Androgenetic alopecia in children: report of 20 cases

Androgenetic alopecia (AGA) is the most common type of hair loss in adults. Although there are differences in the age at onset, the disease starts after puberty when enough testosterone is available to be transformed into dihydrotestosterone. We report 20 prepubertal children with AGA, 12 girls and eight boys, age range 6-10 years, observed over the last 4 years. All had normal physical development. Clinical examination showed hair loss with thinning and widening of the central parting of the scalp, both in boys and girls. In eight cases frontal accentuation and breach of frontal hairline were also present. The clinical diagnosis was confirmed by pull test, trichogram and dermoscopy in all cases, and by scalp biopsy performed in six cases. There was a strong family history of AGA in all patients. The onset of AGA is not expected to be seen in prepubertal patients without abnormal androgen levels. A common feature observed in our series of children with AGA was a strong genetic predisposition to the disease. Although the pathogenesis remains speculative, endocrine evaluation and a strict follow-up are strongly recommended.     

Androgens and hair growth

Hair's importance in human communication means that abnormalities like excess hair in hirsutism or hair loss in alopecia cause psychological distress. Androgens are the main regulator of human hair follicles, changing small vellus follicles producing tiny, virtually invisible hairs into larger intermediate and terminal follicles making bigger, pigmented hairs. The response to androgens varies with the body site as it is specific to the hair follicle itself. Normally around puberty, androgens stimulate axillary and pubic hair in both sexes, plus the beard, etc. in men, while later they may also inhibit scalp hair growth causing androgenetic alopecia. Androgens act within the follicle to alter the mesenchyme-epithelial cell interactions, changing the length of time the hair is growing, the dermal papilla size and dermal papilla cell, keratinocyte and melanocyte activity. Greater understanding of the mechanisms of androgen action in follicles should improve therapies for poorly controlled hair disorders like hirsutism and alopecia.     

一个中国先天性有汗性外胚层发育不良家系的GJB6基因筛查

目的: 先天性有汗性外胚层发育不良是一种常染色体显性遗传病,GJB6基因突变与之相关。调查一个来自中国的先天性有汗性外胚层发育不良家系与GJB6基因的关系。方法: 收集一个共有17个家系成员(患者8人,5男3女)的先天性有汗性外胚层发育不良家系,采集家系成员的外周血,抽提DNA。然后针对GJB6基因的每个外显子设计引物,应用聚合酶链式反应(PCR)方法扩增GJB6基因的整个编码区,测序、筛查突变。结果: 通过对家系患者的GJB6基因筛查,发现了一个杂合错义突变c.31G>A(p.G11R)。结论: GJB6基因错义突变c.31G>A(p.G11R)导致该家系先天性有汗性外胚层发育不良。     

Comparison of the efficacy and safety of topical minoxidil and topical alfatradiol in the treatment of androgenetic alopecia in women

Background: Two drugs which are approved for the treatment of androgenetic alopecia in women in Germany were compared with regard to their influence on hair growth. Patients and Methods: Patients were randomized to group I (n = 52) who used 2% minoxidil solution twice daily for a period of 12 months or to group II (n = 51) who used 0.025% alfatradiol solution once daily for 6 months and were then switched to 2% minoxidil solution for months 7–12. Changes in hair growth parameters were determined using the TrichoScan. Results:Topical treatment with 2% minoxidil solution for 6 months resulted in a significant increase of cumulative hair thickness (p < 0.0001) and absolute hair density (p ≤ 0.0025), whereas these parameters of hair growth remained nearly unchanged after 6 months of treatment with alfatradiol solution. Evaluation of the same parameters from month 7 to month 12 demonstrated that 12 months minoxidil treatment resulted in an increasing stabilization (group I). After the alfatradiol→minoxidil switch in group II a significant increase in cumulative hair thickness (p < 0.0001) and absolute hair density (p < 0.0001) was achieved. Both study medications were well tolerated. Conclusions: Treatment with minoxidil can induce an increase in hair density and hair thickness,whereas treatment with alfatradiol results in deceleration or stabilization of hair loss.     

