梅毒性脱发一例

临床资料 患者,男,25 岁,未婚. 因头枕部及颞部斑状脱发2周,来我院就诊.2周前患者偶然发现颞部出现散在斑片状脱发,自觉洗头脱发数量明显增加,整体发量减少,无瘙痒、疼痛等不适.患者有不洁性交史,否认输血史,否认家族史,发病前无生殖器、皮肤及黏膜异常.皮肤科查体:头顶、后枕部及颞部可见散在灶状的脱发斑(图1),边界不...     

同一个部位患白癜风和斑秃1例

患者男,６０岁,头皮脱发２年、白斑１年。患者２年前头皮枕部出现一块甲盖大脱发,渐扩大,不痛不痒,近１年来枕部脱发区皮肤发白,顶部又出现一枚脱发区,局部皮肤发白,无家族史。体检：系统检查无异常。皮肤科情况：枕部头皮有一块４０ｃｍ×６０ｃｍ的脱发区,...     

毛囊性扁平苔藓1例

患者女,43岁.因头皮出现紫红色斑伴脱发及轻度瘙痒1年,于2008年6月来我院就诊.患者1年前无明显诱因部出现小片状脱发,约指甲大,局部头皮呈紫色,上覆白色鳞屑,伴有轻度瘙痒.随后脱发区面积逐渐扩大至4cm×1.5 cm,为进一步诊治至我院就诊.患者白发病以来精神、食欲及睡眠均可,二便正常,体重无明显改变.既往体健,否认有类似疾病家族史.     

Brocq假性斑秃1例

正1 病历摘要患者女,52岁。因顶枕部头发斑片状脱失1年,2015年5月4日就诊于我科。患者1年前无诱因顶枕部出现不规则的脱发,无自觉症状,脱发现象持续半个月后自然停止。半个月前,右侧后枕部再次出现离散的簇状分布的小的秃发区,部分融合成大片状。既往无其他病史,否认家族成员中有类似病史。     

毛发扁平苔藓三例分析

目的 探讨毛发扁平苔藓的临床和组织病理特征。方法 分析3例毛发扁平苔藓患者的临床、组织病理学特征。结果 3例患者均为女性,平均年龄49岁。1例患者临床表现为额部、顶部及枕部大面积斑片状脱发,2例表现为头皮不规则斑片状脱发及皮肤萎缩。1例患者除头发外,眉毛、腋毛亦脱落。组织病理均为毛囊壁基底层细胞液化变性及淋巴细胞浸润。1例血管附件周围亦可见少量淋巴细胞浸润。结论 毛发扁平苔藓可仅累及头皮,亦可累及全身其他部位皮肤,多表现为头皮斑片状脱发伴皮肤萎缩。病理学典型改变为毛囊基底细胞液化变性,淋巴细胞浸润。     

肩关节复位术颞部压迫致斑秃样脱发1例

患者男，２５岁，因肩关节脱臼于２００１年４月１０日行全麻下肩关节复位术。术中双侧颞部头皮外罩铁托套固定。７h后摘除铁托套。术后患者即感铁托套压迫局部疼痛，并发现该处皮肤发红。２０天后，患者两侧颞部头皮出现两处分布大致对称的圆形约３cm×３cm大小斑片状脱发区。患者不痛不痒，无自觉症状。检查：患者一般情况良好，全身检查未见异常。皮肤科检查见两侧颞部头皮２处分布对称的圆形约３cm×３cm斑片状脱发区。脱发区皮肤光滑，无炎症反应；脱发区边缘头发松动，很易拔出，其余头皮正常。诊断：斑秃样脱发。常规金属斑贴试验（…     

以脱发为主要表现的二期梅毒1例

1 临床资料患者男,52岁.头部斑片状脱发1周.患者1周前头部出现散在分布大小不一(点状、钱币状及指甲盖)的圆形、不规则形的脱发斑片;脱发区逐渐增多.4月前曾有不洁性交史.不久包皮系带处黄豆大的溃疡,未就诊,经口服头孢拉啶胶囊及外涂红霉素眼膏后溃疡愈合.系统检查未见异常.皮肤科情况:头部散在分布点状、钱币状及指甲盖大小的圆形和不规则脱发区,以枕、颞部为主,顶部少见.脱发斑片与周围正常毛发区分界不太清楚,脱发区内尚可见稀疏长短不一之断发根.     

