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局部曲安奈德注射辅助手术切除治疗耳部瘢痕疙瘩
瘢痕疙瘩(keloid)是一种临床上常见的纤维组织增生性疾病,是以皮损后真皮异常纤维增生反应为特征的病理性组织,其形成机制尚未明了.而耳部是瘢痕疙瘩的好发部位,临床上大多由于扎耳孔后导致病损超出原有损害范围,常严霞损害患者容貌外观.我们在2003年4月至2007年2月,采用手术切除病变加曲安奈德注射治疗耳部瘢痕疙瘩48例,取得良好疗效.
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增生性瘢痕退行性变的相关影响因素
瘢痕( cicatrix)是正常组织修复过程中的产物.当创伤修复过程发生异常时,以胶原为主的细胞外基质( extracellar matrix,ECM)成分大量沉积,导致真皮组织过度增生,则出现病理性瘢痕( pathologic scar)或称异常瘢痕(abnormal scar),即增生性瘢痕和瘢痕疙瘩( keloid,K).
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瘢痕疙瘩发生的肿瘤源性学说
瘢痕疙瘩是皮肤创伤异常修复的结果,虽然其发病机制仍然没有完全阐明,但已知与以下因素密切相关:(1)成纤维细胞、免疫细胞、角质形成细胞等细胞功能异常;(2)透明质酸、胶原、腱抗原蛋白等细胞外基质异常;(3)转化生长因子β(TGF-β)、碱性成纤维细胞生长因子(bFGF)等生长因子表达异常;(4)细胞凋亡异常;(5)免疫学异常;(6)性激素等内分泌异常;(7)遗传;(8)力学或机械因素;(9)曲安奈德、维A酸、放射等治疗因素.
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转化生长因子-β1对瘢痕疙瘩成纤维细胞 SMAD3,7表达的影响
AIM: To study the expression of SMAD3 and SMAD7 of transforming growth factor-β 1 ( TGF-β 1) on keloid- derived fibroblasts. METHODS: The expression of SMAD3 (at 1,2,4,24,48 h)and SMAD7(at 0.5 1,1.5, 2,4,24 h) were detected by using methods of Western blot after 500 pmol/L TGF-β 1 were added to the monolayer culture system.RESULTS: The level of SMAD3 were down regulated at 24 h and the SMAD7 were maximum up regulated at 4 h when TGF-β 1 were used.CONCLUSION: TGF-β 1 may down regulate the expression of SMAD3,but up regulate that of SMAD7 .
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瘢痕疙瘩154例临床特征及相关因素分析
瘢痕疙瘩(Keloid, K)是由皮肤损伤引发的、以真皮内胶原纤维大量沉积为特征的皮肤病.本病具有瘢痕组织过度生长、超出原损伤界限、并侵犯邻近正常皮肤组织、始终不退化及单纯手术切除后易复发等特点.关于K临床特征方面的研究国外报道较多,1,2 而国内资料甚少.我们于2006年8月至2008年4月对154例K患者进行回顾性研究,采用SPSS 13.0统计软件对其临床特征及各特征间的相关性进行分析,目的是探讨K发生的一般规律,为本病的预防及治疗提供一定的依据.
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病理性瘢痕的治疗研究进展
病理性瘢痕(Pathologic scar)是临床常见病、多发病,包括增生性瘢痕( Hypertrophic scar)和瘢痕疙瘩(Keloid),主要继发于烧伤、创伤、外科手术等皮肤损伤后组织的过度修复.其组织学特点为大量成纤维细胞增生、细胞外基质中胶原蛋白过量沉积、胶原纤维排列紊乱,临床表现为组织外形的毁损、变形和不同程度的功能障碍,给患者身心带来严重影响.本文拟对病理性瘢痕的各种不同治疗方法进行综述,希望给病理性瘢痕的临床综合治疗提供新的思路和启示.
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信号转导与病理性瘢痕
病理性瘢痕包括增生性瘢痕(hypertrophic scar,HS)和瘢痕疙瘩(keloid,K),是人体对创伤产生过度愈合反应的结果,它们都以成纤维细胞(fibroblast,FB)增殖旺盛并分泌大量细胞外基质,导致胶原的过量合成和沉积为特征.病理性瘢痕作为整形外科的常见疾病,一直是国内外学者研究的热点,其研究报道每年以50%的速度增长[1].
