31例晕痣的临床分析及光电镜观察

本文对31例晕痣的临床资料进行了分析,并作了7例光镜和4例电镜观察.结果表明:31例晕痣患者中伴发白癜风14例(45.1%).晕痣痣细胞周围有密集的淋巴细胞浸润.痣细胞有受损,最后则消失.晕痣的皮肤内郎格罕细胞增多.晕部表皮中黑素细胞消失.结果提示:晕痣的组织学特征符合免疫学改变.此外,本文实验还观察到晕痣组织中一种较为特殊的细胞,推测可能是郎格罕细胞在皮肤内行有丝分裂.     

Fibrosis in regressing melanoma versus nonfibrosis in halo nevus upon melanocyte disappearance: Could it be related to a different cytokine microenvironment?

BACKGROUND: It is not clear why melanocyte disappearance occurs without fibrotic evolution in halo nevus and with fibrotic evolution in regressing melanoma. METHODS: Six halo nevi, seven regressing primary melanomas, and seven primary melanoma (PM) without regression were studied using immunohistochemistry for the phenotype of inflammatory infiltrate and the expression of cytokines involved in fibrogenesis or macrophage regulation. Melanocytes were also evaluated using electron microscopy. RESULTS: CD8(+) lymphocytes predominated in halo nevus, whereas CD4(+) lymphocytes prevailed in melanoma; a few macrophages were only found in melanoma. Fibrogenic cytokines, IL-6, platelet-derived growth factor, and transforming growth factor-beta were only expressed in melanoma, whereas basic fibroblastic growth factor was also expressed in halo nevus. Antifibrotic cytokine tumor necrosis factor (TNF)-alpha was expressed at a higher degree in halo nevus. Cytokines involved in macrophage regulation were only expressed in melanoma. CONCLUSIONS: Fibrogenic cytokines were more frequently expressed in melanoma than in halo nevus, irrespective of regression. At ultrastructural level, melanocytes showed a more activated status in regressing melanoma than in halo nevus, in compliance with a milieu richer in cytokines. Although the cytokine microenvironment does not completely justify the fibrotic evolution in regressing PM, the higher TNF-alpha expression in halo nevus suggests a possible role in nonfibrotic evolution of this lesion.     

Delineation of nevus cell nests in inflammatory infiltrates by immunohistochemical staining for the presence of S100 protein

Fifteen halo nevi were stained for the presence of S100 protein by an unlabelled antibody peroxidase-antiperoxidase method. S100 protein was clearly identifiable within nevus cell nests in the inflammatory infiltrate. The presence of this substance helped to identify nevus cells in dense inflammatory infiltrates and confirm the histologic diagnosis of halo nevus.     

Unusual halo nevi--darkening rather than lightening of the central nevus.

Although the classic halo nevus is a brown nevus with a surrounding rim of depigmentation, i.e. a stage I halo nevus, these nevi can have several clinical stages. The central nevus may lose its pigmentation and appear pink with a surrounding halo (stage II), the central papule may disappear leading to a circular area of depigmentation (stage III) or the depigmented area may repigment (stage IV), leaving no trace of its prior existence. Herein we describe an unusual phenomenon--darkening of the central nevus rather than lightening--following the appearance of the halo phenomenon. An 18-year-old boy who had multiple atypical nevi developed multiple halo nevi beginning at the age of 12 years. Following the appearance of the peripheral halos, 2 of his nevi that were originally solid medium brown in color darkened and the hyperpigmentation had a reticulated pattern with perifollicular sparing. One possible explanation is a postinflammatory hyperpigmentation induced by the infiltrating lymphocytes.     

Development of Halo Nevus Around Nevus Spilus as a Central Nevus,and the Concurrent Vitiligo

Halo nevus is a benign melanocytic nevus that is surrounded by a hypopigmented zone. The most frequent association with halo nevus is vitiligo, and this also appears in nearby regions, as well as at other remote sites. Although the mechanism for developing the depigmentation around nevus spilus is uncertain an immunologic process may be responsible for the finding of inflammatory infiltrates of the upper dermis in the depigmented lesions. We report here on a 13-year-old boy who showed a depigmented zone around a nevus spilus on the right side of his neck with simultaneous vitiligo lesions on the face.     

