毛发扁平苔藓特殊皮肤镜表现一例

患者,女,56岁,脱发4个月.本例患者除皮肤镜下毛发扁平苔藓典型特点毛囊周围的管状鳞屑外,还可以看到较多猪尾状卷曲发、内生发等.病理检查:表皮萎缩、变薄、基底细胞液化变性,真皮浅层淋巴细胞浸润,毛囊周围可见淋巴细胞浸润,毛囊周围纤维化.诊断:毛发扁平苔藓.     

改良的Ho-Vert法切片对21例经典型毛发扁平苔藓临床病理诊断价值的观察

【摘要】 目的 对比传统纵切片法、横切片法及改良的Ho?Vert切片法对经典型毛发扁平苔藓的诊断效能。方法 收集2015年1月1日至2019年1月1日间南京医科大学附属无锡市人民医院皮肤科经典型毛发扁平苔藓患者的临床资料，在皮肤镜辅助下，头皮皮损标本采用改良Ho?Vert法分别进行横、纵切片，采用单一横、纵切片读片和横、纵切片结合读片，观察组织病理学改变。结果 经典型毛发扁平苔藓21例，男15例，女6例，年龄（50.0 ± 13.6）岁，平均病程18个月。患者表现为多灶性或融合性斑片状脱发，其他还可见头皮萎缩、毛周角化过度、毛囊开口消失、纤维性白点、轨道征等。在横切片中，所有患者毛囊漏斗部及峡部均可见苔藓样淋巴细胞浸润，均可见毛囊性微瘢痕，7例可显示真表皮界面。而在纵切片中，只有9例观察到毛囊漏斗部及峡部的淋巴细胞苔藓样浸润，4例观察到毛囊性微瘢痕，所有切片均可显示真表皮界面。横、纵切片中组织病理学结果有差异的表现还有毛囊间皮肤界面皮炎改变、毛囊角栓、皮脂腺周围淋巴细胞浸润、皮脂腺萎缩或消失、毛球周围炎性浸润。结合临床表现，通过单一横切片仅有7例可确诊毛发扁平苔藓，单一纵切片仅9例可确诊，结合纵、横切片组织病理表现，21例均可确诊。结论 皮肤镜辅助下改良的Ho?Vert标本纵横组合切片处理技术，可多维显示组织病理改变，提高病理诊断效率。     

线状皮肤红斑狼疮1例

报告1例线状皮肤红斑狼疮。患者男,36岁。左下颌部红斑,头皮红斑脱发3个月。体格检查:左下颌带状红斑,呈"Y"字形分布,边界清楚,皮损表面附着少许白色鳞屑。头皮纵向带状红斑,皮损处毛发稀疏,毛囊萎缩凹陷。左下颌皮损病理检查示:角化过度伴角栓形成,局部角化不全,灶性棘层萎缩或轻度肥厚,基底层细胞液化变性,带状淋巴细胞浸润,血管及附属器周围亦见淋巴细胞为主的炎症浸润。诊断:线状皮肤红斑狼疮。予羟氯喹治疗后皮损明显好转。     

褶皱部色素性扁平苔藓

报告1例褶皱部色素性扁平苔藓。患者男,63岁。腹股沟、腋窝对称性灰褐色斑3个月。皮损组织病理学改变为表皮萎缩,基底细胞液化变性,真皮内可见噬黑素细胞,类性细胞带状浸润不明显,部分血管周围可见淋巴细胞浸润。     

泛发性光泽苔藓并发毛发扁平苔藓

报告1例泛发性光泽苔藓并发毛发扁平苔藓。患儿女,4岁。头皮、颈项部、背部及四肢出现肤色丘疹4年余。皮肤科检查:头皮可见毛囊性针头大丘疹,毛发稀疏卷曲;颈项、背部及四肢可见针头大肤色坚实丘疹,有光泽。皮损组织病理检查:角化过度伴角化不全,基底细胞液化变性,真皮乳头浅层半球形浸润性细胞团块,团块两侧表皮突延长,呈典型的"抱球状"外观;同时可见毛囊上皮基底细胞液化变性,周围可见淋巴细胞为主的带状浸润。免疫组化显示浸润细胞以CD4~+细胞为主。诊断:泛发性光泽苔藓并发毛发扁平苔藓。治疗:给予他克莫司软膏,维A酸乳膏外用,转移因子口服液治疗,病情好转。     

