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The recognition of follicular mucinosis as a distinct entity is accorded to Pinkus in a 1957 paper under the title Alopecia mucinosa. A primary and a secondary form is recognised. Recently secondary follicular mucinosis was observed in our laboratory in association with an intradermal and a compound melanocytic nevus. To my knowledge this association has not been reported previously.
BACKGROUND: The relationship of adhesion molecules in the dermis to immunologically mediated cutaneous inflammation can be understood by focusing on a serendipitous phenomenon: a lack of dermatitis within the margins of a nevus anemicus (NA) in generalized contact dermatitis. The expression and induction of endothelial and epithelial adhesion molecules with intradermally injected cytokines were investigated. OBSERVATIONS: Nevus anemicus without dermatitis lacked histopathological changes consistent with inflammatory cellular infiltration. The surrounding skin of the dermatitic lesion expressed HLA-DR, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1, and E-selectin on endothelial cells, and HLA-DR and ICAM-1 in the epidermis. However, the skin of the NA lacked endothelial E-selectin and epidermal HLA-DR and ICAM-1 expression. Interferon gamma, injected intradermally, induced endothelial and epidermal HLA-DR and ICAM-1 expression in the NA and surrounding normal skin. While interferon gamma strongly induced E-selectin expression on endothelial cells in normal skin, it failed to induce endothelial E-selectin expression in the NA. CONCLUSIONS: This study suggests that vessels in the NA do not respond normally to proinflammatory cytokines, at least at the level of E-selectin expression. The absence of keratinocyte ICAM-1 and HLA-DR expression in the NA lesion in contact dermatitis is likely caused by the absence of infiltrating lymphocytes, rather than by the intrinsic unresponsiveness of keratinocytes to interferon gamma. Among the endothelial cell adhesion molecules in delayed hypersensitivity, E-selectin appears to be indispensable in recruiting circulating T lymphocytes to the skin.
OBJECTIVE: To present the clinical experience during an 18-year period of a series of 11 cases of pigmented nevus of the external auditory canal (EAC). STUDY DESIGN AND SETTING: Retrospective medical review of 11 consecutive patients with lesions seen in 2 departments of otolaryngology in Taiwan. RESULTS: 12 pigmented nevi, 2 to 12 mm (average, 6.4 mm) in diameter, were excised under otomicroscopy, and the EAC was packed with a temporary Penrose stent. One large lesion developed a postobstructive external auditory canal cholesteatoma (EACC). Histopathologic examination revealed 11 intradermal nevi and 1 compound nevus. There have been no recurrences or stenoses of EACs after 3 months to 17 years (average, 6 years) of follow-up. CONCLUSION: If a pigmented nevus causes symptoms, especially when it is large enough to obstruct the lumen of the EAC and has the possibility of developing into an EACC, it should be excised. EBM RATING: C-4.
Antimelanosome-associated monoclonal antibody has recognized the common antigenic determinant of melanosomes and cell surface of pigment cells, and it is suggested that melanosomes play a significant role as an antigen in progressive depigmentary disorders, in which melanocytes are selectively altered and disappear presumably by auto-antibodies in vivo. Mouse myeloma cells were fused with spleen cells from BALB/c mice immunized with a melanosomal fraction separated from human melanotic melanoma cells (Mm-1-JCK). The monoclonal antibody (MoAb) A4F11 has been found to react with premelanosomes, melanosomes, and probably with Golgi-associated endoplasmic reticulum lysosomes, but not with mitochondria, nuclei, and cytosol from human melanoma cells, by immunoelectron microscopy using the saponin permeation method, which was carried out together with indirect radioimmunoassay and quantitative absorption assay. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting using melanosome preparations have revealed the antigen(s) reactive with the MoAb A4F11 in 3 bands corresponding to Mr 50,000, 18,000, and 17,000. Cell binding assay has shown the reactivity of the MoAb A4F11 with the cell surface of human normal melanocytes and melanoma cells, but not with other mammalian melanoma cells or with human nonpigment cells examined. Indirect immunofluorescence on cultured cells and frozen sections has revealed distinct granular reactivity not only with human melanotic melanoma, but also with junctional and intradermal nevi, cultured malignant blue nevus cells, as well as normal melanocytes. The above evidence has indicated the presence of an antigenic determinant common to the intracellular melanogenic compartments and to the cell surface of human pigment cells, regardless of their oncogenic differentiation status.