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瘢痕疙瘩的遗传学及相关基因研究进展
瘢痕疙瘩(Keloid)是皮肤损伤如创伤、烧伤或手术后引发的以成纤维细胞过度增生和细胞外基质的异常积聚为特征的皮肤胶原性疾病.临床表现差异较大,皮损一般高出周围正常皮肤,范围超过原伤口界限而侵犯临近组织呈瘤样生长,触之较硬,伴有不同程度的瘙痒和疼痛,常造成功能障碍和外形破坏.早期表面呈粉红或暗红色,晚期多为苍白色,可伴色素沉着,与正常皮肤界限明显[1].
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瘢痕疙瘩的遗传学及相关基因研究进展
瘢痕疙瘩(Keloid)是皮肤损伤如创伤、烧伤或手术后引发的以成纤维细胞过度增生和细胞外基质的异常积聚为特征的皮肤胶原性疾病.临床表现差异较大,皮损一般高出周围正常皮肤,范围超过原伤口界限而侵犯临近组织呈瘤样生长,触之较硬,伴有不同程度的瘙痒和疼痛,常造成功能障碍和外形破坏.早期表面呈粉红或暗红色,晚期多为苍白色,可伴色素沉着,与正常皮肤界限明显[1].
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病理性瘢痕的蛋白质组学研究
病理性瘢痕分为增生性瘢痕和瘢痕疙瘩两种类型.增生性瘢痕(hypertrophicscar,HS)是由创伤引起的,以成纤维细胞过度增殖和胶原蛋白等细胞外基质过度产生和沉积为特征的病理性瘫痕.临床上表现为:红色、质硬的皮肤表面肿物,可有痛痒等症状,如发生在关节部位,还可能出现瘫痕挛缩,影响功能;发生在颜面部则严重影响病人的容貌及心理.瘢痕疙瘩(Keloid)是皮肤损伤后引发的胶原异常积累所致的过度瘢痕化,临床表现为过度生长,超过原伤口界限,侵犯临近组织,呈瘤样生长,造成功能障碍,有好发部位,不发生退行性变化和单纯手术后极易复发等特点.
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Objective: To study transforming growth factor-β1(TGF-β1) autoproduction in keloid fibroblasts and theregulation effect of blocking TGF-β intracellular signalingon rhTGF-β1 autoproduction.Methods: Keloid fibroblasts cultured in vitro weretreated with either rhTGF-β1 (5 ng/ml ) or recombinantadenovirus containing a truncated type II TGF-β receptorgene (50 pfu/cell ). Their effects of regulating geneexpression of TGF-β1 and its receptor I and II wereobserved with Northern blot.Results: rhTGF-β1 up-regulated the gene expressionof TGF-β1 and receptor I, but not receptor II. Over-expression of the truncated receptor II down-regulated thegene expression of TGF-β1 and its receptor I, but notreceptor II.Conclusions: TGF-β1 autoproduction was observed inkeloid fibroblasts. Over-expression of the truncated TGF-βreceptor H decreased TGF-β1 autoproduction via blockingTGF-β receptor signaling.
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Aim: This study aimed to investigate the efficacy of the myocutaneous flap of the rectus abdominis in the surgical treatment of a large defect on the female chest following keloid excision.Methods: According to the location and size of the keloid on the chest, a myocutaneous flap based on the left or right rectus abdominis muscle was designed and transferred for repair of a chest defect following keloid resection. Radiotherapy was performed in the surgical area on the first and seventh postoperative days.Results: From January 2015 to March 2016, rectus abdominis myocutaneous flap coverage and early radiotherapy were used to treat 7 cases of keloids on the female chest. A postoperative follow-up of 10-14 months (average 12 months) was conducted. All the flaps survived well without evidence of keloid recurrence, and all patients achieved an improved chest shape.Conclusion:The rectus abdominis myocutaneous flap is a viablemethod for wound closure following resection of large keloids on the female chest.