Search

Bullous pemphigoid (BP) is the most common autoimmune blistering disorder of the skin. It is typified by tense blisters with a subepidermal split and mixed dermal inflammatory infiltrate on histology. Biopsy of the perilesional skin for direct immunofluorescence (DIF) has become the gold standard in the diagnosis of BP. Currently there is a pervasive clinical opinion that the lower extremity is a site with a high false-negative rate (FNR) for DIF in the diagnosis of BP. This notion is primarily based on 2 early studies from the 1980s without more recent confirmatory studies. To readdress this question regarding the lower extremities, a retrospective study from 2012 to 2018 was performed in our institution that evaluated the FNR of DIF by an anatomical site in the diagnosis of BP. Cases of BP were identified using standard criteria (clinical and histological data reviewed in cases with negative DIF), and overall, 79 patients were included in the study. A total of 4 false-negative DIF biopsies were verified. Two negative DIF were from the lower extremity yielding a FNR of 10% compared with 4% on the trunk and 3% from the upper extremity, with no statistically significant difference by anatomical sites. Our study fails to demonstrate a high FNR of DIF from the lower extremity in the diagnosis of BP.

Syringotropic mycosis fungoides (MF) is classified under folliculotropic MF. Although there is significant overlap between the 2, this study demonstrates that folliculotropism is frequently present in syringotropic MF, and when not present, the specimen did not include a follicle to examine. In addition, few of the pathology reports mentioned folliculotropism or syringotropism, although this is an important prognostic feature.

Spindle cell and pleomorphic lipoma constitute a spectrum of lipomatous lesions with characteristic clinical, morphologic, immunohistochemical, and molecular features. Multiple variants have been previously described including vascular, fibrous, plexiform, and those with significantly less fat termed “low-fat” and “fat-free” by Folpe. Cytogenetically, spindle cell lipomas frequently display monoallelic loss of 13q14 region, an abnormality also found in cellular angiofibroma and mammary-type myofibroblastoma. Pseudoangiomatous spindle cell lipoma, originally described by Fletcher et al in 1994, is a rare variant within the spindle cell/pleomorphic lipoma spectrum, with less than 20 published cases. It consists of an admixture of spindle cells, “ropey” collagen, variable amounts of mature fat, and irregular, branching slit-like vascular spaces. The authors present a case of a 1-cm subcutaneous lesion excised from the neck of a 70-year-old man with classic histologic and immunohistochemical features of “low-fat” pseudoangiomatous spindle cell lipoma. Fluorescence in situ hybridization demonstrated a loss of 13q14 region, a characteristic presumed cytogenetic finding of spindle cell lipoma, which has been previously unconfirmed in this variant.

Background The scalp has been proposed as an anatomic site that harbors melanocytic nevi with distinctive histologic attributes, so-called "special-site" nevi, similar to nevi on the breast and genitalia. However, detailed studies are lacking. Objective We sought to better delineate the features of scalp melanocytic nevi, particularly lesions that may qualify as special-site nevi. Methods The histologic features of 365 total melanocytic nevi of the scalp were studied from 322 patients over a consecutive period of 18 months from July 2007 through January 2009. Results A total of 56 nevi with characteristic features were identified. The most common features were: (1) random melanocytes containing large nuclei (92.9%) and abundant pale cytoplasm with dusty melanin granules (96.4%); (2) large nests (76.8%) situated along the sides of rete and between rete ridges (85.7%); (3) nests of poorly cohesive melanocytes (82.1%); (4) overlap features with Clark nevi (75.0%); and (5) overlap features with superficial congenital nevi (50.0%). Pagetoid spread (14.3%), asymmetry (23.2%), and poor lateral demarcation (16.1%) were less common. These 56 lesions predominated in the first 2 decades of life and were not observed after age 35 years. Limitations Lack of long-term clinical follow-up of patients is a limitation; however, no recurrences or malignancies from these patients' scalps were submitted in the time period (≥3 years) since the initial biopsies. Conclusion A special site scalp nevus is recognizable amongst scalp melanocytic nevi, and this lesion is more common in younger patients. Familiarization of its features should assist in the diagnosis and management of scalp melanocytic lesions.