A critical area of chromosomal loss at region p16(9p21-22) and p53(17p13) has been implicated in the genesis of malignant melanoma. It is still unclear whether the genetic alterations can be detected in dysplastic nevus, a premalignant lesion of malignant melanoma. We have searched the frequency of p16 and p53 deletion in nine dysplastic nevi and 13 benign intradermal nevi with five microsatellite markers. Hemizygous deletion was detected in seven of nine (78%) dysplastic nevi at one or more loci for p16 and three of seven (43%) for p53, respectively. No loss of heterozygosity (LOH) was detected in any of the benign intradermal nevi. All three dysplastic nevi with LOH for p53 also showed LOH at p16. However, not all dysplastic nevi showing p16 deletion showed p53 gene deletion. Therefore, these data suggest that deletion of p16 may play an important role in the development of dysplastic nevus as an early event and that the changes may represent an early event in the development of malignant melanoma.
Pigment freckles seen in donor and recipient sites at intermediate skin grafting were studied, chiefly by means of Falck & Hillarp's fluorescence method, with the following results. (1) An important role is played by the regenerative eccrine sweat ducts in the mechanism of recurrence of so-called "lentigines" after incomplete removal. (2) Junctional activity, not associated with the regeneration of epidermal appendages, can recommence in the epidermis of intradermal nevi. (3) B-type nevus cells once again actively produce melanin. (4) Specific fluorescence was observed corresponding to the melanin granules distributed in the manner of "nuclear caps" in keratinocytes around junctional activities. This latter finding may indicate that melanosomes which still contain DOPA are transferred from melanin-producing cells to keratinocytes.
Interleukin-1 alpha and -1 beta, interleukin-6, and tumor necrosis factor-alpha may have a protective effect against malignant transformation of melanocytes. By using monoclonal and polyclonal antisera we investigated, in paraformaldehyde-fixed tissue, the cellular distribution of these cytokines in human common and dysplastic nevocellular nevi and in malignant melanoma. Generally, the immunolabeling for all of these cytokines was both cytoplasmic and perinuclear as well as present in the basement membrane, which surrounds the individual cells or cellular nests of some of the nevi. In compound and intradermal nevi the immunolabeling was abundant, although there was a variation in the staining intensity between individual cells and even inside a single nevus cell, ranging from weak to strong. There was a strong labeling of the basement membrane around the cellular nests and around individual cells inside or outside the nests in the papillary and reticular dermis. With regard to the common junctional and dysplastic nevi and malignant melanoma, occasional immunolabeling could be seen in some cells within the cellular nests in the junctional area or papillary dermis, ranging from faint to moderate in intensity, but in this case the basement membrane around individual cells or cellular nests was not stained. The staining of nevocellular nevi and malignant melanoma indicates the possibility of these cytokines being synthesized by the nevi and melanoma cells. The labeling of the basement membrane in compound and intradermal nevi suggests that cytokines produced by nevocellular cells may be stored in the basement membrane, from which they could be released upon environmental or mechanical challenge. This distribution pattern would support the hypothesis that these cytokines may protect the common nevi from malignant transformation.
Forty-two nevus cell nevi excised surgically from 40 patients were processed for primary culture. The characteristic features of cultured nevi were compared with those of neurofibroma reported previously. 1) Based on phase-microscopic findings, S-100 protein staining, and slow motion picture, most of the cultured macrophage-like cells or cells with dendrites were considered to be nevocytes. 2) The emigration of nevocytes was observed in 31 of the 42 nevus cultures (73%). Nevocytes classified histologically as the intradermal type with fatty degeneration and nevi obtained from the face and aged patients exhibited higher tendencies to ward emigration when they were cultured. 3) The cultured Schwann cells in neurofibroma and the nevus cell nevus, mainly c-type nevocytes, are both of neural crest origin. They were observed to have closely similar morphological and S-100 protein staining features.