斑秃患者皮损处T淋巴细胞表型的研究及Fas的表达

目的　研究斑秃患者皮损处浸润T淋巴细胞的表型及Fas的表达情况。方法　应用免疫组织化学技术检测斑秃患者皮损处CD4和CD8T淋巴细胞及Fas的表达。结果　CD4和CD8:活动期和稳定期斑秃患者皮损处无论是毛囊周围还是血管周围CD4T淋巴细胞浸润数量均明显多于CD8T淋巴细胞 (P <0 .0 5 ) ;斑秃活动期的CD4和CD8T淋巴细胞浸润数量与稳定期和对照组相比较差异有统计学意义 (P <0 .0 5 )。Fas :与对照组相比较 ,斑秃患者皮损处毛囊角质形成细胞Fas的表达例数较多 (P <0 .0 5 )。结论　斑秃患者皮损处浸润T淋巴细胞以CD4T细胞占优势 ;Fas在斑秃皮损处毛囊角质形成细胞异常表达。     

斑秃患者甲襞微循环改变及实验性治疗

目的；探讨斑秃病人甲襞微循环的改变及实验性治疗效果。方法：对门诊斑秃病人进行甲襞微循环观测，以正常人作对照。结果：32例斑秃病人甲襞微循环的清晰度稍有下降，异形管襻比正常人增多（P＜0．05）。红细胞有轻、中度聚集，血流速度减慢，部分病人有轻度襻周渗出，少数病人有襻顶出血。甲襞汗腺导管多于正常人，全秃病人又比一般斑秃病人多（P＜0．001）。654－2促进了毛发生长，且新生毛发不易脱落。结论：斑秃病人存在微循环障碍。654－2对治疗斑秃是有意义的。     

油菜花粉通过提高bFGF和VEGF水平改善小鼠雄激素源性脱发

目的 探索油菜花粉对小鼠雄激素源性脱发的改善作用并研究其作用机制。方法 设立空白组、模型组、阳性药组及给药组,通过脱毛后涂抹0.2%睾酮诱导建立小鼠雄激素源性脱发模型,采用市售5%米诺地尔为阳性药物,0.4 g·mL^-1油菜花粉油溶液为给药组,分别观察小鼠毛发生长速度。通过扫描电子显微镜(scanning electron microscope,SEM)、病理组织HE染色观察小鼠毛发质量及毛囊情况。使用免疫荧光染色、免疫印迹试验检测皮肤中VEGF、bFGF水平,ELISA检测血清性激素及活性氧水平。结果 与模型组相比,油菜花粉能显著促进小鼠毛发生长,且能够改善小鼠毛发毛鳞片的状态。机制探究试验表明油菜花粉不能通过调节小鼠激素水平或抗氧化应激起到促进毛发再生作用,但油菜花粉可以提高造模部位皮肤血管生成相关因子bFGF和VEGF的表达。结论 油菜花粉可以促进雄激素源性脱发小鼠毛发再生,其作用机制可能是通过提高bFGF和VEGF水平,促进毛囊周围血管再生从而达到促进毛发再生作用。     

头皮局限性神经纤维瘤伴脱发一例

患者,男,22岁。脱发1年余,头皮棕褐色肿物6个月。病理可见毛囊微小化,真皮下部大量细长梭形瘤细胞,波浪状排列。S-100多克隆(+),SOX-10(+),MelanA(+),Vimentin-10(+)。诊断为头皮局限性神经纤维瘤。后行手术治疗,随访中。     

茶皂素为乳化剂制备黄芩苷纳米乳及其促小鼠毛发生长的药效学研究

目的 以茶皂素为天然乳化剂制备黄芩苷纳米乳（baicalin nanoemulsion,Bai-NE）,并探究其对C57BL/6小鼠毛发生长的促进作用。方法 采用超声乳化法制备Bai-NE,利用单因素实验法对Bai-NE的处方和制备工艺进行优化,并对最优处方和工艺制备的Bai-NE进行理化性质和稳定性考察。以C57BL/6小鼠为研究对象,评价Bai-NE对毛发生长的促进作用。结果 Bai-NE的最佳处方为茶皂素用量为0.5%,油相用量为5%,最佳制备工艺为超声功率180W,超声时间10min,超声次数1次。制得的Bai-NE为O/W型乳液,外观均一,平均粒径为（225.1±0.6）nm,多分散指数（polydispersity index,PDI）为0.082±0.031,载药量为1.10mg/g,pH值为7.25±0.20。稳定性结果显示,Bai-NE具有良好的离心稳定性和储存稳定性。Bai-NE能显著促进C57BL/6小鼠的毛发生长。结论 茶皂素可作为一种潜在的天然乳化剂用于Bai-NE的制备,制备的Bai-NE对C57BL/6小鼠的毛发生长有促进作用。     

Blood endotyping distinguishes the profile of vitiligo from that of other inflammatory and autoimmune skin diseases

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