Dermatologists and dermatopathologists face the difficulties of accurately diagnosing and treating atypical melanocytic lesions and melanomas. Despite huge advances in medicine, our management of melanoma has not significantly changed in many years. The biggest gains made recently have been in the identification of common mutations in melanoma and the use of these mutations to aid in the diagnosis and treatment of melanoma. To understand these gains one must first be familiar with the regulatory pathways of melanoma and the most common mutations found there. This article will review the function and significance of the most studied mutations in melanoma and briefly discuss new and planned treatment options.

We present two unique cases of fibrous hamartoma of infancy defined by giant-sized and/or multicentric cutaneous and subcuticular lesions--features not, to our knowledge, reported to coexist. We review the nature of such tumors and examine the clinical implications of tumor size and multicentricity on risk for recurrence and likelihood of visceral involvement.

Congress is grappling with ways to fund health care in the future. Much of the focus rests on paying physicians for their patients' outcomes, rather than the current system of payment for services provided during each visit. The years ahead will be years of change for American health care, with an increasing emphasis on the comparison of patient outcomes and measures of quality. Patient safety initiatives will be an integral part of the overall strategy to improve American health care. Part one of this two-part series on patient safety examines what we know about patient safety in dermatology, including data from medicolegal claims and published data on patient safety in the setting of office-based surgery. The article also focuses on how medical societies, payers, the US government, and the Board of Medical Specialties are responding to calls for accountability and improvements in patient safety. Learning objectives After completing this learning activity, participants should be able to identify risks to patient safety based on an understanding of the major causes of legal claims against dermatologists, use published patient safety data to improve the practice of office surgery, and be able to improve patient safety through an understanding of requirements for maintenance of certification.

Objective The definition and management of the atypical nevus remains a controversial issue. Some believe that atypical nevi are common variants of benign melanocytic nevi while others believe they are lesions intermediate between benign melanocytic nevi and melanoma. Therefore, the question of whether or not partially removed atypical nevi should be re-excised with clear margins in order to prevent their evolution into melanoma remains unanswered. Although studies have shown that most atypical nevi will never progress into melanoma, re-excision, when biopsy margins are positive, is commonly practiced. We argue that re-excision in such cases is not necessary. Methods Our cohort study includes 55 previously biopsied atypical nevi that were not re-excised and which were followed for at least 5 years with a mean follow up time of 6.12 years. Results The experimental group included 26 atypical nevi whose biopsy revealed at least one involved margin. The control group included 29 atypical nevi whose biopsy revealed clear margins. No melanomas were observed to arise in association with a pre-existing atypical nevus in either the experimental or control group during the follow-up period. Conclusions The results of our study support observation as a safe alternative to re-excision for incompletely removed atypical nevi. A large prospective study with longer follow up would be necessary to better answer the question of how often atypical nevi evolve into melanoma and over what time period this occurs.

Primary cutaneous inoculation blastomycosis occurs less commonly than secondary blastomycosis, in which cutaneous lesions most often originate from a primary pulmonary infection which disseminates through the blood or lymphatics to involve the skin. In secondary cutaneous blastomycosis, the primary pulmonary infection is frequently subclinical at the time cutaneous lesions manifest. Here we report two cases that illustrate the difficulty in distinguishing between primary and secondary cutaneous involvement. We also review the expanding literature on blastomycosis since its identification over a century ago.

