进行性斑状色素减少症一例

患者男,28岁.因躯干色素减退斑8年就诊.皮疹为色素减退性斑片,大小不一,境界不清,表面无鳞屑,色减斑片在躯干近中线处融合.真菌学直接镜检阴性.Wood灯检查显示皮损区域毛囊性红色荧光.组织病理学仅提示基底层见色素减少,皮肤电镜提示皮损处黑素小体数目较临近正常处皮肤减少,且以Ⅰ～Ⅲ期为主,周围正常皮肤处黑素小体以Ⅳ期为主.根据患者临床表现、Wood灯检查及组织病理、皮肤电镜结果,确诊为进行性班状色素减少症.窄谱UVB治疗有效.     

播散性复发性漏斗部毛囊炎1例

播散性复发性漏斗部毛囊炎(DRIF)临床少见,查阅文献,近20年来,国内共9例报道。我们所见1例报道如下。临床资料患者男,20岁,学生。全身皮肤起皮疹伴瘙痒7年来诊。患者于7年前自觉皮肤瘙痒,继而全身起疹,皮疹以夏季遇热出汗时明显,冬季减轻。近2年来双上臂瘙痒明显加重。曾在多处     

播散性复发性漏斗部毛囊炎一例北大核心CSCD

患者女,44岁,因前胸出现粟粒样小丘疹5个月,于2014年7月来广东省皮肤病医院皮肤科就诊。患者5个月前无明显诱因于胸部出现淡红褐色实性小丘疹,质韧,皮疹渐渐增多,觉瘙痒,夏重冬轻：体检。     

进行性斑状色素减少症30例临床分析

目的:探讨进行性斑状色素减少症的临床特点并对其治疗情况进行分析。方法:回顾性分析我院于2013年10月-2018年10月间诊治的30例进行性斑状色素减少症患者的临床表现和治疗情况。结果:进行性斑状色素减少症主要的临床表现为躯干部出现边界不清的圆形、无鳞屑的色素减退斑,中央可发生融合。真菌镜检阴性。伍德氏灯:色素减退皮损区可见点状红色荧光。皮肤共聚焦扫描显微镜:色素环均正常,25例色素颗粒减少。30例患者均经过10周外涂异维A酸红霉素凝胶联合1周2次窄谱中波紫外线照射治疗,10例痊愈,7例基本治愈,7例显效,3例有效,3例无效,显效率为80.00%。结论:进行性斑状色素减少症临床表现轻微,无明显自觉症状,缺乏特异性的实验室检查,易被忽略及误诊。外涂异维A酸红霉素凝胶联合窄谱中波紫外线照射治疗疗效较好,且无严重的系统性不良反应发生,值得在临床上推广。     

进行性斑状色素减少症的临床及实验研究

目的 探讨进行性斑状色素减少症（PMH）的临床特点和诊断要点。方法 用Wood灯及活体共聚焦激光扫描显微镜（皮肤CT）观察皮损特点、致病菌培养、黑素细胞培养,并应用S-100和TRP-1免疫组化分析皮损区黑素细胞数量、电镜观察其超微结构特征。结果 Wood灯检查示皮损区可见点状红色荧光,皮肤CT观察示皮损区色素环完整,但与周围正常皮肤相比其内所含的黑素颗粒含量减少。致病菌培养可见产红色荧光的革兰阳性棒状杆菌,经鉴定为痤疮丙酸杆菌。S-100染色示皮损区阳性细胞数（8.25 ± 0.96）与周围正常皮肤（8.75 ± 1.71）相比无统计学意义（P > 0.05）。TRP-1染色示皮损区阳性细胞数（4.25 ± 0.96）与周围正常皮肤（4.50 ± 1.29）相比也无统计学意义（P > 0.05）。电镜观察发现,皮损区Ⅳ期黑素小体的数量明显下降,并观察到较多的膜结合体,内含成簇状分布的多个体积较小的Ⅱ ～ Ⅳ期黑素小体。成功培养出黑素细胞,其形态与正常细胞相比未见明显异常。结论 初步提出进行性斑状色素减少症的诊断要点。     

播散性复发性漏斗部毛囊炎1例

播散性复发性漏斗部毛囊炎１例郑伟德，孙栩患者男，１７岁。全身皮肤瘙痒、起疹２年。２年前感皮肤瘙痒，继而全身起疹，至今未消退。瘙痒夏季甚，冬季减轻，出汗时加重。近来两上臂瘙痒明显加重。曾在外院诊治，皮损无改善。患者平素体健，无结核病史。体检：发育正常，...     

播散性复发性漏斗部毛囊炎

报告1例播散性复发性漏斗部毛囊炎。患者女,26岁。颈背部及上肢丘疹伴瘙痒1年余。皮肤科检查:颈背部及上肢密集均匀分布以毛囊口为中心的肤色粟粒大丘疹,大小一致。皮损组织病理检查:表皮轻度角化过度,基底层色素增加,真皮浅层小血管周围淋巴单核样细胞浸润,小血管略增生,毛囊漏斗部见淋巴细胞浸润,海绵水肿。诊断:播散性复发性漏斗部毛囊炎。口服维生素A,配合外用维A酸,治疗效果良好。     