Periocular vitiligo with onset around a congenital divided nevus of the eyelid

Leukoderma in association with congenital melanocytic nevi is a rare phenomenon; nevertheless several reports have been published in the literature. We present a 15-year-old boy born with a pigmented lesion on the lower and upper eyelid diagnosed as a congenital divided nevus of the eyelid. At the age of 13, he developed a depigmented area around the nevus and was diagnosed at first as having a halo nevus in a congenital nevus. Over the next two years, an area of depigmentation appeared around the contralateral eye. At the present time, the patient has bilateral periocular depigmentation. Congenital divided nevus of the eyelid is a rare lesion, and no reports have been published to date of depigmentation in association with this lesion. Our patient presented with depigmentation around the nevus as in a halo nevus phenomenon, although at the present time, the depigmented area has a symmetric periocular distribution, and therefore can be labeled as periocular vitiligo associated with a congenital divided nevus.     

Characterization of the mononuclear infiltrate involved in regression of halo nevi

Halo nevi are characterized by progressive degeneration of nevus cells surrounded by a mononuclear cell infiltrate. We studied the morphological features of the nevus cells and the composition of the mononuclear cell infiltrate in 15 cases of halo nevi using immunohistochemical techniques and a battery of antibodies to different subsets of lymphocytes and histiocytes. Regression could be divided into four more or less identifiable stages, associated with different subsets of lymphocytes and monocyte-macrophage lineage cells. Stage I (preregression): nests of unremarkable nevus cells were surrounded by a moderate number of T lymphocytes (relatively small percentage of helper/inducer T cells), occasional B cells and macrophages. Stage II (early regression): large number of T lymphocytes and FXIIIa-positive cells were in close contact with nevus cell clusters which showed ragged edges. Lysozymepositive cells and epidermal Langerhans cells were mildly increased. Stage III (late regression): single nevomelanocytes showing mild atypia were present. Numerous T lymphocytes and macrophages positive for lysozyme, KP1 and/or FXIIIa were interspersed between the nevus cells. Increased numbers of epidermal Langerhans cells were present. Stage IV (complete regression): no nevus cells were observed and moderate numbers of T lymphocytes only remained. These results suggest that T cells, especially T-suppressor cells, and different subsets of macrophages participate in the regression of the nevi.     

Langerhans cells in various benign and malignant pigment-cell lesions of the skin

Summary We used immunohistochemistry to study Langerhans cells (LCs) and the composition of the dermal inflammatory infiltrate both in normal skin and in biopsies from various benign and malignant pigment-cell lesions. In normal skin and most benign pigment-cell lesions, epidermal LCs are regularly distributed. OKT₆-Positive cells outnumber the OKIa-positive cells. The inconspicuous dermal infiltrate studied in these biopsies was composed of helper and suppressor/cytotoxic T cells and some dermal LCs. More epidermal LCs with an abnormal cytologic presentation were found in a halo naevus and in the radial growth part of primary malignant melanomas. This finding was associated with a dermal infiltrate composed of suppressor/cytotoxic T cells, suggesting a defense mechanism of the host towards abnormal melanocytes. Epidermal LCs were rare in the central part of the biopsies which showed a primary malignant melanoma in its vertical growth. A dermal inflammatory infiltrate was absent in that area. These findings are interpreted as the morphologic expression of a damaged immune system.F. Facchetti is on leave from Istituto di Anatomia Patologica, Spedali Civili di Brescia, Brescia, Italy     

A case of halo nevus with effete melanocytes.

Epidermal melanocytes in the depigmenting lesion were examined in one typical case of halo nevus. Vacuolated melanocytes found in the upper layers of epidermis were not, as observed in serial sections, connected to the basal lamina. These melanocytes contained individual as well as aggregated melanosomes in what appeared to be autophagosomes. Part of the cytoplasm of these melanocytes appeared condensed and segregated and their nuclei were often pyknotic. These melanocytes were considered to be degenerated cells which had been detached from the basal layer and were being shed from the skin. Although epidermal keratinocytes, particularly basal cells, were also vacolated. Langerhans cells and non-specific dendritic cells were more or less intact. The total number of these dendritic cells seemed to be increased.     

