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【病例分析】面中部及周围无症状丘疹

2022-08-08 12:18:56

获奖名单

答案正确的获奖者:

Catherine萌、丫头、吴泳、Dr.Xj、Hautarzt Wong、yangli

附详细解析的获奖者:

rupa、康康、韩飞


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精彩解析

rupa:皮肤淋巴样增生,本例特点年轻女性,额部,鼻部,面颊中部多发性针帽至小米粒大小皮色丘疹,密集但不融合,感觉为实性较硬,类似粟丘疹样。A光泽苔癣,如果是光化性LN的话,发生在颜面曝光部位是可以的,皮损形态也比较符合,日照后也可以出现烧灼或瘙痒感,但到了冬季或数月数年后多数可以有自发性消退,但本例老皮损持续7年不消退,同一部位持续出现新皮疹有些反常。C大家都知道好发于眼周尤其是下眼睑,发病年龄和日晒后症状也相符,但皮损多为皮色,红色或淡褐色丘疹,表面有蜡样光泽,皮损体积也应该更大些,没有反复发生的现象。D皮损形态和发病部位都很符合,但皮损一般没有自觉症状,日晒后也不应有不适感,皮损体积更大,表面也比较光滑圆润些,也不会不断在同一部位反复发生。B皮肤淋巴样增生皮损可以这样表现,各年龄均可发生,常见发病部位,关键是发病过程比较符合,病理下这几个还是比较好鉴别的。


韩飞 :皮肤淋巴样增生。图片上看是多发性小丘疹,无明显炎症,有些闭口粉刺的感觉,当然肯定不是粉刺,粉刺不会一直持续存在;此外还能想到毛发上皮瘤,多发性有家族遗传史的,但这个皮疹大小和位置不符,该患者的皮疹大小太均一了,而且毛发上皮瘤的位置多集中在鼻唇沟,有簇集性,该患者皮疹的分布还是较均一的,不考虑;光泽苔藓的发病位置好发及躯干,面部一般不发生,且皮疹有光泽,排除;汗管瘤不考虑,虽说汗管瘤常见部位是脸上,但其好发眼睑,该患者面部皮疹倒是不少,但眼睑光光,可排除;皮肤淋巴样增生属于皮肤假性淋巴瘤,是病理描述,不是病名,就是做病名一般也要前面缀个T淋巴细胞或B淋巴细胞,病因不清楚,一般认为为反应性,这个病人显然不好解释,这种皮疹也不是常见的表现,但做题毕竟是做题,还是选B吧


康康:皮肤淋巴样增生,主要依据排除法。本例患者表现为多发的米粒大小皮色丘疹,无明显光泽,以面颊、额头为著,散在分布不融合。A光泽苔藓皮损为一致的针尖至粟粒大圆形或平顶丘疹,坚实光亮,好发于躯干和外生殖器等部位,可泛发,但面部极少见。皮损的特点和发病部位均与本例不符,排除。C面部多发的汗管瘤需要鉴别,因为它可以表现为肤色或红棕色小丘疹,散在不融合,表面可有蜡样光泽,但是本例患者皮损以面颊及额头为著,眼睑不明显,非眼睑型,若为发疹型则以前胸、腰腹、上肢好发,因此无论皮损分布及皮疹特点都不似典型的汗管瘤。故不考虑。D毛发上皮瘤面部损害特点是沿鼻唇沟对称分布的多发丘疹或小结节,肤色,部分融合。与本例分布特点不符,不考虑。最后说B皮肤淋巴样增生,又称皮肤淋巴细胞瘤,有局限型和播散型,后一型罕见,可表现为肤色或淡红色粟粒样丘疹。本人未曾见过,需病理最后确诊。




往期回顾

有奖病例问答第三季第3期

病史摘要:患者女性,24岁,面中部皮疹7年余,无明显自觉症状。在同一部位老皮疹持续存在而新皮疹成批出现。在日光曝露下局部有轻微的烧灼感或痒感。

可能的诊断:

A,光泽苔藓;

B,皮肤淋巴样增生;

C,汗管瘤;

D,毛发上皮瘤。

正确答案:B,皮肤淋巴样增生;(具体请看全文)



摘要


本文报道了1例24岁女大学生病例,面中部暴发多个痤疮样丘疹。


简介


面部丘疹性皮损,有时会给诊断带来一些挑战。本文报道了1例24岁女性患者的罕见病例,其面中部及周围暴发类似于寻常痤疮样的皮损。


病例报道


患者女性,24岁,在校大学生,于门诊处就诊。主诉面中部 (颧骨、鼻部、前额、下颌)多个小的、无症状、隆起性皮损7年余(图1)。患者称在同一部位老皮疹持续存在而新皮疹成批出现。在日光曝露下局部有轻微的烧灼感或痒感。无明显的口服、外用药物或感染史。早期确诊为寻常痤疮,并采用抗痤疮药物治疗,但未有任何改善。体格检查发现在颧骨区,鼻部、前额及下颌伴有多个坚实、圆顶状、肤色丘疹。皮损无压痛、鳞屑,大小在2~ 8 mm之间。表面无毛,未见毛细血管扩张。患者身体健康。所有血常规检查,包括全血细胞计数、肝功能检查、尿素、肌酐和胸片均在正常范围。临床需考虑与寻常痤疮、皮脂腺增生、痤疮型药疹、汗腺腺瘤、毛发上皮瘤、粟丘疹、丘疹性肉样瘤和颜面播散性粟粒性狼疮。组织病理学检查(HPE),丘疹性皮损活检显示,表皮层除局灶萎缩性淋巴滤泡形成,以及一个潜在的边界模糊grenz区外,无明显变化。在真皮上层和中层伴有结节性浸润,主要由淋巴细胞和混和性浆细胞和组织细胞组成。毛囊皮脂腺单位和附属结构未见明显变化。未见非典型细胞或肉芽肿(图2和图3)。免疫组织化学分析显示,在这些细胞中,超过90%的细胞对CD3(泛T细胞标记物)染色呈阳性(图4)。考虑以上特征,确诊为以T细胞为主的皮肤淋巴样增生(CLH)[表1]。给予患者中效局部皮质类固醇(糠酸莫米松)进行治疗,持续三周,大部分皮损消失(图5)。



Figure 1: Numerous papular lesions on erythematous base over central part of face

图1:面中部在红斑基础上的多个丘疹性皮损



Figure 2: Photomicrograph showing lymphoid follicles in the upper and mid dermis (H and E, ×40)

图2:显微照片显示在真皮上层和中层可见淋巴滤泡形成(H&E,×40)



Figure 3: Photomicrograph showing a dense lymphocytic infiltrate in the upper and mid dermis (H and E, ×100) (Arrows indicating focal atrophy of epidermis and lymphoid follicle)

图3:显微照片显示真皮上层和中层伴有致密的淋巴细胞浸润(H&E,×100)(箭头指示局灶萎缩性表皮和淋巴滤泡形成)



Figure 4: (a) Photomicrograph showing polymorphic infiltrate comprising mainly of lymphocytes, histiocytes, and plasma cells (H and E, ×400), (b) immunohistochemical staining demonstrates numerous CD3+ T‑cells in the dermis (×400)

图4:(a)显微照片显示主要由淋巴细胞、组织细胞和浆细胞组成的多态性浸润(H&E,×400),(b)免疫组织化学染色显示在真皮层可见多个CD3染色呈阳性的T细胞(×400)


Table 1: A differential diagnosis of the case

1:鉴别诊断




Figure 5: Central part of face after 3 weeks of treatment with topical steroid showing disappearance of lesions