Background. Nephrogenic systemic fibrosis is a debilitating disease occurring exclusively in patients with renal failure. The aetiology of nephrogenic systemic fibrosis is unclear, but recent reports suggest that exposure to gadolinium for enhancement of magnetic resonance imaging may play a role. In the present study, we assessed the association of exposure to gadolinium with the development of nephrogenic systemic fibrosis in patients with various stages of chronic kidney disease. Methods. We analysed the exposure to gadolinium and development of nephrogenic systemic fibrosis in 849 patients on renal replacement therapy over 5 years. We also performed inquiry of development of the nephrogenic systemic fibrosis in 592 patients exposed to gadolinium and estimated to be in stages 3 and 4 of chronic kidney disease. Results. In 849 patients undergoing chronic dialysis from 2001 through 2006 time period, four of the 261 who had received gadolinium (1.5%) and none of the 588 not exposed to gadolinium developed clinically apparent disease. The odds ratio for developing nephrogenic systemic fibrosis was 6.671 [95% confidence interval (CI) 1.537–53.97] in patients with a single gadolinium exposure compared to patients without gadolinium exposure. This ratio increased to 44.5 (95% CI 2.362–2913) in patients with multiple gadolinium exposures compared to patients not receiving gadolinium. None of the 592 patients estimated to be in stage 3 or 4 of chronic kidney disease developed nephrogenic systemic fibrosis after exposure to gadolinium. Conclusion. Gadolinium exposure is associated with nephrogenic systemic fibrosis in patients on chronic renal replacement therapy at a low rate. This association appears to increase with repeated exposure to gadolinium. Since nephrogenic systemic fibrosis may be clinically occult, its prevalence may be higher than reported. Despite this association, it is unclear if gadolinium is the sole or most important factor in the pathogenesis of the disease.

BACKGROUND The determination of clear margins during Mohs surgery for melanoma in situ arising on sun-damaged skin is often made difficult by the presence of background atypical melanocytic hyperplasia. OBJECTIVE To determine the density and distribution patterns of melanocytes adjacent to melanoma and nonmelanoma skin cancers. METHODS 180 skin specimens obtained during the routine repair of defects resulting from the removal of melanoma and nonmelanoma skin cancers were analyzed using H&E-stained permanent sections to determine the quantity and distribution of epidermal melanocytes. RESULTS The mean melanocyte density was 7.97 melanocytes per 1 mm of epidermis (SD,±6.7). Contiguous melanocytes were found in 30 (16.7%), atypical melanocytes were observed in 8 (4.4%), and follicular extension of melanocytes was observed in 11 (6.1%) of the specimens. These features were significantly associated with higher melanocyte densities (p< .001) and were more commonly observed in specimens from patients with melanoma. CONCLUSIONS There is a high degree of variability in melanocyte densities seen adjacent to melanoma and nonmelanoma skin cancers. Contiguous melanocytes, atypical melanocytes, and follicular melanocytes can be seen in the sun-damaged skin surrounding both melanoma and nonmelanoma skin cancers, but especially with melanoma. Because some of the features of melanoma in situ can be seen in chronically sun-damaged skin, the Mohs surgeon should be cautious when assessing the margins for melanoma in this setting.

We describe a newborn infant who was born with a purpuric rash and subcutaneous nodules. Skin biopsies demonstrated acute myeloid leukemia. Cytogenetic studies revealed an 11q23 rearrangement. Initial bone marrow and cerebrospinal fluid examination did not demonstrate medullary or meningeal disease. Chemotherapy was initiated on the basis of the abnormal cytogenetic findings in the skin biopsy. Intensive chemotherapy was, given but the infant's leukemia progressed. The patient died of refractory leukemia and secondary fungal disease. This case report supports the observation that leukemia cutis with an 11q23 rearrangement should be treated aggressively.

Blue nevi are benign dermal melanocytic proliferations that can sometimes share overlapping microscopic features with melanoma. We used comparative genomic hybridization to analyze three groups of dermal melanocytic proliferations. Group 1 consisted of 10 cellular blue nevi and 1 deep penetrating nevus, none of which showed chromosomal aberrations. Group 2 consisted of 11 lesions that were histopathologically ambiguous. Three of these lesions demonstrated chromosomal aberrations (three or fewer per lesion). Group 3 consisted of seven histopathologically malignant lesions, each showing three or more chromosomal aberrations. Moderate to severe cytologic atypia and a mitotic rate of three or more mitoses per 10 high power fields were present in six of eight (75%) lesions that had at least three chromosomal aberrations but were absent in 15 of 20 (75%) lesions without chromosomal aberrations. Necrosis was present in four of the 29 (13%) lesions, with every lesion with necrosis demonstrating three or more genomic abnormalities. In conclusion, histopathologically unequivocally benign or malignant dermal melanocytic proliferations show nonoverlapping patterns of chromosomal aberrations. Ambiguous lesions can be separated into lesions with and without chromosomal aberrations. Future studies with clinical follow-up are necessary to determine which aberrations are most informative for classification of these lesions.

