83 research outputs found

    Chronic allergic contact dermatitis promotes skin cancer

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    Allergic contact dermatitis (ACD) is well recognized as an adverse event associated with implantable medical devices that contain allergenic materials like nickel; however, other cutaneous consequences of chronic exposure to allergens in implanted devices are not well understood. Here, we present a clinical case of Marjolin’s ulcer, an invasive squamous cell carcinoma (SCC) that developed in response to chronic ACD caused by an orthopedic implant. We used a standard murine model of contact hypersensitivity to determine whether chronic ACD promotes skin carcinogenesis. Chronic application of 1-fluoro-2,4-dinitrobenzene (DNFB) to carcinogen-treated skin led to the development of papillomas and aggressive SCC. DNFB-driven chronic ACD was marked by type 2 inflammation, which mediated skin carcinogenesis, as mice unable to mount an inflammatory response were less likely to develop skin tumors. Importantly, we found similar tumor-promoting inflammation surrounding the SCC in our patient. Our findings demonstrate that chronic ACD caused by constant exposure to an allergen can promote tumorigenesis at skin sites with preexisting cancer-initiated cells. Moreover, our results suggest that patients with implantable devices placed in close proximity to the skin should be monitored for ACD and highlight the importance of patch testing prior to the placement of such devices

    Does Complement Have a Role in the Pathogenesis of Alopecia Areata?

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    Alopecia areata (AA) is an autoimmune disorder in which immune attack of the anagen follicle causes hair loss in approximately 2% of the population. Although the pathogenesis of AA has not been fully determined, most likely it is mediated by a variety of factors including cellular/humoral immunity and genetic predisposition. Researchers have been interested in the possible role of the complement pathway in AA since the 1970s. Given recent evidence suggesting that complement plays a role in many immunologic and inflammatory dermatologic diseases including systemic lupus erythematosus, bullous diseases, angioedema, lipodystrophy, and skin infections, it is likely that complement also contributes to AA pathogenesis. Although early serum studies and immunohistochemical staining have been unimpressive, recent genetics studies may provide evidence that complement does indeed contribute to AA. By determining if complement plays a role in AA, options for novel targeted treatments will become available for those patients with refractory disease

    Hair Follicle Melanogenesis Reflected in Hair Pigmentation as a Developmental Factor in Alopecia Areata

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    The mechanism of alopecia areata (AA) is not well-elucidated, and hair follicle melanogenesis pathways are implicated as possible sources for autoantigens. After a retrospective medical record review at a single tertiary medical center, the hair color of 112 AA patients were identified and compared to a control group of 104 androgenetic alopecia patients. There were no statistically significant differences in the natural hair color prevalence between the 2 groups (p = 0.164), and hair color was not a predictor of the alopecia type. Our results suggest hair pigmentation, determined by the eumelanin-to-pheomelanin ratio, is not a positive risk factor for AA development. We hope that our study will encourage multiple large-scale, collaborative, retrospective medical reviews to determine if our results are reproducible in diverse patient populations
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