局部注射曲安奈德及浅层X光局部照射配合手术治疗皮肤瘢痕疙瘩的临床体会

目的探讨采取多种方法综合治疗皮肤瘢痕疙瘩的临床疗效。方法自2002年开始我科采用局部注射曲安奈德、伤口局部浅层X照射配合手术切除治疗皮肤瘢痕疙瘩患者22例。结果除2例术后3个月复查伤口有轻度瘢痕增生外，其余患者随访伤口均愈合良好，无明显瘢痕增生，绝大多数对疗效满意。结论在目前对皮肤瘢痕疙瘩无特效治疗方法的情况下，临床采用手术切除配合局部药物注射、浅层X光照射等多种方法综合治疗，常能取得较满意的效果。     

增生性瘢痕和瘢痕疙瘩药物注射治疗进展

增生性瘢痕和瘢痕疙瘩有着不同的临床表现及预后,但均有组织修复和再生的调节机制出现障碍,从而导致创伤修复出现异常的纤维化的特点。临床上增生性瘢痕和瘢痕疙瘩不仅给患者带来面容损毁,且即使使用手术方法切除也易复发。药物局部注射广泛应用于增生性瘢痕和瘢痕疙瘩的治疗,其方法简单且疗效确切,在预防和早期治疗上有明显优势;在这方面研究进展也较快。该文主要就常用的注射治疗药物及研究现状进行综述。     

瘢痕下埋置扩张器治疗痤疮多发性增生性瘢痕16例

目的总结采用瘢痕下埋置扩张器治疗痤疮多发性增生性瘢痕的疗效。方法 2014年7月-2017年9月,收治16例痤疮多发性增生性瘢痕患者。一期手术于瘢痕下埋置容量为30～200 mL的扩张器,扩张3个月行二期手术取出扩张器,切除瘢痕。结果术后创面均一期愈合,术后随访1～3年,皮瓣恢复良好,少量瘢痕轻度增生,外观改善满意。结论采用瘢痕下埋置扩张器治疗痤疮多发性增生性瘢痕,美容效果好,可作为综合治疗痤疮增生性瘢痕的一项选择。     

髓核剥离术联合脉冲染料激光治疗耳垂瘢痕疙瘩64例疗效观察

目的 探究耳垂瘢痕疙瘩髓核剥离术联合脉冲染料激光综合治疗的效果。方法 选取2018年1月—2020年12月本院收治的128例耳垂瘢痕疙瘩患者,根据治疗手段的不同分为治疗组和对照组,每组64例。治疗组给予髓核剥离术加术后脉冲染料激光治疗,对照组手术加得宝松注射治疗。观察比较2组患者临床疗效及满意度。结果 治疗组48例治愈、12例显效、4例无效,临床有效率（93.75%）显著高于对照组（78.13%）,差异有统计学意义（P<0.05）,治疗组有49例对治疗十分满意,13例一般满意,2例不满意,满意度（96.87%）明显高于对照组（79.69%）,差异有统计学意义（P<0.05）。结论 耳垂瘢痕疙瘩髓核剥离术加脉冲染料激光可有效改善耳垂瘢痕疙瘩患者的瘢痕状态,减轻患者疼痛度,促进患者面容改善,提升疗效,满意度很高,值得在临床应用中推广。     

强脉冲光联合点阵铒激光治疗痤疮后增生性瘢痕的效果观察

目的观察痤疮后增生性瘢痕患者应用强脉冲光联合点阵铒激光治疗后效果。方法随机将我院91例痤疮后增生性瘢痕患者分组,对照组45例给予强脉冲光治疗,观察组46例联合点阵铒激光治疗,对比治疗疗效。结果观察组VSS评分低于对照组,总有效率高于对照组(P <0.05)。结论强脉冲光联合点阵铒激光有效改善瘢痕色泽、血管分布、厚度及柔软度,治疗痤疮后增生性瘢痕效果显著。     