The adjuvant treatment of high-risk malignant melanoma remains problematic. Previously we reported moderate success in the treatment of metastatic disease using tamoxifen, cisplatin, dacarbazine and carmustine. Based upon data that suggested tamoxifen and cisplatin were the active agents in this regimen, we initiated a phase II trial of this combination in the adjuvant setting. We treated 153 patients with 4 cycles of tamoxifen (160 mg day–1, days 1–7) and cisplatin (100 mg m–2, day 2) for 28-day intervals. Patients received an anti-nausea regimen of dexamethasone with ondansetron or granisetron. During the first 2 years of follow-up, patients were evaluated every 2 months with a history, physical exam, laboratory work and computed tomography scans of the chest, abdomen and pelvis every 4 months. Thereafter, patients were evaluated every 3 months and radiographic studies were performed if necessary. Currently, with a median follow-up of 36 months, the disease-free survival (DFS) is 68.4% and overall survival (OS) is 84.5%. Kaplan–Meier analysis predicts a 5-year DFS of 62% with an OS of 79%. Relapses after 20 months have been rare. No effect of gender or number of positive lymph nodes was noted, however, stage of disease prior treatment was a factor. The major toxicity proved to be gastrointestinal in nature with nausea the most prevalent symptom. Minimal renal, haematologic and neurologic toxicity occurred. These preliminary results suggest that there is a positive impact of tamoxifen and cisplatin on both the DFS and OS of high-risk malignant melanoma patients. The 5-year projected DFS and OS compare favourably with those reported for the ECOG 1684 trial and warrant confirmation in a prospective randomized trial. © 2000 Cancer Research Campaign

"Clark's nevi" is the name we apply to lesions that have been referred to in the past as dysplastic nevi or nevi with architectural and/or cytologic atypia. Our criteria for this histopathologic diagnosis include such architectural features as: (1) uneven distribution of melanocytes along the dermoepidermal junction; (2) irregularly spaced junctional nests that sometimes bridge between rete; and (3) ill-defined margins often characterized by a lentiginous growth pattern. If dermal nests are present, the junctional component usually extends laterally for some distance beyond the dermal nests. When there is cytologic atypia, it involves scattered melanocytes. Clark's nevi are of doubtful significance if few in number and occurring in a young patient in whom there is no family history of melanoma. When many are found in a patient with a family history of melanoma, their presence serves as a marker for dysplastic nevus syndrome (familial atypical mole-melanoma syndrome). When Clark's nevi develop in patients older than 40 or 50 years of age who have no family history of melanoma, their significance is less clear. However, they might signify a defect in those mechanisms that normally control formation and growth of melanocytic neoplasms.

Four patients with late stage cutaneous T cell lymphoma (IB-IVA) who had failed at least two previous therapies were treated with DAB389IL2 at 9 or 18 microg/kg as 15-min intravenous infusions daily for 5 days every 3 weeks for eight cycles. Mild vascular leak syndrome (VLS) with transient edema, hypoalbuminemia, weight gain, and myalgias was observed in two of the patients lasting 7-10 days and only occurring on the first cycle. One stage IB patient had a pathologic complete remission (CR) lasting 11+ months from treatment initiation, one stage IIB patient had a complete clinical remission (CCR) lasting >6 months with complete clearing of a large tumor lasting >18 months, and one stage IIB and the one stage IVA patient had partial remissions (80-99% reduction in tumor masses) lasting 5 months. While IL2 receptor (IL2R) was expressed on 20-50% of tumor cells prior to therapy, recurrent tumor was IL2R negative in three of the patients. DAB389IL2 at tolerable doses decreased tumor burden in each of these four standard treatment refractory CTCL patients and may offer an important alternative to standard palliative chemotherapy regimens.