早发性雄激素性秃发1例

患儿男,12岁.因脱发半年就诊.患儿半年前无明显诱因开始脱发,伴夜间多梦.4岁时曾患"斑秃",后治愈.其父患雄激素性秃发.体格检查:发育正常,营养良好,系统检查无异常.皮肤科检查:头顶部弥漫性毛发稀疏,发质细软,头皮及头发油腻感(图 1).颞部、枕部头发正常.拉发试验阴性.面部及胸背部无痤疮.     

梅毒性脱发1例

二期梅毒皮损表现多样 ,梅毒性脱发相对少见。我科见到梅毒性脱发 1例 ,现报告如下。患者男 ,3 8岁。头部片状断发 1月。 1月前无明显诱因头部出现不规则地片状脱发 ,头皮不痒 ,无脱屑。追问病史 ,患者于 6～ 8月前曾有多次不洁性交史 ,4～ 5个月前阴茎有过小硬结 ,未治自愈。但近 1～ 2月肛门部出现小疙瘩。体检 :系统检查仅触及腹股沟浅表淋巴结肿大 ,约黄豆至蚕豆大 ,无粘连 ,轻压痛 ,表面皮肤不红。余未见异常。皮肤科情况 :头部散在 1～5分币大虫蚀状断发区 ,以颞、枕部为著 ,断发残端约 1～ 3ｍｍ ,无发鞘 ,头皮无鳞屑 (图 1)。肛门周…     

姐妹3人同患先天性秃发

先天性秃发临床较少见。笔者于门诊遇到同胞姐妹 3人同患本病 ,现报告如下。例 1　女 ,14岁。自 1周岁起 ,额顶部头发逐渐变细软 ,失去光泽。继之呈弥漫性脱落 ,至 9岁时基本完全脱落 ,趋于稳定 ,至今仍未恢复。脱发区边缘整齐 ,状似男性型脱发 ,中心残存少量细软毛发。颞部及枕部毛发正常。例 2　女 ,11岁。自 4岁起 ,枕部开始脱发 ,渐波及额顶部 ,至今未见缓解。枕部脱发区边缘较清晰 ,呈三角形 ,边长约 5ｃｍ。中央头皮光滑 ,无毛发存留 ,毛孔消失。额部及顶部脱发区呈小片状类似斑秃。周边毛发细软 ,但不易拔除 ,用力拔除可带有毛根及毛…     

The genetic basis of alopecia areata: HLA associations with patchy alopecia areata versus alopecia totalis and alopecia universalis

Many diseases, notably those having a strong autoimmune component, have been shown to have an association with specific human leukocyte antigens (HLA). The molecular basis for this genetic association with disease is the fact that HLA bind and present peptides derived from self and foreign protein antigens to the immune system for recognition and activation of the immune response. Previous studies with heterogeneous groups of alopecia areata (AA) patients have suggested associations with some HLA class I and class II antigens. For this study we selected only patients with long-standing disease and stratified them into two groups by strict definitions of duration and extent of disease: those with patchy AA and those with either alopecia totalis (AT) or alopecia universalis (AU). The patients were tissue typed for HLA class II antigens by biomolecular methods that provided antigen discrimination at an allele level. More than 80% of all of the AA patients typed were positive for the antigen DQB1*03 (DQ3), suggesting that this antigen is a marker for general susceptibility to AA. In addition, two other antigens were found significantly increased in frequency only in the group of AT/AU patients, DRB1*0401 (DR4) and DQB1*0301(DQ7). This strongly suggests that the two clinical types of AA, namely patchy AA versus AT/AU, can be distinguished by a genetically based predisposition to extent of disease.     

Scarring alopecia

Scarring alopecia refers to a group of disorders of various etiologies that cause permanent hair loss. In this article, we focus on primary cicatricial alopecia, a group of diseases in which the hair follicle is the main target of the inflammatory process. These disorders are currently classified as lymphocytic, neutrophilic, or mixed according to the cells that make up the inflammatory infiltrate. The pathogenesis of the majority of these conditions is not fully understood and they may have similar clinical features, often making it necessary to perform 1 or more skin biopsies in order to reach a diagnosis. Management depends on early and accurate diagnosis and aggressive treatment in some cases in order to prevent follicular destruction and scarring.     

