93例光线性角化病和62例鲍恩病临床病理回顾性分析

对2014年1月1日至2018年12月31日我院皮肤科门诊临床诊断为光线性角化病(AK)和鲍恩病患者的临床和病理资料进行回顾性分析。结果示组织病理确诊AK和鲍恩病分别为93例和62例,临床诊断与组织病理报告均AK和鲍恩病患者分别为50例和29例,诊断符合率分别为54%和50%。AK与鲍恩病在临床诊断上易误诊为脂溢性角化病（21例）和基底细胞癌（11例）。AK好发部位为头面部（94%）,鲍恩病则好发于躯干（52%）。     

330例光线性角化病临床与组织病理特征回顾性分析

目的回顾性分析光线性角化病患者临床及组织病理特征。方法对昆明医科大学第一附属医院2000年1月～2015年7月临床及病理确诊为光线性角化病的330例患者进行回顾性分析。患者的基本信息、临床特征和病理类型、KIN分级等其他临床数据均来自医疗记录,并由2位经验丰富的病理医生对病理类型和KIN分级进行复核。结果光线性角化病多见于中老年女性,主要见于曝光部位,冬季就诊患者较少,患者病理类型常见为肥厚型,KINⅠ级较多见。结论光线性角化病受紫外线辐射影响较大,其临床特点和病理学分类特征可能与季节、日照、生活方式等因素有关,需要进行进一步的前瞻性观察研究来证实这些发现。     

播散性浅表性光线性汗孔角化病1例

患者男,52岁,藏族.双下肢角化性丘疹2年余,加重1年,于2008年5月至我院就诊.2年前患者无明显诱因于双下肢伸侧出现散在对称性浅褐色丘疹,约米粒大小,无自觉症状,未诊治.近1年皮损增多,累及双下肢屈侧和双七肢.伴瘙痒,皮损夏重冬轻.23年前曾因肝包虫病行手术治疗,半个月前诊断脑包虫病,可疑肺部包虫病.否认家族中有类似疾病患者.     

棘层松解型光线性角化病1例

报告1例棘层松解型光线性角化病.患者男,80岁,因左颞部皮肤斑块伴疼痛1年余就诊.皮肤组织病理检查示:表皮增生,角化过度,棘层松解,基底层不典型细胞向真皮上部生长.免疫组化检查示:CK(+)、P63(+),ki67约20%(+).诊断为棘层松解型光线性角化病.     

光线性角化病皮损的细胞DNA含量流式细胞分析

光线性角化病的病理组织学特征为不同程度的表皮细胞的非典型增生。为了更加客观地反映该病的这一特征，应用流式细胞技术定量分析了２７例光线性角化病皮损细胞的ＤＮＡ含量及细胞增殖活性。结果：光线性角化病细胞的增殖指数（ＰＩ）同于正常人皮肤的ＰＩ值（Ｐ〈０．０５），８例非典型增生严重的光线性角化病细胞的ＤＮＡ指数（ＤＩ）高于其余１９例光线性角化病的ＤＩ值（Ｐ〈０．０５）。提示：光线性角化病皮损细胞增殖活跃，     

光线性角化病的皮肤镜特征研究进展

光线性角化病(AK)是皮肤长期暴露于日光下所引起的一种癌前病变,有发展为鳞癌的风险,皮肤镜已广泛应用于AK的诊断与鉴别诊断,其皮肤镜特征包括:基底假网状红斑、毛囊口周围白晕、毛囊口黄色角栓等,本文对AK的皮肤镜表现及鉴别诊断进行了综述.     

播散性浅表光线性汗孔角化病1例及家系调查

先证者(Ⅲ3),女,49 岁.面部、颈部及前臂广泛分布棕褐色丘疹20 年,光照后皮损加重,于2010 年11 月12 日在我院就诊.无明显不适,患者平素体健,无其他疾病.系统检查未发现明显异常.皮肤科检查:面部、颈部及前臂广泛分布棕褐色角化性丘疹,边缘隆起,中央平坦(图1A、B),绿豆至黄豆大.掌跖、黏膜以及臀部等非暴露部位未见皮损.     

皮肤镜诊断面部光线性角化病的初步研究

目的 评价皮肤镜在面部光线性角化病诊断中的价值.方法 面部疑似光线性角化病患者40例,其中男27例,女13例;年龄46～88岁;病程2～20年.分别对其行皮肤镜检查及组织病理学检查;以病理诊断为"金标准",通过诊断性试验的研究方法,研究皮肤镜诊断面部非色素性光线性角化病的敏感性、特异性及一致性.结果 与病理诊断比较,两位医生皮肤镜诊断面部非色素性光线性角化病的灵敏度、特异度、Youden指数及Kappa值分别为90.91%、88.89%、79.80%、0.798(χ2=0.25,P>0.05)和86.36%、94.44%、80.80%、0.800(χ2=0.25,P>0.05).结论 皮肤镜检查对面部非色素性光线性角化病诊断与病理组织检查结果存在较好的一致性.     