Background Epidermolysis bullosa acquisita (EBA) is a rare antibody-mediated autoimmune blistering disease of adults. Likewise, acquired factor VIII deficiency is a rare antibody-mediated disease of adulthood. Both diseases can be exceedingly difficult to treat and refractory to immunomodulatory therapies. Methods Herein, we report a challenging case of EBA and acquired factor VIII deficiency in the same patient. Results Cyclosporine 4 mg/kg/day rapidly controlled both disease processes after the patient failed to respond to prednisone, colchicine, and pulse cyclophosphamide. The EBA relapsed when the cyclosporine was decreased to 2 mg/kg/day and the patient wore snuggly fitting new shoes, but it cleared quickly when the dose was increased. Cyclosporine has since been decreased gradually to 1.5 mg/kg/day without relapse of either condition or detectable side-effects. Conclusions Cyclosporine should be considered when EBA and/or acquired factor VIII deficiency fail to respond to conservative therapy. Both conditions usually respond rapidly to cyclosporine 4–6 mg/kg/day.

As of 2013, keratoacanthomas (KAs) have not been decided on as either a benign or a malignant entity. Originally considered benign epidermal growths, the assertion by Hodak, Jones, and Ackerman that these lesions are truly "an expression of squamous cell carcinoma" (SCC) fueled the controversy and placed some of the biggest names in the field on opposite sides of the issue. Without a clear understanding of the etiology of KAs and without stringent diagnostic criteria, the literature in regard to KA contains scant reports of their "metastatic potential." Four hundred forty-five cases of KA with reported follow-up and outcomes were reviewed from 113 published articles. In our data set, none of these cases resulted in death or distant metastases. When compared with 429 cases of SCC of the skin, with 61 cases of metastases and 24 deaths as a direct result of SCC, the biologic behavior of the 2 entities is distinct and evident. KAs are benign epidermal growths and not a malignant variant of SCC.

The Tsc2 gene, which is mutationally inactivated in the germ line of some families with tuberous sclerosis, encodes a large, membrane-associated GTPase activating protein (GAP) designated tuberin. Studies of the Eker rat model of hereditary cancer strongly support the role of Tsc2 as a tumor suppressor gene. In this study, the biological activity of tuberin was assessed by expressing the wild-type Tsc2 gene in tumor cell lines lacking functional tuberin and also in rat fibroblasts with normal levels of endogenous tuberin. The colony forming efficiency of Eker rat-derived renal carcinoma cells was significantly reduced following reintroduction of wild-type Tsc2. Tumor cells expressing the transfected Tsc2 gene became more anchorage-dependent and lost their ability to form tumors in severe combined immunodeficient mice. At the cellular level, restoration of tuberin expression caused morphological changes characterized by enlargement of the cells and increased contact inhibition. As with the full-length Tsc2 gene, a clone encoding only the C terminus of tuberin (amino acids 1049-1809, including the GAP domain) was capable of reducing both colony formation and in vivo tumorigenicity when transfected into the Eker rat tumor cells. In normal Rat1 fibroblasts, conditional overexpression of tuberin also suppressed colony formation and cell growth in vitro. These results provide direct experimental evidence for the tumor suppressor function of Tsc2 and suggest that the tuberin C terminus plays an important role in this activity.

We review the clinical features, histopathology, and immunohistochemistry in three cases of eosinophilic histiocytosis, comparing lymphomatoid papulosis and eosinophilic histiocytosis. Each of the patients presented with self-healing recurrent papules and ulcerative nodules that were associated with pruritus. Disease duration was 5 months to 9 years. Histologically, the lesions demonstrated spongiosis and lymphocytic exocytosis, epidermal hyperplasia, papillary dermal edema, and a superficial and deep mixed perivascular inflammatory infiltrate. The infiltrate showed numerous eosinophils, histiocytoid cells, lymphocytes, and large mononuclear cells with atypical hyperchromatic nuclei. Most of the lymphocytes and large mononuclear cells with atypical nuclei marked with UCHL-1 (T-cell marker). The histiocytoid cells marked with S-100 and were dendritic both in the epidermis and the dermis. Eosinophilic histiocytosis appears to differ from classic lymphomatoid papulosis. It presents with recurrent papules and nodules associated with marked pruritus. Eosinophilic histiocytosis uniformly has more eosinophils and does not have the Reed-Sternberg cells often observed in lymphomatoid papulosis type A. Eosinophilic histiocytosis does not have cells that mark with Ki-1 and shows numerous S-100-positive histiocytoid cells that are most likely Langerhans cells, unlike lymphomatoid papulosis. However, eosinophilic histiocytosis may be an unusual Ki-1-negative variant of lymphomatoid papulosis with histopathologic changes not typical of type A or type B. In addition, eosinophilic histiocytosis lacks multinucleated histiocytes and the atypical histiocyte with a reniform nucleus, findings that are characteristic of histiocytosis X. Further studies are needed to define the pathophysiology and prognosis of this apparently distinct entity more accurately.