Sarcoidosis-induced alopecia

Cutaneous sarcoidosis of the scalp may induce scarring alopecia, which clinically resembles other forms of primary cicatricial alopecia. Differentiation via histologic evaluation is necessary because sarcoidosis demonstrates classical non-caseating granulomas. Review of the literature reveals that sarcoidosis-induced alopecia occurs more commonly in black females age 23 to 78, with the majority of patients having coexisting facial sarcoidosis with pulmonary and lymph node involvement. Given the strong association between sarcoidal alopecia and systemic sarcoidosis, evaluation of the patient is indicated if alopecia is the initial presenting manifestation.     

Scarring alopecia

The scarring alopecias are a diverse group of diseases characterized by the combination of follicular destruction and dermal scarring. In this article we divide scarring alopecias into three broad categories, pediatric diseases, perifollicular lymphocytic diseases, and folliculopustular diseases, and discuss selected entities from each category.     

Psoriatic alopecia

Alopecia and other hair abnormalities occurring in patients with psoriasis were first recognized over four decades ago, yet psoriatic alopecia is not a well‐known concept among clinicians. Alopecia may be directly related to the psoriasis itself, and can affect both the scalp and other parts of the body. On the scalp, psoriatic alopecia most commonly affects lesional skin, but may present as a generalized telogen effluvium. In most cases, there is regrowth of hair, but in rare cases it can cause scarring alopecia. Histological findings include features of psoriasis in the interfollicular epithelium, along with perifollicular inflammation and atrophy or loss of the sebaceous glands. Late changes include destruction of the hair follicle, with perifollicular fibrosis and ‘naked’ hair shafts lying free in the dermis. In addition to the hair loss caused by the psoriasis itself, data from population and genetic studies reveal that patients with psoriasis are at greater risk of developing alopecia areata. Psoriasis treatments may also contribute to hair loss. Application of topical preparations may cause hair loss through friction, and many of the systemic treatments used for psoriasis can also cause hair problems. Treatment with anti‐tumour necrosis factor‐α agents can precipitate de novo psoriasis and subsequent psoriatic alopecia.     

Cicatricial alopecia

In the classification of the North American Hair Research Society, primary cicatricial alopecias (PCA) are divided into four groups according to their prominent inflammatory infiltrate: PCAs with lymphocytic, neutrophilic, mixed or nonspecific cell inflammation pattern. The hair loss can begin subclinically and progress slowly so that the exact onset of the disease is often difficult to determine. The diagnosis is often delayed. While most forms of cicatricial alopecia can be clearly diagnosed based on clinical presentation in the acute disease stage, diagnosis can be challenging in the subacute, early or late disease stages. At first presentation, a detailed patient history and dermatological examination of the body, including trichoscopy, should be performed. In clinically unclear cases, a biopsy should be performed. Due to the scarcity of primary cicatricial alopecia, there is little evidence on the efficacy of the various therapies. The aims of treatment are to stop or at least delay hair loss and progression of the scarring process, reduce clinical inflammation signs as well as to alleviate subjective symptoms. Hair re‐growth in already scarred areas should not be expected. Anti‐inflammatory treatment with topical corticosteroids class III to IV and / or with intracutaneous intralesional triamcinolone acetonide injections can be considered in most of the primary cicatricial alopecias. The choice of systemic therapy depends on the type of predominant inflammatory infiltrate and includes antimicrobial, antibiotic or immunomodulating/immunosuppressive agents. Psychological support and camouflage techniques should be offered to the patients.     

压力性脱发

压力性脱发(pressure alopecia,PA)的病理生理过程与长期卧床所致的压力性溃疡相类似,常发生在枕部,患者在过去数周内曾有手术或较长时间在重症监护病房的持续静卧、头位固定史,有些患者脱发前曾有头皮压痛、肿胀、甚至溃疡的表现,但部分患者可能仅直接表现为脱发。该文总结已有文献对其作一综述。