线状皮肤红斑狼疮1例

报告1例线状皮肤红斑狼疮。患者男,36岁。左下颌部红斑,头皮红斑脱发3个月。体格检查:左下颌带状红斑,呈"Y"字形分布,边界清楚,皮损表面附着少许白色鳞屑。头皮纵向带状红斑,皮损处毛发稀疏,毛囊萎缩凹陷。左下颌皮损病理检查示:角化过度伴角栓形成,局部角化不全,灶性棘层萎缩或轻度肥厚,基底层细胞液化变性,带状淋巴细胞浸润,血管及附属器周围亦见淋巴细胞为主的炎症浸润。诊断:线状皮肤红斑狼疮。予羟氯喹治疗后皮损明显好转。     

光化性扁平苔藓1例

报告1例光化性扁平苔藓。患者女，80岁。右耳前皮肤棕褐色斑疹伴做痒1年余。皮肤组织病理检查显示角化过度、表皮萎缩，基底细胞液化变性伴明显的色素失禁．真皮浅层中等量淋巴细胞带状浸润或片状分布于毛细血管周围，未见异形细胞。     

前额纤维化性脱发二例

例1女,44岁,额颞部发际线后移4年,面部多发性肤色小丘疹2年.皮肤科检查:额颞部发际线后移,局部皮肤光滑菲薄,可见残存的细小毛发;眉毛、腋毛和阴毛部分脱落;额颞部、双下颌角处可见弥漫性分布许多粟粒大小的肤色小丘疹.皮肤镜下可见毛囊开口数减少,毛发直径不一,瘢痕性白斑和毛囊周围红斑.例2女,55岁,额颞部毛发稀少2年.皮肤科检查:双侧额颞部发际线后移,眉毛、腋毛和阴毛部分脱落.2例患者的组织病理检查均可见毛囊周围以淋巴细胞为主的浸润,基底细胞液化变性,毛囊周围有板层状纤维化.2例患者的临床和组织病理表现均符合前额纤维化性脱发的诊断.     

经典型毛发扁平苔藓反射式共聚焦显微镜图像特征分析

目的：明确经典型毛发扁平苔藓反射式共聚焦显微镜(reflectance confocal microscopy，RCM)图像特征及其在诊断中的意义。方法：对2018年1月至2020年6月就诊于我院皮肤科的24例临床确诊为经典型毛发扁平苔藓的患者进行RCM和组织病理检查，并将两者结果进行对比研究。结果：24例患者的RCM图像主要特征为：表皮萎缩、变薄9例(37.5%)，毛囊角栓4例(16.67%)，表皮基底细胞液化变性10例(41.67%)，真皮浅层单一核细胞浸润9例(37.5%)，毛囊壁基底细胞液化并周围大小不一的单核细胞及油煎蛋样的噬色素细胞浸润24例(100%)，毛囊周围胶原明显增生7例(29.17%)，和组织病理学检查的一致率分别为91.67%、83.33%、91.67%、96.43%、100%及83.33%。结论：经典型毛发扁平苔藓RCM主要特征与组织病理具有较高的一致性，可以为经典型毛发扁平藓的诊断、疗效判断等提供有效的帮助。     

毛囊扁平苔藓

报告1例毛囊扁平苔藓。患者男,51岁。头皮隆起性斑块伴瘙痒1年。皮肤科检查:枕部左侧头皮可见数个淡紫色斑块,最大者约2.5 cm×1.5 cm,上有较多粟粒大毛囊角化性白色丘疹,伴有头发脱失,拉发试验(-)。皮损组织病理检查:表皮角化过度,毛囊口扩张,内含角质栓,漏斗部颗粒层增厚,毛囊上皮基底细胞液化变性,可见胶样小体,上皮与真皮间有裂隙形成,真皮内于毛囊周围大量淋巴细胞呈带状浸润。诊断:毛囊扁平苔藓。     

Lichen planopilaris.

P, a 20-year-old laborer displayed initial symptoms of the disease in question when he was 10 years old. Initially he had an asymptomatic progressive loss of hair on the scalp. A couple of years later he had mild to moderate pruritis, and the appearance of slate-blue eruptions on the scalp and elsewhere on the body. This resulted in a complete loss of hair on the vault of the scalp, which led him to seek specialist opinion. Skin surface examination revealed the presence of grayish-blue acuminate follicular papules, disposed singly and in groups (plaques). The pilo-sebaceous orifices were conspicuously obliterated and filled by keratin plugs. Perifollicular erythema was a predominant feature on the scalp. The lesions were present over the scalp, around the neck, chest, back, axillae, groin and legs. Shiny atrophied scalp skin depicting scarring alopecia mimicking male-type baldness was a salient feature. In addition, it was studded with conspicuous acuminate papules in its center (Fig. 1a). The known nonhairy (glabrous) skin had classic lichen planus lesions (Fig. 1b). Hemotoxylin-eosin stained microsections prepared from typical lichen planus (LP) lesions over the abdomen and those of lichen planopilaris (LPP) of the scalp were simultaneously studied. The former revealed changes in the epidermis comprising of hyperkeratosis, increase in thickness of stratum granulosum, hydropic degeneration of the basal cell layer and band-like lympho-histiocytic infiltrate pressing against and invading the epidermis, while the latter revealed uniform atrophy of the epidermis and vacuolization of basal cells. The hair follicles were dilated and were filled with keratin plugs. In addition to fibrosis of the dermis, pigment laden microphages and lympho-histiocytic infiltrate was prominent. The follicles and the sebaceous glands were absent. However, arrectores pilorum and sweat glands were preserved (Fig. 2a,b).     