Background: Nevi that are clinically atypical and histologically dysplastic have been associated with increased melanoma risk. There are few reproducibility studies or population-based studies of nevus histology. Objective: Our purpose was to quantify concordance in histologic diagnosis of melanocytic lesions among a diverse group of pathologists, to assess intraobserver concordance by comparing readings of the same slide as well as of adjacent recuts from the same block, to correlate histology with nevus appearance and melanoma risk, and to estimate the range of prevalence of histologic dysplasia. Methods: Histologic slides were prepared from 149 tissue blocks of pigmented lesions from melanoma cases, relatives, and controls. Six dermatopathologists independently evaluated the lesions for histologic dysplasia, without prior agreement on criteria. Results: According to κ statistics, intraobserver reproducibility was substantial, and interobserver concordance was fair, despite differences in criteria. The estimated prevalences of histologic dysplasia for the six pathologists ranged from 7% to 32%. Histologic dysplasia was correlated with nevus size for most observers, confounding the observed correlation between nevus appearance and histology. Conclusion: Although experienced dermatopathologists use different diagnostic criteria for histologic dysplasia, their usage is consistent. Histologic changes ascribed to melanocytic dysplasia are prevalent in the white population for all pathologists. The term nevus with histologic dysplasia should be used in preference to dysplastic nevus.

Background: We observed four patients with mid-dermal elastolysis (MDE) that was either precipitated or aggravated by UV light (UVL) exposure or was primarily confined to areas of UVL exposure. Objective: Our purpose was to report four cases of MDE occurring after significant UVL exposure and to demonstrate why we suspect that MDE in some instances may be photoinduced or photoaggravated. We also wish to demonstrate the varied clinical presentation of this disorder. Methods: Because all our patients had MDE involving skin exposed to UVL, biopsies were performed on clinically uninvolved sun-exposed and sun-protected skin in one patient to elucidate further the role of UVL in this process. Results: On routine histopathologic examination we found that uninvolved sun-exposed skin but not sun-protected skin demonstrated early MDE. Ultrastructural examination revealed a spectrum of elastic fiber changes in involved and clinically uninvolved sun-exposed skin. Phagocytosis of elastic fibers was not present. Conclusion: We conclude that UVL, exposure was a major causative or aggravating factor of MDE in our patients and that the clinical appearance of this disorder is variable.

Bloom syndrome is a rare genodermatosis of autosomal recessive inheritance. Although lupus-like skin lesions characterize this disorder, mechanisms of photosensitivity are poorly understood. In this case presentation, the authors report a patient with Bloom syndrome whose lupus-like facial rash revealed striking histopathologic similarities to cutaneous lupus erythematosus.

Symmetric skin thickening of the limbs with deep fascial inflammation is the hallmark of eosinophilic fasciitis. We describe a woman who presented with unilateral progressive skin thickening. Examination of a full thickness skin biopsy revealed an inflammatory process and fascial changes consistent with eosinophilic fasciitis. In contrast to other scleroderma mimics, eosinophilic fasciitis generally responds rapidly to glucocorticoid therapy. It is possible that unilateral eosinophilic fasciitis is under-recognized and can easily be misdiagnosed as another scleroderma variant if a full thickness biopsy is not reviewed by a dermatopathologist. Recognition of this subtype of eosinophilic fasciitis is important given the profound differences in prognosis of eosinophilic fasciitis and other scleroderma variants.

In some individuals habitual cheek and lip biting becomes a fixed neurosis. Pieces of oral mucosa are actually torn free from the surface, producing a distinctive clinical appearance termed morsicatio buccarum et labiorum. Sometimes it may be confused with other dermatological disorders involving the oral mucosa, and can lead to misdiagnosis. Most patients with this condition are unaware of their habit and will not aid in the diagnosis. We suggest that the histopathological features of this condition are distinctive, if not pathognomonic, and that an accurate diagnosis should be rendered if a biopsy sample is taken. Two cases are reported herein that were originally misdiagnosed as pemphigus, one of which resulted in complications of improper oral corticosteroid use.

