通路介导,并受微管动态稳定性调节。
Circ Res. 2004 Mar 19;94(5):617-25. doi: 10.1161/01.RES.0000118599.25944.D5. Epub 2004 Jan 22.
8
Dexamethasone enhances osteoclast formation synergistically with transforming growth factor-beta by stimulating the priming of osteoclast progenitors for differentiation into osteoclasts.地塞米松通过刺激破骨细胞祖细胞向破骨细胞分化的启动,与转化生长因子-β协同增强破骨细胞的形成。
J Biol Chem. 2003 Nov 7;278(45):44667-74. doi: 10.1074/jbc.M300213200. Epub 2003 Aug 27.
9
Bisphosphonate treatment of osteoporosis.双膦酸盐治疗骨质疏松症。
Clin Geriatr Med. 2003 May;19(2):395-414. doi: 10.1016/s0749-0690(02)00069-1.
10
Long-term linear growth of children with severe steroid-responsive nephrotic syndrome.重度类固醇反应性肾病综合征患儿的长期线性生长
Pediatr Nephrol. 2003 Aug;18(8):783-8. doi: 10.1007/s00467-003-1176-3. Epub 2003 Jun 13.

卡姆拉蒂-恩格尔曼病:24个家族的临床、放射学及分子数据回顾以及对诊断和治疗的意义

Camurati-Engelmann disease: review of the clinical, radiological, and molecular data of 24 families and implications for diagnosis and treatment.

作者信息

Janssens K, Vanhoenacker F, Bonduelle M, Verbruggen L, Van Maldergem L, Ralston S, Guañabens N, Migone N, Wientroub S, Divizia M T, Bergmann C, Bennett C, Simsek S, Melançon S, Cundy T, Van Hul W

机构信息

Department of Medical Genetics, University of Antwerp, Antwerp, Belgium.

出版信息

J Med Genet. 2006 Jan;43(1):1-11. doi: 10.1136/jmg.2005.033522. Epub 2005 May 13.

DOI:10.1136/jmg.2005.033522
PMID:15894597
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2564495/
Abstract

Camurati-Engelmann disease (CED) is a rare autosomal dominant type of bone dysplasia. This review is based on the unpublished and detailed clinical, radiological, and molecular findings in 14 CED families, comprising 41 patients, combined with data from 10 other previously reported CED families. For all 100 cases, molecular evidence for CED was available, as a mutation was detected in TGFB1, the gene encoding transforming growth factor (TGF) beta1. Pain in the extremities was the most common clinical symptom, present in 68% of the patients. A waddling gait (48%), easy fatigability (44%), and muscle weakness (39%) were other important features. Radiological symptoms were not fully penetrant, with 94% of the patients showing the typical long bone involvement. A large percentage of the patients also showed involvement of the skull (54%) and pelvis (63%). The review provides an overview of possible treatments, diagnostic guidelines, and considerations for prenatal testing. The detailed description of such a large set of CED patients will be of value in establishing the correct diagnosis, genetic counselling, and treatment.

摘要

卡穆拉蒂-恩格尔曼病(CED)是一种罕见的常染色体显性骨发育不良类型。本综述基于14个CED家族(共41例患者)未发表的详细临床、放射学和分子学研究结果,并结合其他10个先前报道的CED家族的数据。在所有100例病例中,均有CED的分子学证据,因为在编码转化生长因子(TGF)β1的基因TGFB1中检测到了突变。肢体疼痛是最常见的临床症状,68%的患者出现该症状。蹒跚步态(48%)、易疲劳(44%)和肌肉无力(39%)是其他重要特征。放射学症状并非完全显性,94%的患者表现出典型的长骨受累。很大比例的患者还表现出头骨(54%)和骨盆(63%)受累。本综述概述了可能的治疗方法、诊断指南以及产前检测的注意事项。如此大量CED患者的详细描述对于确立正确诊断、遗传咨询和治疗具有重要价值。