Multiple Basaloid Cell Hamartoma with Alopecia and Autoimmune Disease (Systemic Lupus Erythematosus)

We report a 22-year-old Japanese woman with multiple basaloid cell hamartoma with alopecia and autoimmune disease (systemic lupus erythematosus). She presented with infiltrated large annular, brown-violet, erythematous plaques with atrophic areas in the center on her right cheek, left abdomen and left knee. She also had progressive multiple follicular keratotic papules on her scalp, face, neck, and both axilla and hair loss from her scalp, eyebrow, and axilla. Serologically, reumatoid factor (+++), rheumatoid arthritis hemagglutination test (x1280), and anti-nuclear antigen (x160) were positive. Histological findings of the annular lesion showed liquefaction degeneration of basal cells, lymphocytic infiltration around hair follicles and capillaries, and panniculitis with lymphoid cell infiltration, which was diagnosed as lupus erythematosus profundus. The histological findings of multiple follicular papular lesions of the scalp and neck showed aggregations of basaloid cells, partially with hair-bulb-like structures, which was diagnosed as trichoepithelioma. Taken together, the histogenesis of multiple basaloid cell hamartoma is thought to share the same basis with autoimmune disease.     

IL-17-positive mast cell infiltration in the lesional skin of lichen planopilaris: Possible role of mast cells in inducing inflammation and dermal fibrosis in cicatricial alopecia

Lichen planopilaris (LPP) is a primary cicatricial alopecia characterized by the infiltration of lymphocytes in the upper portion of hair follicles. Inflammation around the bulge region of hair follicles induces destruction of hair follicle stem cells and tissue fibrosis, resulting in permanent hair loss. Treatment is still challenging, and the precise pathophysiology of this disorder is unknown. To clarify the pathogenesis of LPP, we performed histological and immunohistochemical analysis on specimens obtained from LPP patients. Formalin-fixed and paraffin-embedded samples were evaluated by staining with haematoxylin and eosin (HE), toluidine blue stain, immunohistochemistry and immunofluorescence. The immunohistochemical analysis demonstrated that CD4-positive T cells preferentially infiltrated into the follicular infundibulum in the LPP lesions. Toluidine blue stain detected a large number of mast cells in the inflammatory lesions of LPP. Interestingly, immunohistochemical analysis demonstrated that the mast cells harboured IL-17A- and IL-23-producing activity and expressed the IL-23 receptor. The number of IL-17A-positive mast cells was significantly higher in the LPP lesions than in normal scalp. Moreover, the IL-17 receptor was expressed exclusively in the follicular epithelial cells in the LPP lesions. These results suggested that mast cells infiltrating hair follicles might play a role in the pathogenesis of LPP via the IL-23/IL-17 axis.     

Using biopsies to study the differences between two hair loss disorders: lichen planopilaris and frontal fibrosing alopecia

Lichen planopilaris (LPP) and frontal fibrosing alopecia (FFA) are two uncommon disorders that both cause permanent, scarring alopecia (hair loss) and inflammation of the hair follicles. LPP affects both sexes and typically causes patchy alopecia over the central scalp, whereas FFA generally affects women and causes the hairline at the front of the scalp to recede. It can also cause eyebrow and body hair loss. Despite these distinct phenotypes (physical characteristics), FFA has traditionally been regarded as a variant of LPP. The authors sought to distinguish the two conditions using a wide array of markers for different cell types around the hair follicles. Markers are substances in the body, such as certain proteins, which act as signs to show, for example, the presence of certain cells or inflammation. The authors took skin punch biopsies (a type of tissue sample) from affected areas of scalp in patients with a diagnosis of LPP or FFA, and from healthy controls (people without LPP or FFA). In this study, the authors present a detailed, systematic analysis of a range of key inflammatory cell markers in LPP, FFA and controls. There were many similarities in the numbers and type of inflammatory cells in the two conditions. The study focussed on the different types of cells called macrophages seen in LPP and FFA. Broadly, these cells can be divided into two types, M1 cells, associated with inflammation and cell death, and M2 cells, involved in tissue repair. The two conditions differed in that more markers for M2 cells were seen in LPP in comparison to FFA. The authors hope that therapies directed against specific macrophage cell types may be developed in the future, preventing irreversible hair loss. Linked Article:   Harries et al. Br J Dermatol 2020; 183 :537–547 .     