Melanocytic nevi may microscopically associate with clefts or slits of the nests resembling lymphatic or vascular spaces. This unique histologic feature has been known as an artifact of injection or tissue-processing. We present a case of melanocytic nevus with a prominent vascular space-like structure. We also studied whether intralesional injection of local anesthetic could reproduce similar histologic findings. A 45-year-old Japanese female visited us with a solitary, brownish papule on the chest. Histology revealed numerous nests composed of round to oval-shaped nevus cells throughout the entire dermis. In the mid-dermis, nevus cells were lined up in a layer anastomosing and forming a vascular space-like structure. These nevus cells were uniformly stained with vimentin and S100 protein but not with factor VIII-related antigen. They were also positively immunoreactive with anti-type IV collagen and anti-fibronectin. There were no significant differences in staining intensity in the nevus cells between the solid portion and the vascular space-like structure. In the experimental study, eight melanocytic nevi were removed under local anesthesia. The local anesthetic solution was then injected into the excised nevus. Intralesional injection of a considerable volume of local anesthetic was capable of causing slits or clefts of the nests and dermal edema; however, it failed to reproduce a vascular space-like structure similar to that in the present case. These findings suggest that a vascular space-like structure in melanocytic nevus is not caused by the injection alone. Some other factor(s) may play a major role in the development of such structures in melanocytic nevus.
BACKGROUND: The presence of mature adipose cells among the dermal melanocytes of nevi (nevi with fat) has previously been reported. However, its clinical features are not well characterized. OBJECTIVE: Our goal was to develop a better clinical understanding and insight into the histogenesis of nevi with fat by characterizing the patients' age, sex, height, weight, and location of lesion. METHODS: This was a prospective study of 100 nevi with fat from 89 patients over an 18-month period. RESULTS: Nevi with fat occur 4 times more commonly in women than men. They were diagnosed most often in patients between the ages of 40 to 49 years. The most frequent location is the head and neck. Most nevi with fat are intradermal. CONCLUSION: The appearance of fat within nevi is probably a multifactorial process. Age, weight, and sun exposure may be factors associated with the occurrence of nevi with fat.
Benign juvenile melanoma was originally described and differentiated from malignant melanoma by Sophie Spitz in 1948. The solitary form is the most frequent and usually appears on the face and extremities of young children and adolescents as a solitary, hairless, dome-shaped papule or nodule, varying in size from 3 to 15 mm. It can be of a wide spectrum of colors including pink, yellow, red, brown, purple and black, representing 1% to 8% of melanocytic tumors in children. Histologically, Spitz nevus has been subdivided into junctional, compound and intradermal type according to the location of neoplastic melanocytes in the skin. Rarely multiple benign juvenile melanoma arranged in clusters (agminated) or widespread (disseminated) are described. Less than 50 cases have been reported in the world literature. The grouped form usually occurs on the face of children on normal, but also hyperpigmented or hypopigmented skin, while the disseminated one in adults. A case of multiple agminated Spitz nevus arised on the face of a 2 years old girl is reported. The clinical presentations with a 3 years follow-up and the histologic features of this nevus are described as well as the therapeutic approach.
Using fluorescent-labeled estrogen and progesterone, congenital nevi from fifteen patients, six male and 9 female, were studied for the presence of corresponding cytoplasmic receptor binding. Similar studies were done in a control population of twenty-one patients, ten male and 11 female, with acquired intradermal nevi. Congenital nevi contained high concentrations of estrogen-binding and progesterone-binding nevus cells in both male (6/6) and female patients (5/9). Lesser concentrations of estrogen-binding and progesterone-binding nevus cells were found in congenital nevi from the remaining four female patients. In contrast, acquired intradermal nevi from the control group of patients had little or no detectable estrogen or progesterone binding. These data indicate that congenital nevi are similar in hormonal-binding properties to melanomas and dysplastic nevi, in contrast to acquired intradermal nevi.