复发性播散性漏斗部毛囊炎

本病系由Hitch首先发现,在1968年以复发性播散性漏斗部毛囊炎(disseminate and recurrent infundibulofoliculitis)为名作首例报告的.以后其他作者相继作了同类病例的报告.据Owen综合了截至1979年为止的世界文献,已先后报告了19例,多见于黑人,男∶女为4∶1.本病的特点是反复发生的弥漫性瘙痒性呈正常肤色的大小一致的毛囊性丘疹性发疹,其组织学所见为毛囊漏斗部的淋巴细胞浸润性毛囊炎.现复习有关本病的资料并归纳如下:     

伊藤色素减少症五例

<正>临床资料患儿共5例,男2例,女3例。均因皮肤白斑来我科就诊。皮肤表现的共同点为白色斑疹、斑片,呈条索状,沿Blaschko线分布。1例为不对称性分布,仅累及左侧躯干及左侧上下肢(图1a,1b)。5例中4例为对称性分布,其中1例累及躯干和四肢,2例累及四肢,1例累及眼周和双下肢。发病年龄为出生后即刻至3月龄,平均1.5个月。除皮损外,1例并发骨骼系统损害,5例中4例并发神经系统损害。骨骼系统损害表现为双足6趾(图2a-2c)。神经系统损害的发现年龄为3~12个月,平均6.3个月,表现为癫痫伴四肢肌张力偏低,癫痫伴语言、行走落后,智力落后,走路不稳及智、体力发育迟缓,竖头不稳,追物慢等;其中1例患儿伴左面部及左侧上、下肢     

播散性复发性漏斗部毛囊炎1例

正播散性复发性漏斗部毛囊炎(Dissminateandrecurrentinfundibularfolliculitis,DRIF)临床少见,国外文献中仅见于黑人,近年来发现本病在黄种人当中偶有发病,我科诊断1例该病患者,报告如下:1临床资料患者,女,39岁,主因全身皮肤起皮疹伴瘙痒2年于2006年10月来我院就诊。患者自2年前开始无明显诱因自觉皮肤瘙痒,继而全身起皮疹,皮疹可逐渐消退但反复发生。夏季皮疹明显,搔抓后继发感染伴有渗出,冬季皮疹减轻但不能完全消失。曾     

Adolescent extra-truncal progressive macular hypomelanosis

Two adolescent females presented to outpatient clinic with isolated, non-scaly, asymptomatic hypopigmented macules and patches on the arm(s). Both cases had Wood's lamp exams notable for extralesional punctiform coral-red perifollicular fluorescence on the back and faint intralesional enhancement. In one case, biopsy was performed and deemed consistent with progressive macular hypomelanosis. The patient had complete response to antimicrobial therapy and sun exposure.     

Propionibacterium acnes and the pathogenesis of progressive macular hypomelanosis

BACKGROUND: Progressive macular hypomelanosis is a common hypopigmentation mainly on the central parts of the trunk, predominantly in young adults, especially women. It is often mistaken for pityriasis versicolor and pityriasis alba. It occurs in all races and has been described in many parts of the world. We discovered follicular red fluorescence restricted to lesional skin. We suspected a relation with a porphyrin-producing bacteria residing in sebum of the pilosebaceous duct, and we therefore performed a study in 8 patients.Observation In all biopsy specimens taken from lesional skin of 8 women, we could demonstrate gram-positive bacteria in the pilosebaceous duct, and a mild perifollicular lymphocytic infiltrate was seen. In all but 1 patient, Propionibacterium acnes was yielded from cultured biopsy specimens taken from follicular lesional skin. Healthy follicular skin did not show bacteria in histological sections, and cultures did not yield anaerobic bacteria. CONCLUSIONS: There seems to be a relation between the presence of P acnes and the hypopigmented macules. We propose that a factor is produced by these strains of P acnes, which interfere with melanogenesis. Based on these observations, we are undertaking a clinical trial to find a treatment for this troubling, intractable disease.     

A case of disseminated and recurrent infundibulofolliculitis responsive to treatment with systemic isotretinoin

We report a 16-year-old Turkish patient who developed disseminated and recurrent infundibulofolliculitis (DRIF) and responded well to systemic isotretinoin therapy after three months.     

Ultrastructural findings in progressive macular hypomelanosis indicate decreased melanin production

Background The pathogenesis of progressive macular hypomelanosis (PMH) is unknown. Recently, Westerhof et al. (Arch Dermatol 2004; 140: 210–214) hypothesized that Propionibacterium acnes produces a depigmenting factor that interferes with melanogenesis in the skin, resulting in hypopigmented spots. The purpose of the study is to gain an insight into the pathogenesis of PMH. Materials and methods We took a biopsy of 2‐mm diameter from normal and lesional skin in eight PMH patients. Using electron microscopy, we compared melanization of melanosomes, melanosome transfer and amount of epidermal melanin in normal and lesional skin. Result Compared to non‐lesional skin, we observed a decrease of epidermal melanin and less melanized melanosomes in lesional skin of all patients. When comparing normal and lesional skin of patients with skin type V and VI, we observed a difference in melanosome size and maturation and a switch of transferred melanosomes from single stage IV transferred melanosomes to aggregated stage I, II and III transferred melanosomes, as seen in healthy skin of skin type I to IV. Conclusion Hypopigmentation in PMH seems to be the result of an altered melanogenesis based on a decrease in melanin formation and a change in the distribution of melanosomes. In lesional skin of PMH patients with skin type V and VI less melanized, aggregated melanosomes in stead of single, mature melanosomes are transferred from melanocytes to keratinocytes. This results in a decrease of epidermal melanin. Further investigations are needed to determine the precise role of Propionibacterium acnes in this alteration of melanogenesis.