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BACKGROUND: The Floating Sign is a histopathologic clue to the diagnosis of autoimmune sclerosing skin disorders such as morphea and interstitial granulomatous dermatitis (IGD). On the other hand, the "free-floating" sign has been associated with neoplasms, for example, dermatofibroma and interstitial mycosis fungoides. Herein, we report the Free Sign in sclerosing skin disorders. METHODS: In a case-control study, we applied detailed histopathologic definitions of Floating Sign and Free Sign to assess their presence in morphea, IGD, and other sclerosing disorders. RESULTS: Free Sign was present in most cases of morphea (46/55, 84%) and IGD (7/13, 54%) but not necrobiosis lipoidica (NL) (6/14, 42.8%) or sclerodermoid graft versus host disease (SGVHD) (2/7, 28.5%). The sensitivity and specificity of Free Sign for morphea versus other disorders was 84% and 56%, respectively. Floating Sign was not identified in most cases: NL (3/14, 21.4%), SGVHD (1/7, 14.2%), morphea (5/55, 9%), IGD (1/13, 7.7%). The diagnostic sensitivity of Floating Sign in morphea was 9%. CONCLUSIONS: The Free Sign was present in most cases of morphea in our series and may represent a clue to the presence of evolving sclerosis. Free Sign may be seen in other sclerosing disorders. Technical artifact is a potential cause of a false-positive Free Sign.

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Interleukin-17 (IL-17) and tumor necrosis factor (TNF) regulate tissue remodeling through matrix metalloproteinases (MMPs). It is not yet clear whether these cytokines have a functional hierarchy in psoriasis. Serum levels of TNF (1,403 versus 1,058 pg/mL), IL-17 (1,528 versus 820 pg/mL), MMP-1 (1,999 versus 1,039 pg/mL), and MMP-9 (1,950 versus 1,561 pg/mL) were higher in psoriasis subjects (n = 60) than in control subjects (n = 60). Tissue inhibitor of MMPs (TIMP-1; 1,374 versus 1,218 pg/mL) was lower in psoriasis subjects. Serum IL-17 was correlated with MMP-2 (rs = 0.40) and TIMP-1 (rs = -0.26) levels. Unstimulated production of MMP-1, MMP-2, and MMP-9 by monocytes was higher in psoriasis subjects, whereas TIMP-1 production was lower. TNF stimulation increased all MMPs, whereas TIMP-1 production was unchanged. IL-17 stimulation increased all MMPs, whereas TIMP-1 production was decreased in psoriasis subjects. MMP-9 production was higher in monocytes stimulated with IL-17 compared with TNF. TIMP-1 production was decreased more by IL-17 than by TNF, but only in psoriasis cells. MMP-1/TIMP-1, MMP-2/TIMP-1, and MMP-9/TIMP-1 ratios were higher after IL-17 stimulation (compared with TNF stimulation) in psoriasis subjects; this occurred in controls only for the MMP-2/TIMP-1 ratio. IL-17 has a greater ability than TNF to dysregulate the MMPs/TIMP-1 balance, supporting IL-17 blockade as first-line treatment in cutaneous psoriasis.

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Alopecia areata (AA) is a common form of nonscarring hair loss. It is believed to be a consequence of an immune-mediated stimulus, probably involving autoreactive T cells against antigens present in the hair follicle. The exact antigen is still unknown; however, some authors have proposed that melanogenesis-associated molecules might trigger autoimmunity. Although transient white hair regrowth is a common and well-known situation in AA, there are other types of white hair phenomena in this context, including permanent white hair regrowth, sparing of white hair in a patchy pattern, or sparing in a diffuse pattern, giving the appearance of the so-called overnight graying phenomena or canitis subita. In this review, we aim to describe the different clinical aspects of white hair in AA, as well as the proposed pathophysiologic mechanisms involved in this phenomena.

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Fillers are frequently used in aesthetic medicine and, although usually safe, complications can occur. Vascular occlusion leading to tissue necrosis is a rare but severe complication. Alopecia after hyaluronic acid injection has been recently reported, being a vascular compromise the most probable physiopathological mechanism. The trichoscopic findings in this entity have not been described yet. A case report of a 30-year-old female who developed this complication following a hyaluronic acid injection as well as the description of the trichoscopic findings are presented in this report.

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We describe the case of a 45-year-old man who presented with a 5-month history of unilateral pruritic linear erythematous papules and atrophy on the chin and mandibular area. Dermoscopy showed areas of cicatricial alopecia with absence of follicular openings, perifollicular erythema and pigment. Lichen planopilaris of the face is a rare variant with only 13 cases reported in the literature.

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Yeasts cause only 5-10% of onychomycosis; the most common yeast is Candida albicans, and rarely Trichosporon spp. is found. Recently, it has become an important cause of fungemia with a high mortality rate in immunocompromised patients. Superficial infections caused by Trichosporon spp., including piedra and onychomycosis, occur in immunocompetent patients. Herein, we report a case of a fungal nail infection characterized by onycholysis and chromonychia caused by Trichosporon inkin.