Sezer Engin, Özturk Durmaz Emel, Çetin Emel, Şahin Sedef
Engin Sezer, MD, Acıbadem University School of Medicine, Department of Dermatology, Buyukdere Caddesi No: 40, Istanbul, Turkey;
Acta Dermatovenerol Croat. 2016 Apr;24(1):81-2.
Meyerson phenomenon (MP) is characterized by a symmetrical area of erythema and scales encircling a central lesion, which is most commonly a banal melanocytic nevus. Herein, we describe an unusual case with MP representing an eczematized response to a melanoma in situ and review the literature covering this entity. A 56-year-old man presented with a 6-month history of a pruritic, pigmented lesion on the trunk. The patient had no other significant medical history and no notable family history of similar lesions. Physical examination revealed an irregular, hyperpigmented plaque, 1 cm in diameter, with a surrounding halo of erythematous, scaly areas on the right abdominal region (Figure 1, a). On dermatoscopical examination, an irregular, broadened pigment network, radial streaming, and a focal blue-white veil, encircled by a homogenous, erythematous zone was observed (Figure 1, b). Based on clinical and dermatoscopical findings, a presumptive diagnosis of MP occurring on an early melanoma was made and the lesion was excised with a 5 mm safety margin. Histopathological examination of the excised material revealed a central intraepidermal atypical, confluent melanocytic proliferation with angular, hyperkeratotic, and irregular nuclei and a prominent fixation artifact around the cells (Figure 1, c). Human melanoma black (HMB-45) immunostaining highlighted the confluence of the neoplastic melanocytic proliferation. Lymphohistiocytic infiltration with melanophages was also identified in the upper dermis. An interesting feature was the presence of subacute spongiotic dermatitis around the melanocytic lesions (i.e. parakeratosis, serum/crusting, spongiosis, lymphocyte exocytosis, and acanthosis). Immunohistochemical staining with the Langerhans cell marker, CD1a, revealed an increased cell population in the perilesional, erythematous halo (Figure 1, d). A diagnosis of MP existing on melanoma in situ was established with clinical and histopathological findings. No recurrence of the eczematized components or melanocytic lesions was identified despite 1-year follow-up. Also called halo dermatitis and halo eczema, MP presents as an eczematized, perilesional plaque around various lesions, mainly of banal melanocytic nevi (1). Occurrence of halo dermatitis around a melanocytic nevus was first described by Meyerson in 1971. Other cutaneous disorders with MP include those of dysplastic nevus, melanoma, seborrheic keratosis, stucco keratosis, nevus sebaceous, dermatofibroma, vascular malformations, nevus flammeus, molluscum contagiosum, basal cell carcinoma, squamous cell carcinoma, and keloid formation (2-7). History of atopy and atopic dermatitis is observed in a subset of patients, which was absent in our case. Rarely, patients with Behçet's disease, severe sunburn, and cessation of interferon therapy have also been associated with this entity. MP is described to be more frequent in young males and has a tendency to occur in summer. As far as we are aware, there are only two cases of melanoma with features of MP in the literature. Rodin et al. presented a case report showing features of MP around a melanoma in situ arising on a dysplastic nevus (8). By way of comparison, a pre-existing precursor dysplastic nevus was not identified in our case. Dermatoscopic features including scar-like depigmentation and negative pigment network also differed from our case which featured a broadened pigment network, radial streaming, and blue-white veil. The other case report was of a 50-year-old man, presenting with an atypical melanocytic lesion several years in duration showing an erythematous halo (9). Histopathological examination was consistent with a Clark level 2 superficial spreading melanoma, which was cured with excision with no recurrence despite long-term follow-up. As far as we are aware, our case report is the first to describe de novo melanoma in situ without dermal invasion or a precursor dysplastic nevus. The etiopathology of MP is unclear; however it is considered to be immune-mediated. Up-regulation of intercellular adhesion molecule-1 on keratinocytes and dermal endothelial cell surfaces has been shown, suggesting the involvement of adhesion molecules in pathogenesis (10). We hypothesize that increased Langerhans cell population, as observed in our case, results in a delayed immune response reminiscent of an eczematous process in MP. Excision of the central lesion has been reported to precipitate the resolution of dermatitis, as in our case, in which recurrence of the erythematous, scaly eruption was not observed after removal of the central lesion despite a 1-year follow-up period. Some authors recommend pre-treatment of the lesion with topical corticosteroids to suppress the eczematous process in the adjacent skin. Coexistence of MP around a melanocytic nevus (Meyerson nevus) with halo nevus and progression of Meyerson nevus to halo nevus has also been reported. We suggest that melanoma may occur as a component of MP, and careful dermatoscopic examination is essential to differentiate between pigmented lesions with a perilesional erythematous halo.
