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排序方式: 共有145条查询结果,搜索用时 15 毫秒
31.
患者男,39岁,面部皮肤肥厚、四肢肢端肥大20年,间断头晕乏力1年.查体:重度贫血貌,睑结膜、口唇及甲床苍白;头面部皮肤肥厚、皱褶、呈回状颅皮;双下肢皮肤肥厚,手指及足趾呈杵状;皮损颜色正常,触之略韧;踝关节肿胀无压痛、活动自如.X线检查提示右腓骨中段髓腔密度增多,腓骨中段及胫骨下段后缘骨皮质增厚.血常规重度正常细胞低... 相似文献
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观察12 例骨关节病及10 例正常关节的滑膜内衬细胞的细胞凋亡情况,作定量分析且用滑膜组织的DNA 凝胶电泳加以证实。结果示,骨关节病滑膜内衬细胞凋亡指数(2-04 % ) 明显高于正常关节组(0-60 % ) ;DNA 凝胶电泳亦示病理组在200 bp 处有明显的梯带,对照组则无。提示骨关节病滑膜内衬细胞有高于正常的转换频率,其凋亡作用增强可能在骨关节病的发生发展中有重要意义。 相似文献
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A patient with nasopharyngeal carcinoma developed clubbing and hypertrophic osteoarthropathy 6 months before radiological detection of secondary deposits in the lung. Another patient with nasopharyngeal carcinoma developed digital clubbing and hypertrophic osteoarthropathy 6 months after the discovery of lung metastases. Development of a paraneoplastic syndrome in the form of hypertrophic osteoarthropathy and digital clubbing is very rare. This manifestation of nasopharyngeal cancers is presented, with a short review of its biology and pathogenesis. 相似文献
34.
Martinez-Lavin M 《Seminars in arthritis and rheumatism》2007,36(6):380-385
OBJECTIVE: Digital clubbing is regarded as the oldest clinical sign of medicine. The cause of this unique finger deformity has remained elusive throughout the centuries. For 3 decades our group has studied the etiology of this acropachy. This article reviews the current knowledge on the cause of digital clubbing. METHODS: PubMed database (www.pubmed.gov) was accessed. In clinical queries/clinical study service we entered "clubbing" or "hypertrophic osteoarthropathy," choosing the "etiology" category with a "broad sensitive" search scope. The time span was from January 1975 to August 2006. Additionally, this article narrates the chronology of our research on the pathogenesis of clubbing. RESULTS: The many dreadful internal illnesses associated with digital clubbing have in common enhanced platelet/endothelial cell activation. Emerging evidence suggests that, in hypoxic conditions with extrapulmonary shunting of blood, large megakaryocyte fragments fail to enter the pulmonary circulation. Instead they gain access to the systemic circulation impacting at the most distal sites, there releasing growth factors and thus inducing clubbing. In cases of lung cancer, the purported growth factor could gain direct entrance to the systemic circulation. Vascular endothelial growth factor (VEGF) may play a central role in the development of digital clubbing. It is a platelet-derived factor induced by hypoxia, and it is also abnormally produced by diverse malignant tumors fostering their uncontrolled growth. On the other hand VEGF produces vascular hyperplasia, edema, and fibroblast/osteoblast proliferation. Such are clubbing histologic characteristics. Enhanced VEGF expression has been reported in practically all internal illnesses associated with this type of finger deformity. Recent studies have demonstrated high circulating levels as well as increased local expression of VEGF in different groups of patients with digital clubbing. CONCLUSION: Abnormal expression of VEGF may be the cause of digital clubbing. 相似文献
35.
颈椎退行性骨关节病的X线平片分析 总被引:1,自引:0,他引:1
目的分析X线平片对颈椎退行性骨关节病的诊断价值。方法对380例颈椎退行性骨关节病患者X线平片进行回顾性分析。结果380例颈椎退行性骨关节病X线表现为:钩椎关节增生、退变占47.89%;颈椎生理曲度发生改变者,占56.05%;颈椎骨质增生者占46.32%;椎间隙狭窄、椎间盘退变患者占60.79%;椎间孔变形、变小占69.47%;颈椎失稳、移位占21.32%;韧带钙化者占38.42%。结论X线平片能够观察到颈椎退行性骨关节病的大部分征象,在该病的初步诊断特别是早期诊断中具有重要意义。 相似文献
36.
Castori M Sinibaldi L Mingarelli R Lachman RS Rimoin DL Dallapiccola B 《Clinical genetics》2005,68(6):477-486
Pachydermoperiostosis (PDP) is a rare genodermatosis, characterized by pachydermia, digital clubbing, periostosis and an excess of affected males. Although an autosomal dominant model with incomplete penetrance and variable expression has been proved, both autosomal recessive and X-linked inheritance have been suggested. However, at present, genetic heterogeneity is not fully supported. The aim of this study is to review the clinical and pedigree data of 68 published PDP families, including 204 patients. This analysis has confirmed an autosomal dominant mutation in 37 families and suggested the existence of an autosomal recessive form in the remaining families. The two forms may differ in clinical severity, intrafamilial variability and prevalence of some features. Additionally, the marked skewed sex ratio could not be easily explained by an X-linked mutation, but alternative explanations (i.e. testosterone promoting proliferation) are discussed. 相似文献
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