Unaffected Skin Research Articles

DNA Methyltransferases in Malar Melasma and Their Modification by Sunscreen in Combination with 4% Niacinamide, 0.05% Retinoic Acid, or Placebo.

Background Malar melasma has a chronic and recurrent character that may be related to epigenetic changes. Objective To recognize the expression and DNA methylation of DNA methyltransferases (DNMTs) in malar melasma and perilesional skin, as well as the changes in DNMTs after their treatment with sunscreen in combination with 4% niacinamide, 0.05% retinoic acid, or placebo. Methods Thirty female patients were clinically evaluated for the expression of DNMT1 and DNMT3b using real-time PCR and immunofluorescence. These initial results were compared to results after eight weeks of treatment with sunscreen in combination with niacinamide, retinoic acid, or placebo. Results The relative expression of DNMT1 was significantly elevated in melasma compared with unaffected skin in all subjects, indicating DNA hypermethylation. After treatment, it was decreased in all groups: niacinamide (7 versus 1; p<0.01), retinoic acid (7 versus 2; p<0.05), and placebo (7 versus 3; p<0.05), which correlates with clinical improvement. DNMT3b was not overexpressed in lesional skin but reduced in all groups. Conclusions We found DNA hypermethylation in melasma lesions. Environmental factors such as solar radiation may induce cellular changes that trigger hyperpigmentation through the activation of pathways regulated by epigenetic modifications. However, limiting or decreasing DNA methylation through sunscreen, niacinamide, and retinoic acid treatments that provide photoprotection and genetic transcription can counteract this.

The identification of CCL18 as biomarker of disease activity in localized scleroderma

BackgroundLocalized Scleroderma (LoS) encompasses a group of idiopathic skin conditions characterized by (sub)cutaneous inflammation and subsequent development of fibrosis. Currently, lack of accurate tools enabling disease activity assessment leads to suboptimal treatment approaches. ObjectiveTo investigate serum concentrations of cytokines and chemokines implicated in inflammation and angiogenesis in LoS and explore their potential to be utilized as biomarker of disease activity. Additionally, to investigate the implication of potential biomarkers in disease pathogenesis. MethodsA 39-plex Luminex immuno-assay was performed in serum samples of 74 LoS and 22 Healthy Controls. The relation between a validated clinical measure of disease activity (mLoSSI) and serum analytes was investigated. Additionally, gene and protein expression were investigated in circulating cells and skin biopsies. ResultsFrom the total of 39, 10 analytes (CCL18, CXCL9, CXCL10, CXCL13, TNFRII, Galectin-9, TIE-1, sVCAM, IL-18, CCL19) were elevated in LoS serum. Cluster analysis of serum samples revealed CCL18 as most important analyte to discriminate between active and inactive disease. At individual patient level, CCL18 serum levels correlated strongest with mLoSSI-scores (rs = 0.4604, P < 0.0001) and in longitudinal measures CCL18 concentrations normalised with declining disease activity upon treatment initiation. Additionally, CCL18 was elevated in LoS serum, and not in (juvenile) dermatomyositis or spinal muscular atrophy. Importantly, CCL18 gene and protein expression was increased at the inflammatory border of cutaneous LoS lesions, with normal expression in unaffected skin and circulating immune cells. ConclusionCCL18 is specific for disease activity in LoS thereby providing relevance as a biomarker for this debilitating disease.

Dysbiosis of Skin Microbiota in Psoriatic Patients: Co-occurrence of Fungal and Bacterial Communities.

Psoriasis is a chronic inflammatory skin disease, whose pathogenesis involves dysregulated interplay among immune cells, keratinocytes and environmental triggers, including microbiota. Bacterial and fungal dysbiosis has been recently associated with several chronic immune-mediated diseases including psoriasis. In this comprehensive study, we investigated how different sampling sites and methods reflect the uncovered skin microbiota composition. After establishing the most suitable approach, we further examined correlations between bacteria and fungi on the psoriatic skin. We compared microbiota composition determined in the same sample by sequencing two distinct hypervariable regions of the 16S rRNA gene. We showed that using the V3V4 region led to higher species richness and evenness than using the V1V2 region. In particular, genera, such as Staphylococcus and Micrococcus were more abundant when using the V3V4 region, while Planococcaceae, on the other hand, were detected only by the V1V2 region. We performed a detailed analysis of skin microbiota composition of psoriatic lesions, unaffected psoriatic skin, and healthy control skin from the back and elbow. Only a few discriminative features were uncovered, mostly specific for the sampling site or method (swab, scraping, or biopsy). Swabs from psoriatic lesions on the back and the elbow were associated with increased abundance of Brevibacterium and Kocuria palustris and Gordonia, respectively. In the same samples from psoriatic lesions, we found a significantly higher abundance of the fungus Malassezia restricta on the back, while Malassezia sympodialis dominated the elbow mycobiota. In psoriatic elbow skin, we found significant correlation between occurrence of Kocuria, Lactobacillus, and Streptococcus with Saccharomyces, which was not observed in healthy skin. For the first time, we showed here a psoriasis-specific correlation between fungal and bacterial species, suggesting a link between competition for niche occupancy and psoriasis. However, it still remains to be elucidated whether observed microbial shift and specific inter-kingdom relationship pattern are of primary etiological significance or secondary to the disease.