The histopathologic criteria used in the diagnosis of dysplastic nevi have been a source of controversy, as has the clinical significance of these lesions. Several dermatopathologists noted for their work on dysplastic nevi were asked to contribute responses to questions regarding the architectural and cytological criteria used to classify a melanocytic nevus as dysplastic, the terminology used to describe these lesions, and the role of dysplastic nevi as precursors of melanoma. Although no consensus has been reached regarding the cytologic features required for diagnosis of dysplastic nevi, there is substantial agreement regarding the architectural features of these lesions.

Background: Previous studies suggest that chemokines and chemokine receptors have a role in the metastatic process. A correlation exists between the specific expression of these chemoattractive, pro-inflammatory cytokines and the ability of cancer to disseminate. Prior studies have shown that in metastatic melanoma and squamous cell carcinoma of the head and neck upregulation of CXC (α) chemokine receptor (CXCR)4 and CC (β) chemokine receptor (CCR)7 expression is accompanied by downregulation of the chemokine receptor CCR6. However, the expression patterns of CCR6, CCR7 and CXCR4 in non-melanoma skin cancer have yet to be elucidated. Methods: The expression patterns of CCR6, CCR7 and CXCR4 were determined using an immunohistochemical approach on formalin-fixed, paraffin-embedded normal, pre-cancerous actinic (solar) keratosis, squamous cell carcinoma and basal cell carcinoma tissues. Results: Analysis of chemokine receptor expression showed downregulation of CCR6 and upregulation of CCR7 and CXCR4 in potentially metastatic non-melanoma skin cancer, invasive squamous cell carcinoma, but this pattern did not exist in non-melanoma skin cancer with no metastatic potential, basal cell carcinoma; or actinic keratosis, when compared with normal skin. Conclusions: Chemokine receptor expression may influence the biological behavior of non-melanoma skin cancer. The exact mechanism by which this occurs requires further study.

Localized cutaneous argyria presenting as an asymptomatic blue-gray macule has been rarely reported from diverse etiologies including occupational exposures, topical medications, alternative medical therapies, body jewelry, and dental procedures (amalgam tattoos). The lesions often are clinically indistinguishable from blue nevi and malignant melanoma. We present a case of localized cutaneous argyria from an acupuncture needle in a patient with a history of malignant melanoma. Fine granules of nonbleachable dark particles coating collagen and elastin fibers, altered yellow-brown collagen bundles similar to ochronosis, and involvement of eccrine structures were histologically consistent with the pseudo-ochronosis pattern of localized cutaneous argyria, demonstrating that clinicopathologic correlation is of crucial importance.

• A 46-year-old woman developed localized scleroderma after surgical manipulation of her silicone gel-filled breast prostheses. She developed firm, shiny plaques on her legs that progressed to involve the thighs. Histopathologic examination of a deep-skin biopsy specimen confirmed the diagnosis of scleroderma. On surgical removal of the silicone implants, and their replacement with saline-filled implants, the scleroderma gradually resolved. Histopathologic examination of the removed implant capsules revealed evidence of silicone leakage. All new female patients with scleroderma should be questioned and examined regarding augmentation mammoplasty. Until prospective studies are completed on the possible association between scleroderma and silicone breast implants, it would seem prudent to use the saline-filled, elastomeric envelope-type breast implant for augmentation mammoplasty rather than the silicone gel-filled implant. (Arch Dermatol. 1990;126:1198-1202)

Squamous metaplasia of eccrine sweat glands has been most frequently described in chronic cutaneous ulcerations with associated epidermal hyperplasia. We found examples of the process in skin biopsy specimens from five patients: three had associated lobular panniculitis and two had lesions of pyoderma gangrenosum. The metaplasia was located in the mid-to-deep reticular dermis in all five patients and extended into the superficial subcutis in one. Immunohistochemical stains for CEA and S-100 protein were used to accentuate the relationship of the metaplastic islands with eccrine ducts. It is postulated that necrosis of a portion of the eccrine duct is the stimulus for this process.