光线性角化病159例与皮肤鳞状细胞癌51例临床病理特征分析

目的了解滇东地区光线性角化病与鳞状细胞癌的疾病构成比、一般情况和临床病理特征。方法采用回顾性研究方法对曲靖市第一人民医院皮肤科2014年1月-2018年12月共5年行病理检查确诊的光线性角化病和皮肤鳞状细胞癌患者的临床和病理检查资料进行分析。结果159例光线性角化病(AK)与51例(SCC)鳞状细胞癌患者中女性多于男性,光线性角化病和鳞状细胞癌的发病平均年龄分别为(66.32±14.63)岁和(65.00±16.26)岁。光线性角化病和鳞状细胞癌患者皮损发生于曝光部位的分别占98.11%和78.43%。51例鳞状细胞癌患者中,有3例均是光线性角化病继发鳞状细胞癌,均为女性,年龄均>70岁,发病部位均为曝光部位。5年确诊光线性角化病患者占总病检患者的构成比相对稳定,其中鳞状细胞癌有所波动。AK病理分型分为肥厚型98例(61.64%)、萎缩型26例(16.35%)、棘层松解型12例(7.55%)、色素型9例(5.66%)、苔藓样型9例(5.66%)、鲍温样型5例(3.14%);SCC病理分级Ⅰ级39例(76.47%)、Ⅱ级11例(21.57%)、Ⅲ级1例(1.96%)、Ⅳ级0例。光线性角化病与鳞状细胞癌中临床诊断与病理诊断符合率分别为61.00%和56.86%,易被误诊为其他疾病。结论滇东地区光线性角化病与鳞状细胞癌以中老年女性为主,主要位于头面颈部等曝光部位,与紫外线关系密切,其中发生于曝光部位、皮损多样、病程长的老年女性光线性角化病患者易继发鳞状细胞癌,但临床病理诊断符合率较低,需引起重视。     

播散性浅表性光线性汗孔角化症21例临床病理分析

目的探讨播散性浅表性光线性汗孔角化症临床和组织病理学特点。方法回顾性分析本科1995年1月～2012年1月间断收治的21例播散性浅表性光线性汗孔角化症患者的临床和组织病理学资料。结果 21例患者中男女比例为1.1∶1(男11例,女10例)。20岁前发病者13例(61.91%),(20～50)岁7例(33.33%),>50岁1例(4.76%),平均发病年龄18.36岁。皮损位于曝光部位,累及面部者10例(47.62%),累及颈部者9例(42.86%),累及上肢者19例(90.48%),累及下肢者7例(33.33%),累及躯干者6例(28.57%)。其中4例有家族史(占19.05%)。3例合并有系统疾病。组织病理资料分析均可见典型的角化不全柱,其下方颗粒层减少或消失。结论播散性浅表性光线性汗孔角化症20岁前发病多见,男女发病率大致相当,皮损位于暴露部位。组织学上以表皮角质层内典型的角化不全柱伴其下方颗粒层减少或消失为特征。     

Standardized AgNOR analysis in actinic keratosis.

To assess if the quantity of silver-stained nucleolar organizer region (AgNOR) proteins predicts the behavior of actinic keratosis (AK), we performed a standardized AgNOR analysis on 51 cases of AK; in addition, 10 cases of squamous cell (SCC) and 10 cases of basal cell (BCC) carcinomas and 10 normal skin samples were also studied. AgNOR analysis was performed on formalin-fixed and paraffin-embedded sections according to the guidelines of the Committee on AgNOR Quantification (1995), evaluating the mean area (microm(2)) of AgNORs per nucleus (NORA). A highly significant P value (< 0.001) was found in the comparison among NORA values of normal skin (1.869 microm(2); SD + 0.332), AK (3.988 microm(2); SD + 0.914), BCC (3.044 microm(2); SD + 0.254), and SCC (5.286 microm(2); SD + 0.920). In AK, a progressive increase of mean NORA values was observed moving from Stage I (3.161 microm(2); SD + 0.600) to Stage II (3.455 microm(2); SD + 0.562), Stage III (4.360 microm(2); SD + 0.295), and Stage IV (5.168 microm(2); SD + 0.694); highly significant differences (P < 0.001) were noted when Stages I or II were compared with Stage III or Stage IV or between these latter stages. The AgNOR quantity may identify AKs with high proliferative activity and increased tendency to develop into invasive SCC.     