Bacterial biofilm is associated with higher levels of regulatory T cells in unaffected hidradenitis suppurativa skin.

The role of bacterial biofilm in hidradenitis suppurativa (HS) is highly debated. Less biofilm is found in clinically unaffected axillary perilesional skin of HS patients compared with healthy controls. To study the correlation between biofilm and the phenotypical characterization of the preclinical inflammatory infiltrate. An exploratory comparative study of punch biopsies from unaffected axillary HS skin compared to similarly biopsies from healthy controls underwent standard staining procedures for CD4, CD8, CD25, FoxP3 and IL17. Standard-sized inflammatory histological hotspots were identified manually. Slides were scanned into Leica Biosystems' Digital Image Hub. Number of stained cells per slide and hotspot was found using an algorithm. 12.5% of HS had biofilm compared to 85% of controls. For full slides, HS patients had more CD4+ cells than controls; HS patients with biofilm had higher CD4+ cell number than controls with or without biofilm and HS patients without biofilm. For hotspots, HS patients with biofilm had higher number of CD4+FoxP3+ cells than HS patients without biofilm and controls with biofilm. The association between biofilm and the number of regulatory T cells in HS patients supports the concept of dysbiosis as a factor in the preclinical HS lesions.

Global gene expression of histologically normal primary skin cells from BCNS subjects reveals "single-hit" effects that are influenced by rapamycin.

Studies of dominantly heritable cancers enabled insights about tumor progression. BCNS is a dominantly inherited disorder that is characterized by developmental abnormalities and postnatal neoplasms, principally BCCs. We performed an exploratory gene expression profiling of primary cell cultures derived from clinically unaffected skin biopsies of BCNS gene-carriers (PTCH1 +/-) and normal individuals. PCA and HC of untreated keratinocytes or fibroblasts failed to clearly distinguish BCNS samples from controls. These results are presumably due to the common suppression of canonical HH signaling in vitro. We then used a relaxed threshold (p-value <0.05, no FDR cut-off; FC 1.3) that identified a total of 585 and 857 genes differentially expressed in BCNS keratinocytes and fibroblasts samples, respectively. A GSEA identified pancreatic β cell hallmark and mTOR signaling genes in BCNS keratinocytes, whereas analyses of BCNS fibroblasts identified gene signatures regulating pluripotency of stem cells, including WNT pathway. Significantly, rapamycin treatment (FDR<0.05), affected a total of 1411 and 4959 genes in BCNS keratinocytes and BCNS fibroblasts, respectively. In contrast, rapamycin treatment affected a total of 3214 and 4797 genes in normal keratinocytes and normal fibroblasts, respectively. The differential response of BCNS cells to rapamycin involved 599 and 1463 unique probe sets in keratinocytes and fibroblasts, respectively. An IPA of these genes in the presence of rapamycin pointed to hepatic fibrosis/stellate cell activation, and HIPPO signaling in BCNS keratinocytes, whereas mitochondrial dysfunction and AGRN expression were uniquely enriched in BCNS fibroblasts. The gene expression changes seen here are likely involved in the etiology of BCCs and they may represent biomarkers/targets for early intervention.

Evidence for neurogenic inflammation in lichen planopilaris and frontal fibrosing alopecia pathogenic mechanism.

Lichen planopilaris (LPP) and frontal fibrosing alopecia (FFA) are lymphocytic scarring alopecias affecting primarily the scalp. Although both diseases may share some clinical and histopathological features, in the last decade, FFA has become an "epidemic" particularly in Europe, North and South America with unique clinical manifestations compared to LPP, thus, raising the idea that this disease may have a different pathogenesis. Symptoms such as scalp burning, pruritus or pain are usually present in both diseases, suggesting a possible role for nerves and neuropeptides in the pathogenesis of both diseases. Based on some previous studies, neuropeptides, such as substance P (SP) and calcitonin gene-related peptide (CGRP), have been associated with lipid metabolism and many chronic inflammatory disorders. In this study, we asked if these neuropeptides are associated with LPP and FFA scalp lesions. Alteration in the expression of SP and CGRP in affected and unaffected scalp skin from patients with both diseases was found with examination of sections using immunohistochemical techniques and confocal microscopy. We then quantitatively assessed and compared SP and CGRP expression from control, LPP and FFA scalp biopsies. Although LPP and FFA share similar histopathologic findings, opposite results were found in affected and unaffected scalp in the ELISA tests, suggesting that these diseases may have different pathogenic mechanisms. We also found presence of histopathological inflammation irrespective of evident clinical lesions, which raises the possibility that both diseases may be more generalized processes affecting the scalp.