One hundred and forty-two (142) halo nevi were reviewed. For 66 cases the diagnosis of halo nevus was made both clinically and pathologically, and for 76 cases the diagnosis was based on histological grounds alone. The nevi were classified by type and by degree of atypia. Of the 142 nevi, all were compound, junctional, or intradermal nevi except for one case of a Spitz nevus and two cases that could not be further classified. For those with a clinicopathological diagnosis of halo nevus, 11% exhibited moderate atypia; 16% exhibited minimal atypia to only focally moderate atypia; 24% minimal atypia; and 49% exhibited no significant atypia. For those cases where the diagnosis was pathological only, there was also a broad spectrum of atypia identified, with 8% exhibiting focally severe or severe atypia. This study supports the concept that the halo nevus should not be regarded as a single clinicopathological entity, but rather that the halo phenomenon occurs in a wide spectrum of nevus types exhibiting a wide spectrum of histological atypia. The pathologist is therefore encouraged to classify halo nevi on the basis of the nevus cell population alone, using whatever classification normally utilized.
Dye lasers are useful for treating pigmented skin lesions, but their equipment is expensive and bulky. A simple and cheap phototherapy would be acceptable to dermatologists for treating pigmented skin lesions such as nevus of Ota. We investigated as a pilot study whether dermal injection of riboflavin and exposure to near-ultraviolet/visible radiation (ribophototherapy) decreases the dermal pigment of blue nevi which are recalcitrant to laser therapy. The therapeutic efficacy was assessed by comparison of the amount of dermal pigment in hematoxylin-eosin specimens taken before and after treatment. Pigmentation of the nevus became faint to the depth of 1 mm with little noticeable epidermal change after 21 treatments. At the deeper dermis somewhere between 3 and 4 mm from the epidermis, ballooning degeneration of the dermal cells was observed in hematoxylin-eosin specimens. Ribophototherapy is hopeful for treating pigmented skin lesions.
The metaplastic synovial cyst (synovial metaplasia of the skin) is a recently described intradermal cyst lined by a membrane that resembles hyperplastic synovium. All of the reported cases thus far have occurred in adults after surgical incision. A case of metaplastic synovial cyst after partial excision of nevus sebaceus in a 7-year-old girl is herein reported. Pathogenesis and light-microscopic and immunohistochemical features of this case are discussed.
A 2-year-old girl had variably-sized, relatively well demarcated, depressed brownish patches on the left shoulder, back, and both legs from the age of 1 month. The biopsy specimen from the left shoulder showed an increase in the number of normal intradermal eccrine ducts and coils, which was compatible with pure eccrine nevus. The clinical manifestation of our case, including brownish depressed patches, was unique compared to other reported cases.
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BACKGROUND: Metalloproteinases (MMPs) are proteins involved in extracellular matrix breakdown and have been implicated in stages of migration and metastasis. MT1-MMP is an MMP anchored to the cell membrane. During maturation, melanocytic nevi penetrate the extracellular matrix and express MMPs. METHODS: We studied 10 junctional, 10 compound, and 10 intradermal nevi diagnosed by clinical and histological studies and by performing immunohistochemical study to assess MT1-MMP activity. RESULTS: We found evidence of MT1-MMP expression in melanocytic nevus cells, particularly around the entire border of cell nests. Expression was more intense in junctional nevi and gradually decreased with acquisition of intradermal component and became nonexistent in nevi in the deep dermis. CONCLUSIONS: MT1-MMP is expressed in the membrane of nevus cells, with expression greater in nest cells in contact with the extracellular matrix. The intensity of expression correlated inversely with the maturation phase of the nevus, being very high in junctional nevi and low in intradermal nevi.