Plasma cell infiltrate in common acquired melanocytic nevus

The presence of plasma cells in melanocytic lesions has been considered in literature as a sign of concern, when evaluated in the appropriate context. Plasma cells have been evaluated in halo nevus, but they are not frequently reported in non-halo common acquired nevus. Our claim was to study how common and frequent plasma cells are in the latter type of nevi. Therefore, we examined 280 of these nevi and selected the cases with an inflammatory infiltrate, even if mild. We then looked for plasma cells in the inflammatory infiltrate in the hematoxylin-eosin routine sections and selected 17 cases in which plasma cells (even if only occasional) could be found in the hematoxylin-eosin staining. Out of these 17, plasma cells were easily found in four cases, which were then further studied with immunohistochemistry for epithelial membrane antigen. The percentage of plasma cells varied in these four cases from 0.5% to 7%. No relation between the amount of plasma cells and either the location of the nevus or the location of the inflammatory infiltrate could be established. We conclude that the main point of this study is not to trust the presence of plasma cells as a solid criterion on its own, when evaluating a melanocytic lesion.     

晕痣的免疫组化特点与自发性消退机制的研究

目的 研究晕痣自发性消退早期及晚期皮损区炎细胞表型、数目及其分布特点，探讨晕痣自发性消退的免疫机制。方法 应用免疫组化方法对晕痣皮损区、非皮损区及正常对照皮肤进行CD3、CD4、CD8、CD20、CD1a、CD56、CD68染色，用计算机图像分析系统（Image-pro PLUS 6.0）观察及定量分析。结果 晕痣早期及晚期皮损区CD4、CD8、CD20、CD1a阳性细胞数均明显高于非皮损区及正常对照皮肤（P ＜ 0.01），皮损区CD1a、CD68阳性细胞直径明显大于非皮损区及正常对照皮肤（P ＜ 0.01）。消退晚期CD8 与CD4阳性细胞数目比值（2.05 ∶ 1）高于消退早期（1.82 ∶ 1），CD8阳性细胞在痣细胞巢内大量浸润。结论 CD4、CD8、CD20、CD1a、CD56、CD68阳性细胞均参与晕痣自发性消退，CD8阳性T细胞在晕痣消退中起主要作用。     

Behavior of pigment cells on lesions of the pigmented venus with vitiligo.

When vitiligo occurred on lesions of the pigmented nevus, the behavior of pigment cells in this nevus was investigated. Three cases of giant hairy nevi, seven cases of moles, three cases of Mongolian spots and eleven specimens in nine cases of halo nevi were used. Giant hairy nevi combining with vitiligo showed intensive decreases in nevus cells, particularly superficial A and B-type nevus cells. The epidermal dopa-positive melanocytes and melanin granules in the epidermis decreased, but still remained. On the other hand, moles in vitiligo showed an almost complete disappearance of epidermal dopa-positive melanocytes and melanin granules in the epidermis; nevus cells in the dermis decreased only slightly. Mongolian spots with vitiligo showed an epidermis similar to vitiligo, but the dermal melanocytes were hardly changed. Halo nevi exhibited an intensive decrease and degeneration of nevus cells and marked lymphocytic infiltration. Some of them showed disappearance of epidermal dopa-positive melanocytes and melanin granules in the epidermis. The characteristic findings of vitiliginous skin are mostly restricted to epidermis. In contrast, however, it is interesting to note that, on the lesions of nevocellular nevi with vitiligo, the dermis also exhibited some decrease and degeneration of nevus cells and lymphocytic infiltration.     

A case of extramammary Paget's disease with depigmented macules as the sole manifestation

Summary We report a 76-year-old man who had four depigmented macules in the genital area as the sole manifestation of extramammary Paget's disease (EMP). Histologically, many scattered, dissociated, plump Paget cells, and small intraepidermal nests of these cells were seen in all four lesions. The distribution of Paget cells extended beyond the margin of the depigmented areas into adjacent normally pigmented skin. Fontana–Masson staining revealed a reduction in, or absence of, melanin deposition along the basal layer of the depigmented lesions, in contrast with an abundance of melanin along the basal layer of the adjacent normal skin. Pigment-blockade melanocytes and melanophages were seen within or below the affected epidermis. The depigmentation in this case could have been caused by a symbiotic disorder between melanocytes and keratinocytes (including melanocyte destruction), and by a disorder in melanosome transmission to the keratinocytes. This case illustrates that a depigmented macule may be a diagnostic feature of EMP. Moreover, depigmentation is probably one of the earliest clinical features of EMP, and not a neighbouring secondary change such as occurs in the Sutton's halo naevus phenomenon.     