强脉冲光联合皮损内注射曲安奈德治疗痤疮后增生性瘢痕的疗效评价

目的 探讨强脉冲光联合多点注射曲安奈德治疗痤疮后增生性瘢痕的临床疗效。方法 选取2018年3月至2020年12月医院收治的60例痤疮后增生性瘢痕患者为研究对象,随机分为实验组和对照组。分别比较两组患者治疗前及3次治疗结束1月后的温哥华瘢痕量表（VSS）评分。结结果果实验组患者治疗后瘢痕色泽、厚度、血管分布、柔软度及总分均较治疗前有明显改善（P <0.05）;对照组患者治疗后瘢痕色泽、厚度、柔软度及总分均较治疗前有明显改善（P <0.05）,但血管分布与治疗前无明显差异（P> 0.05）;治疗后,实验组患者的瘢痕色泽、厚度、血管分布及总分均低于对照组（P<0.05）。结论 强脉冲光联合多点注射曲安奈德治疗痤疮后增生性瘢痕可抑制瘢痕内血管过度增生,有效改善瘢痕的颜色、厚度等,提高临床疗效。     

自体瘢痕皮回植联合局部注射等治疗胸前巨大瘢痕疙瘩的疗效观察

目的 回顾性分析自体瘢痕皮回植联合局部注射等综合治疗胸前巨大瘢痕疙瘩的临床疗效.方法 对30例胸前巨大瘢痕疙瘩患者,行瘢痕疙瘩切除后自体瘢痕皮回植覆盖修复创面,配合局部注射等综合方法治疗,术后随访1年,评估瘢痕疙瘩复发和瘢痕形成情况.结果 30例患者回植的瘢痕皮均成活.随访1年,3例瘢痕疙瘩所致的疼痛、瘙痒等症状消失,...     

瘢痕的临床类型及治疗进展

瘢痕是机体受到创伤后修复的自然产物,可根据组织病理学和临床特点分为浅表性瘢痕、萎缩性瘢痕、增生性瘢痕及瘢痕疙瘩。其发病机制较复杂,临床治疗较困难,特别是对于增生性瘢痕及瘢痕疙瘩,目前仍没有完全满意的治疗方法,常见的治疗手段包括激光、手术、压迫、药物、放疗等,由于单一治疗手段的局限性,多途径综合治疗是目前推荐的治疗策略。     

氨基酮戊酸光动力疗法治疗新发病理性瘢痕疗效观察

目的探讨氨基酮戊酸光动力疗法(ALA-PDT)治疗新发病理性瘢痕的疗效。方法对10例新发病理性瘢痕的患者进行ALA-PDT治疗,通过温哥华瘢痕量表对瘢痕进行评分,治疗前后对比评价疗效。以11例糖皮质激素皮损内注射的患者为对照组。结果 ALA-PDT治疗10例新发病理性瘢痕患者,7例有效,3例无效,对照组7例有效,ALA-PDT治疗组未见复发,不良反应主要为疼痛及色素沉着。结论 ALA-PDT可作为新发性瘢痕尤其是增生性瘢痕的一种治疗手段。     

耳环孔增生疤痕综合治疗

近五年来 ,我们的美容门诊共收治因耳垂部穿耳孔后致增生性疤痕 42例。采用手术加疤痕敌外贴加药物注射的综合治疗方法 ,效果良好 ,总结如下 :1　临床资料　 42例患者全为女性 ,最大年龄 5 7岁 ,最小年龄 16岁。双侧耳环孔出现增生疤痕者 36例。单侧耳环孔出现增生疤痕者 6例。共 78只耳垂。增生疤痕最大直径2 1ｃｍ ,最小直径 0 3ｃｍ。临床表现均为耳垂穿耳孔后 2月至半年内穿耳孔部位出现较硬的增生疤痕 ,疤痕渐增大。有明显痒痛 ,凸出皮肤表面 ,影响外观。经综合疗法 ,获得良好治疗效果 ,术后耳垂外观正常。随访最长 4年 ,最短半年 ,…     