Severe diffuse non‐scarring hair loss in systemic lupus erythematosus – clinical and histopathological analysis of four cases

Background Although diffuse non‐scarring hair loss been found common in systemic lupus erythematosus (SLE), study that conduted on the severe type has been scarce. Objective This study aims to explore the dermoscopic and pathological features of severe diffuse hair loss in SLE. Method Data including clinico‐laboratory, dermoscopic and histopathological findings of four patients with SLE with severe diffuse hair loss were analysed retrospectively. Results All four patients were women aged 41, 39, 14 and 48 with complaints of hair loss involving 55%, 100%, 60% and 55% of their scalp respectively. Common clinical findings observed in the patients were sparse scalp hair with clusters of newly regrown hair. Scalp dermoscopy showed scaling, perifollicular telangiectasia, increased numbers of short vellus hairs, focal atrichia and decreased hair shaft pigmentation. Scalp tissue histopathology revealed typical changes of SLE such as epidermal atrophy with focal liquefaction, degeneration of the basement membrane zone, pigment incontinence, mild focal perivascular and perifollicular lymphocytic infiltrates and deposition of immunoglobulins at the dermal–epidermal junction. Treatment and improvement in SLE disease activity indices had a favourable impact on hair regrowth. Conclusion The severe type of hair loss in patient with SLE presents a unique set of clinical, dermoscopic and histopathological features.     

外伤性脂膜炎一例

患者女,48岁,因左下肢红斑结节伴痛3个月余就诊。患处10年前有撞伤史,遗留凹陷性瘢痕,3个月前无明显诱因出现红斑结节伴疼痛。既往有双下肢静脉曲张15年,左侧为著,未治疗,近年逐渐加重。否认糖尿病、高血压、冠心病、肾功能不全等病史……     

Dynamic ultrastructural changes of the connective tissue sheath of human hair follicles during hair cycle

Summary Ultrastructural changes of the connective tissue sheath (CTS), including the hyaline membrane, of human hair follicles during the hair cycle, were studied in normal scalp skin specimens. In early anagen, the CTS was composed of a thin basal lamina and surrounding collagen tissue. The collagen tissue gradually thickened during the development of the hair and hair follicle. In mature anagen hair follicles, the collagen tissue was separated into three layers. The inner collagen layer, just outside the basal lamina, was thin and composed of collagen fibres running longitudinally parallel to the hair axis. The middle collagen layer was very thick with its collagen fibres running transversely against the hair axis and surrounding the inner hair tissue. Many fibroblasts were present among the collagen fibres in the middle layer, whereas the inner layer contained almost none. In the outer collagen layer, collagen fibres ran in various directions parallel to the outer surface of the outer root sheath cells. In late anagen, the basal lamina became very thick. In catagen, the basal lamine and the inner collagen layer became corrugated and showed oedematous change and degeneration. Surrounding fibroblasts showed active production of new collagen fibres, which seemed to fill the spaces left by the retraction of the hair follicle and hyaline membrane. These ultrastructural changes of the CTS show that there may be dynamic metabolic changes of the connective tissue around human hair follicles during the hair cycle.     

梅毒性脱发合并HIV感染1例

  报告1例梅毒性脱发合并HIV感染。患者男,44岁,弥漫性斑状脱发伴白发增多11个月余。查体可见前额发际线“M型”上移,全头散在圆形、类圆形脱发斑,边界欠清,白发增多,拉发试验（-）,双手掌、足底红斑、鳞屑。头皮脱发斑处皮肤镜检查示：头皮无毛区内毛囊开口存在,毛干变细,少量黑点。实验室检查:TRUST定性（+）,TRUST定量（1: 128）,TPPA试验＞1:1 280,HIV抗体（+）。头皮脱发区病理组织活检示：真皮毛囊周围少量淋巴组织细胞,见休止期毛囊,周围纤维包绕,毛球部见浆细胞。诊断：梅毒性脱发合并HIV感染。经青霉素治疗5个月后,脱发斑消退,手足红斑、鳞屑消失,无再发脱发斑。