Depletion and repopulation of Langerhans cells in nonsegmental type vitiligo

The role of Langerhans cells in the pathogenesis of nonsegmental type vitiligo is still unknown. In this study, biopsies were taken from 26 patients at various stages of nonsegmental type vitiligo and morphometrically observed to investigate the kinetics of Langerhans cells in patients at various stages of the disease. A marked depletion of OKT6-positive and ATPase-positive epidermal dendritic cells was noted in patients with active nonsegmental type vitiligo. A repopulation of both OKT6-positive and ATPase-positive epidermal dendritic cells was noted in patients with stable nonsegmental type vitiligo. Profound depletion of epidermal OKT6-positive and ATPase-positive dendritic cells was noted in patients with repigmenting nonsegmental type vitiligo receiving treatments involving topical use of 0.05% Fluocinonide cream or PUVA photochemotherapy. Transmission electron microscopy confirmed the absence of epidermal dendritic cells (Langerhans cells and intermediate cells) in patients with active and repigmenting nonsegmental type vitiligo. In active nonsegmental type vitiligo, two possible explanations are proposed for the depletion of OKT6-positive and ATPase-positive epidermal dendritic cells (presumptive Langerhans cells): 1) the cells are destroyed by cytotoxic factors released during the course of destruction of melanocytes in active vitiligo, and/or 2) they leave the epidermis and migrate to regional lymph nodes to present certain antigens which are released from certain destroyed epidermal cells (keratinocytes or melanocytes) during the course of active vitiligo. The repopulated epidermal Langerhans cells may result from phenotypically transformed dermal dendritic cells in the depigmented lesions of patients with stable vitiligo. Since various therapies which result in repigmentation deplete the density of epidermal Langerhans cells markedly, it is suggested that depletion of epidermal Langerhans cells in stable vitiligo may aid in repigmentation. It is also proposed that the repopulated epidermal Langerhans cells may play a role in inhibiting the proliferation of epidermal melanocytes in depigmented lesions of stable vitiligo, thus various methods of treatment which deplete the Langerhans cells may eventually aid in the repigmentation of nonsegmental type vitiligo.     

Architectural features in melanocytic lesions with cellular atypia

According to the quantity of single atypical melanocytes at the dermoepidermal junction 334 nevi were assigned to 3 groups: (1) with pronounced nuclear and cellular atypia (n = 73); (2) with moderate atypia (n = 127), and (3) without atypical melanocytes (n = 134). Three architectural features were almost exclusively observed in groups 1 and 2 with cellular and nuclear atypia: atypical localization of melanocytes in the epidermis, irregular distribution of melanocytes in the junctional zone and atypical nests of melanocytes. A combination of 2 or 3 of these features was seen in 76% of the nevi with pronounced cellular and nuclear atypia, in 28% of those with moderate atypia and in none of those without atypical melanocytes. Regarding 4 other criteria only minor but still statistically significant differences were found between the 3 groups of nevi. We conclude that these 4 other criteria, i.e. inflammatory infiltrate, lamellar and/or concentric fibroplasia, persisting lentiginous hyperplasia and dust-like pigment in melanocytes and nevus cells are not helpful for the diagnosis of a dysplastic nevus because of their low specificity. Minimal requirements for the diagnosis of a dysplastic nevus are suggested.     

几种色素减退性皮肤病的共聚焦激光扫描显微镜图像特点

目的 观察白癜风、无色素痣、进行性斑状色素减少症、贫血痣的活体共聚焦激光扫描显微镜（CLSM）特征。方法 用CLSM观察同一层面（基底层真表皮交界处）皮损处、交界处及白斑周边正常皮肤的镜下特征。结果 进展期白癜风白斑区部分区域色素完全缺失,部分区域可见残存色素环,残存之色素环结构欠完整且色素含量降低;交界处界限模糊;白斑周边正常皮肤可见部分色素环失去完整性。稳定期白癜风白斑处色素完全消失;交界处界限清晰;白斑周边正常皮肤色素环完整,折光明亮;恢复期可见到树突状、折光明亮的黑素细胞。无色素痣和进行性斑状色素减少症的CLSM表现相似：白斑处色素环结构完整,色素含量降低,折光减弱。贫血痣白斑处色素环结构和色素含量与周边正常皮肤无明显差异。结论 结合临床表现,CLSM可以作为鉴别诊断白癜风、无色素痣、进行性斑状色素减少症、贫血痣的一种辅助方法。     