长脉冲1064nm Nd:YAG激光治疗兔耳增生性瘢痕的实验研究

目的 通过建立兔耳增生性瘢痕模型,评价长脉冲1064 nm激光治疗增生性瘢痕的疗效.方法 选用新西兰长耳白兔10只,雌雄各半,体质量2.0～2.5 kg.在所有兔耳腹侧面建立增生性瘢痕模型,每只兔耳4处1.5 cm x 1.5 cm正方形造模.10只兔子共80个创面形成增生性瘢痕74处,将左侧和右侧兔耳增生性瘢痕块分为对照组和治疗组,治疗组应用长脉冲1064 nm激光照射,对照组未予治疗.30 d后观察实验组及对照组瘢痕的颜色、质地;彩色超声测量瘢痕厚度;瘢痕取材,HE染色和CD31免疫组化染色,记数瘢痕成纤维细胞密度和微血管密度;Masson染色观察胶原纤维.结果 激光治疗组较对照组瘢痕颜色变浅,质地变柔软,瘢痕厚度变薄,对照组搬痕的平均厚度为3.089 mill,治疗组为2.137 mm,两组比较,t=5.72,P<0.01.对照组血管密度均值为68.056个/mm2,治疗组为38.333个/mm2,两组比较,t=4.93,P<0.01,治疗组血管密度较对照组明显降低.成纤维细胞数量均值对照组为355.000个/mm2,治疗组为166.940个/mm2,两组比较,t=13.36,P<0.01,治疗组成纤维细胞数量明显减少.Masson染色观察对照组胶原纤维排列紊乱,治疗组胶原纤维排列疏松,规则.结论 长脉冲1064 nm激光可以促进早期增生性瘢痕消退,对瘢痕增生具有抑制作用.

Abstract：

Objective To evaluate the therapeutic effect of long-pulsed Nd:YAG 1064 laser on hyperplastic scars by using a rabbit ear model.Methods Five female and five male New Zealand long-ear white rabbits weighting 2.0-2.5 kg were used in this experiment.Four square full-thickness skin wounds sized 1.5 cm x1.5 cm were created on the ventral surface of each ear to develop a model of hyperplastic scar.Finally,a total of 74 hyperplastic scars developed on the 80 wounds,and the scars on the left and right ears served as the control (unirradiated) and treatment (irradiated with long-pulsed 1064 nm Nd:YAG laser) group,respectively.After 30 days of irradiation,the color and texture of scars were observed and the scar thickness was measured by color Doppler ultrasonogTaphy.Then,the scars were harvested followed by the analysis of density of fibroblasts and microvessels as well as the changes in collagen fibers in scars by HE staining,CD31 staining and Masson staining,respectively.Results A decrease was observed in the color,hardness and thickness of scars in the irradiated ears compared with the unirradiated ears.The average thickness of scars,microvessel density and fibroblast density in scars were significantly lower in the treatment group than in the control group(2.137vs.3.089 am,t=5.72,P<0.01;38.333/mm2vs.68.056/mm2,t=4.93,P<0.01;166.940/mm2vs.355.000/mm2,t=13.36.P<0.01).Masson staining revealed a disorganized arrangement of collagen fibers in the control group but a sparse and regular alignment in the treatment group.Conclusion Long-pulsed 1064 nm Nd:YAG laser may promote the shrinkage and suppress the hyperplasia of scars.     

Hyperpigmented scar due to minocycline therapy

A 20-year-old woman presented with a heavily pigmented scar on the left lower abdomen following excision of a benign compound nevus. Reexcision showed an organizing scar with pronounced hemosiderinlike pigment deposition and no residual melanocytic lesion. Results of further histopathologic workup showed positive staining with both Perls stain for iron and Fontana-Masson stain. These findings led to further questioning of the patient, which revealed a history of minocycline therapy--information that had not been provided during her initial evaluation. Hyperpigmented scars may result from minocycline ingestion. We present a review of the literature, with particular regard to the possible mechanisms of minocycline hyperpigmentation and the differential diagnosis of hyperpigmented scars.     