日光性角化病研究进展

日光性角化病的发病与炎症反应、氧化应激、免疫抑制等有关, 其组织病理表现为表皮结构异常和角质形成细胞发育不良,其他非侵入性的成像方法对诊断该病也有重要意义。治疗方法包括局部药物、光动力、冷冻、激光等。本文对日光性角化病的流行病学、发病机制、临床和组织学特征、诊断及治疗进行综述。     

日光性角化病90例临床及病理特征分析

目的:探讨日光性角化病的临床及组织病理特点.方法:采用回顾性分析,选取门诊患者中病历资料保存完整,经组织病理检查确诊的日光性角化病患者90例,对苏木精-伊红染色的组织切片进行观察并分析其组织病理特征.结果:90例患者平均患病年龄(65.94±10.46)岁,病程(26.63±27.50)个月,男:女为1:1.5,皮损发生于面部占92.2%.临床表现为红褐色斑片46例(51.1%),黑褐色斑片23例(25.6%),黑色丘疹8例(8.9%),皮角7例(7.8%),糜烂性斑片4例(4.4%),并发溃疡2例(2.2%).组织病理上可见表皮不典型角质形成细胞增生、排列紊乱.病理分型为肥厚型36例(40%).萎缩型22例(24.4%),鲍恩样型15例(16.7%),棘层松解型5例(5.6%),苔藓样型6例(6.7%),色素型6例(6.7%).进展为侵袭性鳞状细胞癌2例(2.2%).18例(20%)伴有毛囊受累,11例(12.2%)伴有汗腺导管受累.复发2例(2.2%).84例(93.3%)有真皮日光弹性纤维变性,其中Ⅰ级39例(43.3%),Ⅱ级18例(20%),Ⅲ级27例(30%);6例(6.7%)未见明显日光弹性纤维变性.结论:日光性角化病好发于老年人,面颊部最多发;组织病理示表皮不典型角质形成细胞增生、排列紊乱,以肥厚型、萎缩型、鲍恩样型常见.该病临床易误诊,临床医师应高度警惕.     

Dermoscopic features of actinic keratosis

Actinic keratosis (AK) is a keratinocytic neoplasm that typically develops on sun‐damaged skin of elderly individuals. Only a few reports so far have described the dermoscopic diagnostic features of AK, mainly focusing on facial non‐pigmented AKs. A typical feature of facial non‐pigmented AK is a composite pattern named “strawberry pattern”, characterized by a background erythema/red pseudonetwork consisting of unfocused, large vessels located between the hair follicles, associated with prominent follicular openings surrounded by a white halo. Dermoscopic characteristics of pigmented AK on the face include multiple slate‐gray to dark‐brown dots and globules around the follicular ostia, annular‐granular pattern and brown to gray pseudonetwork. Recognizing specific dermoscopic features of AK can be useful in guiding the clinician in the differential diagnosis of AK with melanocytic skin lesions such as LM and non‐melanocytic lesions. Histopathologic examination should be performed whenever clinical and/or dermoscopic differential diagnosis is inconclusive.     

Tenascin expression in actinic keratosis

BACKGROUND: Tenascin is an extracellular matrix protein frequently expressed around neoplastic and non-neoplastic lesions of the skin. Actinic keratoses (AKs) are intraepidermal neoplastic lesions of the sun-exposed skin. They are classified according to the extension of dysplasia in four stages; they also present different histological varieties. METHODS: We performed an immunohistochemical study using tenascin monoclonal antibody diluted 1 : 50 on 150 cases of AKs classified, respectively, in histotypes (38 hypertrophic, 18 atrophic, 21 bowenoid, 19 acantolytic, and 40 mixed) and in stages (27 stage I, 46 stage II, 42 stage III, and 35 stage IV; 14 in tumoral progression). RESULTS: Tenascin positivity was observed in all cases at the dermal level close to the epithelial lesion. The intensity of reaction increased from stage I to stage IV and, of course, also in tumoral progression. Its expression was not related to the histotypes. In very few cases, the atypical keratinocytes were positive. CONCLUSIONS: Tenascin expression in AKs is related to the stages of dysplasia. In fact, the immunostaining intensity corresponds to the degree of the dysplasia rather than the thickness of the involved epidermis. Tenascin plays a role in neoplastic progression working as an anti-adhesive factor.     

Current therapies for actinic keratosis

Actinic keratosis (AK) is a very common skin disease caused by chronic sun damage, which in 75% of cases arises on chronically sun-exposed areas, such as face, scalp, neck, hands, and forearms. AKs must be considered an early squamous cell carcinoma (SCC) for their probable progression into invasive SCC. For this reason, all AK should be treated, and clinical follow-up is recommended. The aims of treatment are: (i) to clinically eradicate evident and subclinical lesions, (ii) to prevent their evolution into SCC, and (iii) to reduce the number of relapses. Among available treatments, it is possible to distinguish lesion-directed therapies and field-directed therapies. Lesion-directed treatments include: (i) cryotherapy; (ii) laser therapy; (iii) surgery; and (iv) curettage. Whereas, field-directed treatments are: (i) 5-fluorouracil (5-FU); (ii) diclofenac 3% gel; (iii) chemical peeling; (iv) imiquimod; and (v) photodynamic therapy (PDT). Prevention plays an important role in the treatment of AKs, and it is based on the continuous use of sunscreen and protective clothing. This review shows different types of available treatments and describes the characteristics and benefits of each medication, underlining the best choice.