图5:应用局部类固醇治疗3周后,面中部皮损消退


讨论


皮肤淋巴样增生(CLH)通常是一种良性的、反应性、真皮B-或T-淋巴细胞炎性疾病,其病因不明,类似于淋巴瘤。好发于成人,较少累及儿童和女性。于1894年首次描述。临床上CLH表现为孤立的、或罕见少量多发性结节,主要出现在面部或四肢。CLH主要是一种病理性疾病,而非临床疾病。


根据浸润的主要细胞类型,CLH可以是B细胞为主(螺旋菌皮肤淋巴细胞瘤,纹身诱导皮肤淋巴细胞瘤和带状疱疹后疤痕淋巴细胞瘤)或T细胞为主的(淋巴瘤样药物反应,淋巴瘤样接触性皮炎和持久性结节性节肢动物咬合反应)。其中可能涉及多种病因,包括寄生虫感染,(如莱姆病螺旋体和利什曼原虫)、病毒感染、创伤、药物、节肢动物叮咬、纹身、带状疱疹和疫苗接种。然而,大多数情况下,该疾病的病因仍然未知。临床上, T-细胞和B细胞CLH均可能表现为孤立的或多个坚实的、红色至紫罗兰色的丘疹或结节,表面无变化,主要出现在头部、颈部或上肢。一般患者没有任何系统性受累。本例患者的特殊之处在于,其面中部成群出现多个丘疹,并伴有中度红斑,这是CLH中非常罕见的临床表现。


组织病理学检查(HPE),通常CLH在其真皮浅层和深部伴有结节状或弥漫性多态性浸润,主要包括淋巴细胞、组织细胞,偶见浆细胞、树突状细胞和嗜酸性粒细胞。存在一个边界清晰的grenz带。在真皮深层,发现生长中心,通常由混合性BT细胞包围,。通过临床-病理相关性、组织化学研究可将CLH与皮肤淋巴瘤相鉴别,在某些病例中,还需进行基因重排研究。免疫组化研究可有助于进一步证实浸润多态性,其中包括CD3染色呈阳性的T淋巴细胞,CD20染色呈阳性的B淋巴细胞以及CD68染色呈阳性的组织细胞。在本例中,HPE以及浸润中超多90%的细胞对CD3染色呈阳性,证实其为T细胞为主的CLH


大多数病例在数周至数月内症状可自行缓解。初期应当考虑保守的治疗方法。可选择多种治疗方法,其中包括局部或病灶内注射类固醇、冷冻疗法、沙利度胺、干扰素α、激光和手术切除。文献记载中对于CD20染色阳性皮损,可以采用病灶内注射利妥昔单抗治疗。局部皮质类固醇仍然是治疗加重痤疮,CLH的主要药物。


当患者面中部长期出现多个顽固性小丘疹时,应考虑诊断为皮肤淋巴样增生。


下附英文原文

ABSTRACT

We report the case of a 24‑year‑old college girl, presenting with numerous acneiform papular eruptions over the central part of the face.


INTRODUCTION

Facial papular lesions sometimes pose a diagnostic challenge. We report an unusual case of central and pericentral facial popular lesions mimicking acne vulgaris in a 24‑year‑old female.