Tacrolimus action pathways in an ointment base for hypertrophic scar prevention in a rabbit ear model

BackgroundTacrolimus is used to prevent unaesthetic scars due to its action on fibroblast activity and collagen production modulation.ObjectivesTo evaluate the action pathways, from the histopathological point of view and in cytokine control, of tacrolimus ointment in the prevention of hypertrophic scars.MethodsTwenty-two rabbits were submitted to the excision of two 1-cm fragments in each ear, including the perichondrium. The right ear received 0.1% and 0.03% tacrolimus in ointment base twice a day in the upper wound and in the lower wound respectively. The left ear, used as the control, was treated with petrolatum. After 30 days, collagen fibers were evaluated using special staining, and immunohistochemistry analyses for smooth muscle actin, TGF-β and VEGF were performed.ResultsThe wounds treated with 0.1% tacrolimus showed weak labeling and a lower percentage of labeling for smooth muscle actin, a higher proportion of mucin absence, weak staining, fine and organized fibers for Gomori's Trichrome, strong staining and organized fibers for Verhoeff when compared to controls. The wounds treated with 0.03% tacrolimus showed weak labeling for smooth muscle actin, a higher proportion of mucin absence, strong staining for Verhoeff when compared to the controls. There was absence of TGF-β and low VEGF expression.Study limitationsThe analysis was performed by a single pathologist. Second-harmonic imaging microscopy was performed in 2 sample areas of the scar.ConclusionsBoth drug concentrations were effective in suppressing TGF-β and smooth muscle actin, reducing mucin, improving the quality of collagen fibers, and the density of elastic fibers, but only the higher concentration influenced elastic fiber organization.     

The role of ERK and JNK signaling in connective tissue growth factor induced extracellular matrix protein production and scar formation

CCN2 plays an important role in the pathogenesis of hypertrophic scars (HTSs). Although CCN2 is involved in many fibroproliferative events, the CCN2 induction signaling pathway in HTSs is yet to be elucidated. Here, we first investigated the effect of the mitogen-activated protein kinases (MAPKs) on CCN2-induced α-smooth muscle actin (α-SMA) and collagen I expression in human HTS fibroblasts (HTSFs). Then, we established HTSs in a rabbit ear model and determined the effect of MAPKs on the pathogenesis of HTSs. MAPK pathways were activated by CCN2 in HTSFs. Extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) inhibitors significantly inhibited CCN2-induced expression of α-SMA and collagen I in HTSFs. In the rabbit ear model of the HTS, JNK and ERK inhibitors significantly improved the architecture of the rabbit ear scar and reduced scar formation on the rabbit ear. Our results indicate that ERK and JNK mediate collagen I expression and scarring of the rabbit ear, and may be considered for specific drug therapy targets for HTSs.     

CD34 immunoreactivity distinguishes between scar tissue and residual tumor in re-excisional specimens of dermatofibrosarcoma protuberans

Dermatofibrosarcoma protuberans (DFSP) is a locally aggressive tumor that often recurs after simple excision, and therefore usually requires wide surgical re-excision. It is sometimes difficult to distinguish histologically between residual tumor and scar tissue formed in response to the original biopsy. In an effort to solve this diagnostic problem, we have examined CD34 immunoreactivity in 10 primary biopsies of DFSP, 12 scars, and 7 re-excisional DFSP specimens containing residual tumor adjacent to scar tissue. In all 10 primary biopsies of DFSP, the tumor cells strongly and uniformly expressed CD34. In the 12 scars, only periaclnexal cells, enclothclial cells, and rare, scattered dendritic cells in the clermis were immunolabeled for CD34. In the 7 re-excisions of DFSP, the foci of residual DFSP were strongly immunolabeled, while the surrounding scar tissue was not. The pattern of CD34 immunoreactivity distinguishes DFSP from scar tissue, and thereby may permit more accurate assessment of surgical margins in re-excisional specimens of DFSP.     

Marjolin's ulcer: burn scar carcinoma

The term Marjolin's ulcer means the malignant transformation of chronic ulcers, sinus tract and burn scars. The most frequently produced neoplasm is squamous cell carcinoma. The pathogeny is unknown, involving mutations in the Fas gene. Main therapeutic management are consist of prophylactic measures, avoiding repeated traumas and prolonged cure periods. We present the case of a 48-year-old male with squamous cell carcinoma on the old burn scar of legs that evolved favorably after excision.     