Clinical and histopathologic characteristics of trichrome vitiligo

BACKGROUND: The term trichrome vitiligo describes lesions that have a tan zone of varying width between normal and totally depigmented skin, which exhibits an intermediate hue. However, the pathogenesis and the histopathologic characteristics of trichrome vitiligo are unknown. OBJECTIVE: Our purpose was to investigate the clinical and histopathologic characteristics and the pathogenesis of trichrome vitiligo. METHODS: Four punch biopsy specimens were taken from 21 patients with trichrome vitiligo; they were from vitiliginous skin, light brown skin, perilesional normal skin, and normal skin as far as 5 cm from the nearest vitiligo spot. The sections were stained with hematoxylin-eosin; in selected cases, we performed immunohistochemical staining with S-100 protein and CD1a. RESULTS: Trichrome vitiligo occurred most frequently on the trunk in active vitiligo vulgaris. Focal vacuolar degeneration of the basal cell layer and mild inflammatory cell infiltration of the epidermis and dermis were more prominent in light brown skin and perilesional normal skin than in vitiliginous skin and normal skin. The number of melanocytes was decreased in light brown skin compared with perilesional normal skin (P <.05) and in vitiliginous skin compared with light brown skin (P <.05); a few melanocytes were observed even in skin affected by trichrome vitiligo. The number of Langerhans cells was increased in the epidermis of light brown skin and perilesional normal skin compared with vitiliginous and normal skin (P <.05). PUVA therapy yielded excellent repigmentation. CONCLUSION: Trichrome vitiligo is a variant of active vitiligo. The changes of melanocytes, keratinocytes, and Langerhans cells may be involved in the pathogenesis of depigmentation in trichrome vitiligo.     

Targetoid hemosiderotic nevus. A trauma-induced simulator of malignant melanoma

BACKGROUND: Simulators of malignant melanoma comprise a heterogenous group of melanocytic and nonmelanocytic lesions of the skin. Among frequent clinical mimickers of melanoma are injured melanocytic nevi. Any change in the clinical appearance of a pre-existing nevus should alert the clinician to exclude the possibility of malignant transformation in order to early identify a lesion at a stage when complete cure can still be achieved. OBJECTIVE: The purpose of this study was to present the clinical, dermoscopic and histopathologic findings of a series of acquired melanocytic nevi which abruptly developed a pigmented peripheral halo, presumably following minor trauma. METHODS: A series of 6 cases of acquired melanocytic nevi which suddenly developed a targetoid halo were included in the study. All lesions were evaluated by dermoscopy. Three cases were surgically removed at different stages of evolution and submitted to histopathologic examination. In all cases, follow-up was obtained. RESULTS: All the lesions arose on trauma-prone skin sites of young women. The sudden development of an asymptomatic, targetoid halo on a long-lasting, acquired exophytic nevus was the main presentation. Whereas the central nevus persisted, the ecchymotic halo ultimately disappeared. Histopathologic examination disclosed changes of the traumatized nevus in the central part, whereas the ring showed hemorrhage and hemosiderin deposits. Increased numbers of small vessels with hobnail characteristics were associated features. CONCLUSIONS: Targetoid hemosiderotic nevus is a distinctive clinicopathologic variant of traumatized acquired melanocytic nevus which should be included in the list of clinical simulators of melanoma.     

Acquired patch-type blue nevus with overlying vitiligo: a case report

Background Blue nevi are a group of congenital and acquired dermal melanocytoses characterized by a blue‐gray appearance on the skin. The common blue nevus and cellular blue nevus are the most common subtypes. Patch‐type blue nevus is rather rare. Observations We describe a 77‐year‐old Chinese male with a 6 × 8‐cm non‐palpable blue patch overlaid by a depigmented patch on the back of the left scalp. Histological examination of the blue‐gray patch showed numerous spindled and elongated bipolar dendritic melanocytes in the upper reticular dermis and an absence of epidermal melanocytes. Immunohistochemically, these dendritic melanocytes were positive for S‐100 and HMB‐45. A diagnosis of a patch‐type blue nevus with overlying vitiligo was made after the biopsy. Conclusions The patient presents an unusual manifestation of patch‐type blue nevi with overlying vitiligo. To the best of our knowledge, these features have not been previously described.