CASE REPORT

A 24‑year‑old college‑going female presented to the outpatient department with the complaint of numerous asymptomatic, small, raised lesions over the central part of the face (cheekbones, nose, forehead and chin) since 7–8 years [Figure 1]. She reported that while the old lesions persisted, new lesions appeared as crops over the same site. She perceived a mild burning sensation of the face upon going out in the sun and also complained of occasional, mild itching. There was no significant history of drug intake, topical application or infection. A provisional diagnosis of acne vulgaris had been made earlier and she had been treated with antiacne drugs without any improvement. Physical examination revealed multiple firm, dome shaped and skin colored papular lesions over malar region, nose, forehead and chin. The lesions were nontender, nonscaly and the size varied between 2 to 8 mm. The surface was hairless without telangiectasia. She was otherwise healthy. All routine blood investigations including complete blood count, liver function test, urea, creatinine and chest radiograph were within normal limits. The clinical differential diagnosis we considered were acne vulgaris, sebaceous hyperplasia, acneiform drug eruption, syringomas, trichoepitheliomas, milia, papular sarcoid and lupus miliaris disseminatus faciei. On histopathological examination (HPE), biopsy of a papular lesion revealed that epidermis was unremarkable except for focal atrophy over the lymphoid follicles, with an underlying ill defined grenz zone. Dermis showed nodular infiltration in the upper and mid dermis comprising mainly of lymphocytes admixed with plasma cells and histiocytes. Pilosebaceous units and adnexal structures were also unremarkable. No atypical cell or granuloma was evident [Figures 2 and 3]. Immunohistochemical analysis displayed more than 90% CD3 (Pan T‑Cell marker) positivity among the cells [Figure 4]. Considering all the above features we reached at a diagnosis of T‑Cell predominant cutaneous lymphoid hyperplasia (CLH) [Table 1]. We treated our patient with a mid potent topical corticosteroid (mometasone furoate) for three weeks and most of the lesions disappeared [Figure 5].


DISCUSSION

Cutaneous lymphoid hyperplasia (CLH) is usually a benign, reactive, dermal B‑or T-lymphocytic inflammatory response of unknown cause that may mimic lymphoma. It is commonly seen in adults and less often in children with a slight predilection for women. It was first described in 1894. CLH manifests clinically with isolated, or rarely few multiple nodules, mainly on the face and extremities. CLH is mainly a histopathological condition rather than a clinical entity.


Depending on the predominant cell type in the infiltrate, CLH may be B‑cell predominant (borrelial lymphocytoma cutis, tattoo‑induced lymphocytoma cutis and post‑zoster scar lymphocytoma) or T‑cell predominant (lymphomatoid drug reaction, lymphomatoid contact dermatitis and persistent nodular arthropod‑bite reactions). A variety of etiological factors may be involved, including parasitic infections such as Borrelia burgdorferi and Leishmania panamensis, viral infections, trauma, drugs, arthropod bites, tattoos, zoster and vaccinations. However, the cause of the disease most of the time remains obscure. Clinically, both T‑and B‑cell CLH may occur as isolated or multiple cutaneous firm, erythematous to violaceous papules or nodules without surface changes, mainly on head, neck, or upper extremities. Patients do not generally have any systemic involvement. The peculiarity in our case was that the patient presented with numerous papular lesions appearing in crops over the central part of the face with mild erythema, which was a very unusual presentation of CLH.


On HPE, CLH often reveals a superficial and deep dermal, nodular or diffuse polymorphic infiltrate comprising mainly of lymphocytes, and histiocytes and occasional plasma cells, dendritic cells and eosinophils. A clear grenz zone may be present. In deep dermis, well defined germinal centers, often surrounded by a mix of B and T cells may be seen with central large lymphoid cells with abundant cytoplasm. CLH needs to be distinguished from cutaneous lymphomas by clinico‑histopathological correlation, histochemical studies, and in some cases, gene re-arrangement studies. Immunohistochemical studies might be helpful further to demonstrate the polymorphic nature of infiltrate, including CD3‑positive T lymphocytes, CD20‑positive B lymphocytes and CD68‑positive histiocytes. In our case, suggestive HPE and >90% CD3+ cells in the infiltrate were indicative of T‑cell predominant CLH.


Most cases resolve spontaneously within a few weeks to months. A conservative approach should be considered initially. A variety of treatment options are available including topical or intralesional steroids, cryotherapy, thalidomide, interferon‑α, laser and surgical excision. In documented CD20+ lesions, intralesional rituximab may be tried. Topical corticosteroids, which aggravate acne, remain the mainstay of treatment of CLH.


Cutaneous lymphoid hyperplasia should always be suspected whenever a patient presents with numerous recalcitrant small papules over central part of the face for a considerable time period.


由MediCool医库软件冯飞飞 编译

原文来自:IndianDermatology Online Journal - May-June2015 - Volume 6 - Issue 3




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