迈耶森现象(MP)的特征是围绕中心病变出现对称的红斑和鳞屑区域,该中心病变最常见的是普通黑素细胞痣。在此,我们描述了一例不寻常的MP病例,其表现为对原位黑素瘤的湿疹样反应,并回顾了关于该实体的文献。一名56岁男性,躯干出现瘙痒性色素沉着病变6个月。患者无其他重大病史,家族中无类似病变的显著病史。体格检查发现右腹部有一个直径1cm的不规则色素沉着斑,周围有红斑、鳞屑区域形成的晕环(图1a)。皮肤镜检查观察到不规则、增宽的色素网、放射状流注以及局灶性蓝白色面纱,周围有均匀的红斑区域(图1b)。基于临床和皮肤镜检查结果,初步诊断为早期黑素瘤上发生的MP,并以5mm安全切缘切除病变。切除组织的组织病理学检查显示中央表皮内非典型、融合的黑素细胞增生,细胞核呈角形、角化过度且不规则,细胞周围有明显的固定假象(图1c)。人黑素瘤黑色(HMB - 45)免疫染色突出了肿瘤性黑素细胞增生的融合。真皮上层也发现有含黑素巨噬细胞的淋巴细胞组织细胞浸润。一个有趣的特征是黑素细胞病变周围存在亚急性海绵状皮炎(即角化不全、血清/结痂、海绵形成、淋巴细胞外渗和棘层肥厚)。用朗格汉斯细胞标志物CD1a进行免疫组织化学染色显示,病变周围红斑晕环中的细胞数量增加(图1d)。根据临床和组织病理学检查结果,确诊为原位黑素瘤上存在MP。尽管随访1年,但未发现湿疹样成分或黑素细胞病变复发。MP也被称为晕皮炎和晕湿疹,表现为围绕各种病变的湿疹样、病变周围斑块,主要是普通黑素细胞痣(1)。1971年迈耶森首次描述了黑素细胞痣周围出现晕皮炎。其他伴有MP的皮肤疾病包括发育异常痣、黑素瘤、脂溢性角化病、点状角化病、皮脂腺痣、皮肤纤维瘤、血管畸形、鲜红斑痣、传染性软疣、基底细胞癌、鳞状细胞癌和瘢痕疙瘩形成(2 - 7)。部分患者有特应性病史和特应性皮炎,本病例中未出现。罕见情况下,白塞病、严重晒伤和干扰素治疗停止的患者也与该实体有关。据描述,MP在年轻男性中更常见,且有在夏季发生的倾向。据我们所知,文献中仅有两例具有MP特征的黑素瘤病例。罗丁等人发表了一份病例报告,显示发育异常痣上原位黑素瘤周围出现MP特征(8)。相比之下,我们的病例中未发现先前存在的发育异常痣前驱病变。皮肤镜特征包括瘢痕样色素脱失和阴性色素网也与我们的病例不同,我们的病例特征为增宽的色素网、放射状流注和蓝白色面纱。另一例病例报告是一名50岁男性,有一个持续数年的非典型黑素细胞病变,表现为红斑晕环(9)。组织病理学检查与克拉克2级浅表扩散性黑素瘤一致,经切除治愈,长期随访无复发。据我们所知,我们的病例报告是首例描述无真皮浸润或发育异常痣前驱病变的新发原位黑素瘤。MP的病因病理尚不清楚;然而,它被认为是免疫介导的。已显示角质形成细胞和真皮内皮细胞表面的细胞间黏附分子 - 1上调,提示黏附分子参与发病机制(10)。我们推测,如我们病例中观察到的朗格汉斯细胞数量增加,导致免疫反应延迟,类似于MP中的湿疹样过程。据报道,切除中心病变可促使皮炎消退,如我们的病例,切除中心病变后,尽管随访1年,但未观察到红斑、鳞屑性皮疹复发。一些作者建议用外用糖皮质激素预处理病变,以抑制相邻皮肤的湿疹样过程。也有报道黑素细胞痣周围的MP(迈耶森痣)与晕痣共存以及迈耶森痣进展为晕痣。我们认为黑素瘤可能是MP的一个组成部分,仔细的皮肤镜检查对于鉴别有病变周围红斑晕环的色素性病变至关重要。