获得的局限性色素沉着过度斑块和斑块有各种鉴别诊断,包括炎症后色素沉着和真菌病(MF)。白斑是一种罕见的皮肤病,其发病机理尚未完全阐明。据报道,白斑白斑发生在来自氢醌或急性皮肤移植物抗宿主病的过敏性接触性皮炎之后(1,2)。色素沉着MF是一种皮肤T细胞淋巴瘤,具有常见的CD8+表型(3)。在这里,我们报告了一例临床和组织学上类似于色素沉着MF的白斑白斑。一名55岁的日本妇女被转诊到我们的部门,以评估网状色素沉着和面部瘙痒性红斑。她使用市售的脱色化妆品试剂20年,使用含10%氢醌的软膏3个月。体格检查显示面部和颈部弥漫性色素沉着过度和标定的低色素斑(图1,a)。皮肤镜检查显示脱色斑点和网状加上点状色素沉着过度;它呈现假色素网络(图1,b)。从病变活检的组织样本的组织学检查显示真皮中伴随单个细胞或表皮中的小簇的浅表带状淋巴细胞浸润(图1,c)。在真皮中与黑色素细胞一起观察到界面变化。没有Melan-A阳性黑素细胞。免疫组织化学分析表明表皮性淋巴细胞为CD3+CD3-,它们以CD8+细胞为主(图1,d)。这些免疫组织化学结果模仿MF。然而,T细胞受体g基因重排的PCR分析为阴性。用对苯二酚(5%pet。)分为D2(+?)和D3(+)。停用化妆品试剂和氢醌10个月后,色素的变化显示出改善。白斑白斑的发病机制尚不清楚。尽管已经提出了由于过敏性或接触性皮炎引起的炎症后色素沉着以及氢醌使用的直接脱色作用(1),尚未检查T细胞的免疫表型。正如在我们的病人身上观察到的,与黑色素细胞的界面变化,除了常见的CD8+表型的表皮性和淋巴细胞的皮肤浸润,是色素沉着MF(3)的特征。此外,最小的CD7表达是MF的特异性发现(4)。我们患者的T细胞受体克隆性为阴性,但是在多达50%的早期MF患者中,通过PCR似乎可以检测到克隆性(3)。相比之下,我们病人的封闭斑贴试验氢醌呈阳性,据报道,CD8+T细胞被募集到过敏性接触性皮炎患者的表皮和真皮之间的间期(5)。CD8T细胞可能导致急性皮肤移植物抗宿主病样界面改变,并破坏白斑皮损中的黑素细胞。因此,在我们的患者中建议表现为白斑白斑的过敏性接触性皮炎。然而,需要进一步的报告和研究来支持这个问题。因此,我们认为有必要跟踪病人,因为MF没有被绝对淘汰。
Acquired circumscribed hyperpigmented patches and plaques have various differential diagnoses, including post-inflammatory
hyperpigmentation and mycosis fungoides (MF). Leukomelanoderma is an uncommon cutaneous condition in which the pathogenesis is not fully elucidated. It has been reported that leukomelanoderma occurs after allergic contact dermatitis from hydroquinone or acute cutaneous graft-versus-host disease (1,2). Hyperpigmented MF is a cutaneous T-cell lymphoma with a frequent CD8+ phenotype (3). Herein, we report a case of leukomelanoderma clinically and histologically resembling hyperpigmented MF. A 55-year-old Japanese woman was referred to our department for evaluation of reticulate pigmentation with pruritic erythema on the face. She had used commercially available depigmenting cosmetic reagents for 20 years and ointment containing 10% hydroquinone for 3 months. Physical examination revealed diffuse
hyperpigmentation and demarcated hypopigmented macules on the face and neck (Figure 1, a). Dermoscopy showed depigmented spots and reticulated plus dotted
hyperpigmentation; it presented a pseudo-pigment network (Figure 1, b). Histological examination of a tissue specimen biopsied from the lesion showed superficial band-like lymphocytic infiltration in dermis accompanying single cells or small clusters in epidermis (Figure 1, c). Interface changes were observed together with melanophages in the dermis. Melan-A-positive melanocytes were absent. Immunohistochemical analysis demonstrated that the epidermotropic lymphocytes were CD3+CD7-, and they had predominance of CD8+ cells (Figure 1, d). These immunohistochemical results mimicked MF. However, PCR analysis of the T-cell receptor g-gene rearrangement was negative. Closed patch test result with hydroquinone (5% pet.) was graded D2 (+?) and D3 (+). Ten months after discontinuing cosmetic reagents and hydroquinone, the pigmentary changes showed improvement. The pathomechanism of leukomelanoderma is unclear. Although post-inflammatory pigmentation due to allergic or contact dermatitis together with direct depigmenting effects from hydroquinone use has been suggested (1), the immunophenotype of T-cells has not been examined. As observed in our patient, interface changes with melanophages, in addition to frequent CD8+ phenotype of the epidermotropism and dermal infiltrate of lymphocytes, were characteristic for hyperpigmented MF (3). Moreover, minimal CD7 expression was a specific finding for MF (4). T-cell receptor clonality was negative in our patient, but the clonality appears to be detected by PCR in up to 50% of the patients with early MF (3). In contrast, the closed patch test was positive for hydroquinone in our patient, and it is reported that CD8+ T-cells are recruited to the interphase between the epidermis and the dermis of the patients with allergic contact dermatitis (5). CD8+ T-cells might contribute to acute cutaneous graft-versus-host disease-like interface changes and destroy melanocytes in the leukomelanoderma lesion. Allergic contact dermatitis presenting as leukomelanoderma was thus suggested in our patient. However, further reports and studies are required to support this issue. Therefore, we considered it necessary to follow the patient, since MF was not absolutely eliminated.