Elastic fibers in scar tissue

The capacity of the skin to be stretched and to return to its resting position is correlated to the quantity and to the quality of the elastic fiber network. Although elastic fibers have been demonstrated in scars, the time course of their appearance in scars and their role in scar elasticity has not been elucidated. A study was therefore undertaken to evaluate the elastic fiber network in scars.
The scars studied were from re-excision specimens following a biopsy performed for a benign or a malignant process. A total of 182 scars were evaluated in patients of different age groups. Miller's elastic tissue stain, considered to be superior to Verhoeff's van Giesen stain, was used. No elastic fibers were detected in any of 116 scars which were of less than 3 months' duration. In 66 scars present for over 3 months, a progressive increase in elastic fibers was present, first as focal and thin fibers, then as diffuse and thicker fibers. For scars of the same duration, a regional difference was noted in that scars from the back contained more and thicker elastic fibers than those from the cheek. When patients were stratified according to age, no appreciable difference was noted in the density of elastic fibers in both new and old scars between the different age groups. These results show that the synthesis of elastic tissue fibers in scars is a function of duration and site of the scar.     

强功率UVA1照射对增生性瘢痕动物模型瘢痕形成的影响

目的 探讨不同剂量UVA1对全层皮肤缺损诱导的兔耳增生性瘢痕模型的影响情况。方法18只新西兰白兔双耳腹面手术切除2 cm × 5 cm全层皮肤至筋膜,建立兔耳增生性瘢痕模型后,随机分成3组,每组6只兔,将每只兔左耳分别于伤后即刻、1个月、2个月开始用不同剂量大功率UVA1照射,右耳为非照射组。各照射组又分为两个剂量照射组,兔耳分别每次照射UVA1 60 J/cm2、110 J/cm2,连续30次。结果 创伤建模1个月、2个月后开始照射UVA1组,与照射前比较,高剂量组照射后瘢痕处真表皮厚度（282.32 ± 58.60;336.50 ± 98.34）和真皮胶原含量（24.91 ± 16.88;34.47 ± 8.90）均显著降低（P < 0.05）;照射组与非照射组在UVA1照射前后差值的比较,高剂量组照射后瘢痕处表真皮厚度差值（-143.52 ± 42.91;-142.44 ± 49.96）和真皮胶原含量差值（-56.39 ± 15.04;-48.35 ± 10.44）的差异有统计学意义（P < 0.05）;各照射组UVA1对瘢痕皮肤厚度（811.68 ± 79.03;659.08 ± 178.98）和胶原含量（67.80 ± 9.06;61.35 ± 12.91）的影响均存在剂量依赖性（P < 0.05）。而创伤建模的同时照射UVA1组,两种剂量的UVA1照射后瘢痕处皮肤厚度和胶原含量较非照射耳均显著增加（P < 0.05）。结论 上皮化后开始UVA1照射可使瘢痕变软,皮肤变薄,胶原含量降低。创伤同时照射UVA1不仅不能阻止瘢痕模型的建立,反而加重瘢痕。     

Studies on human scar tissue proteoglycans

The proteoglycans (PGs) in pooled normal scars and pooled hypertrophic scars were extracted with 4 M guanidinium chloride and isolated by DEAE-cellulose chromatography. The PG samples were then fractionated further by dissociative CsCl density gradient sedimentation. Following cleavage of the density gradient PG fractions with alkaline NaB3H4, the glycosaminoglycan (GAG) constituents were isolated and analyzed by quantitative cellulose acetate electrophoresis. In addition, single samples of normal skin and a keloid scar were also analyzed. The results showed that the hypertrophic scars had a higher average content of extractable and also residual PGs than did the normal scars but a wide range of values was obtained for each type of scar. Some differences were noted in the amounts and distribution of the GAGs in CsCl gradient fractions, in the different types of scar tissue. The PGs in tissues were distributed in low-, medium-, and high density fractions and are, therefore, heterogeneous. Dermatan sulfate (DS) was the major GAG in each tissue and smaller quantities of chondroitin sulfate (CS), heparan sulfate (HS), and heparin (HP) were also present. In addition, 2 other GAG constituents were also detected. Based on the susceptibility of these GAGs to enzymes and nitrous acid treatments, one was a HS or HP while the second was a DS. The major differences in the PG composition of the scar tissues were the higher proportions of low-density CS-PGs in the keloid scar and of low density DS-PGs in hypertrophic and keloid scars.