An extended high-frequency ultrasound protocol for assessing and quantifying of inflammation and fibrosis in localized scleroderma.

Clinical characteristics of the lesions are used to identify activity and damage in localized scleroderma (LoS). For high-frequency ultrasound (HF-US), the features of active lesions were described. Clinical signs of activity and damage in LoS lesions were assessed with the use of Localized Scleroderma Cutaneous Assessment Tool (LoSCAT) and HF-US by two examiners independently. All US images were obtained using a 20MHz HF-US (DermaLab System, Cortex Technology, Hadsund, Denmark). The dermal thickness (DT) and echogenicity (intensity score, IS) of the LoS lesional dermis were measured in the area of each lesion with the highest score for erythema (ER), skin thickness (ST), and dermal atrophy (DAT). Measurements were compared to the site-matched unaffected skin. The relative difference of DT and IS values was calculated between each lesion and its normal control for comparison among different clinical scores for ER, ST, and DAT. A total of 92 lesions in 40 adult patients were examined with HF-US. Thirty one lesions were erythematous, 26 were in sclerosis, and 35 were in atrophy. A correlation between the clinical evaluation of the LoS lesions and US measurements was found. The sensitivity and specificity of HF-US were 97% and 90%, respectively. The positive predictive value was 83%, negative predictive value-98%. Interrater reliability was excellent for LoSCAT and HF-US findings. High-frequency ultrasound allows an accurate assessment of the inflammatory and fibrotic skin lesions in LoS.

Dynamic Optical Coherence Tomography Is a New Technique for Imaging Skin Around Lower Extremity Wounds.

Chronic wounds such as venous leg ulcers invariably heal slowly and recur. In the case of venous leg ulcers, poor healing of chronic wounds is variously attributed to ambulatory hypertension, impaired perfusion and diffusion, presence of chronic inflammation at wound sites, lipodermatosclerosis, and senescence. The aim of this study was to investigate whether a new technique, optical coherence tomography (OCT), which permits imaging of blood capillaries in the peri-wound skin, can provide new insights into the pathology. OCT and its recent variant, dynamic OCT, permit rapid noninvasive depth-resolved imaging of the capillaries in the superficial dermis via a handheld probe, showing the morphology and density of vessels down to 20 µm in diameter. We used dynamic OCT to investigate 15 chronic wounds and assess characteristics of the vessels at the 4 poles around the wounds, the wound bed, adjacent dermatosclerosis, and unaffected skin. The results of the study show that both vessel morphology and density in the wound edges are dramatically different from that in healthy skin, showing clusters of glomuleri-like vessels (knot-like forms or clumps) and an absence of linear branching vessels, and also greater blood perfusion. Such vessel shapes are reported to be associated with tissue growth. The OCT imaging procedure was rapid and well tolerated by patients and provided new information not available from other devices. Thus, OCT appears to have great promise as a tool for the evaluation and study of chronic ulcers.

Linear IgA bullous dermatosis

Aim: to present a clinical case of linear IgA bullous dermatosis.Materials and methods. A 44 years old patient complaining of skin rashes on the trunk and extremities, accompanied by severe itching was examined. We carried out a morphological investigation of biopsy samples derived from the lesion and apparently unaffected skin areas using the method of indirect immunofluorescence.Results. The patient having rashes in the form of multiple vesicles and small bubbles with a tight cover, which had been grouped into figures resembling pearl necklaces, demonstrated the presence of focal subepidermal cracks (subepidermal bubble in one location), as well as a linear deposition of IgA along the epidermal basement membrane. According to the clinical picture and following the histological and immunofluorescent investigation of skin biopsies, the patient was diagnosed with linear IgA bullous dermatosis. Lesion regression was achieved as a result of systemic therapy with prednisolone at a dose of 50 mg per day.Conclusion. The diagnosis of linear IgA bullous dermatosis should be made on the basis of skin biopsy investigation by the method of indirect immunofluorescence. Systemic glucocorticosteroids are seen as an effective approach to the treatment of such patients.

The Skin Microbiome in Atopic Dermatitis—a Potential Treatment Target?

Staphylococcus aureus (S. aureus) frequently colonize the skin of patients with atopic dermatitis (AD). The abundance of S. aureus increases during flares, accompanied by a reduction in bacterial diversity. This flare-associated imbalance in the cutaneous microflora (dysbiosis) correlates with disease severity. However, the causality of this association has not yet been fully established, and this review aims to further explore the relation between the skin microbiome and AD along with the clinical implications hereof. Recently, it has been shown that the skin microbiome in clinically unaffected skin of AD patients differs from that of healthy individuals. In addition, mutations in the gene encoding the structural protein filaggrin (FLG) have been shown to influence the skin microbiome. Skin barrier impairments, which characterize the AD phenotype, influence the skin microbiome and increase the susceptibility to colonization with S. aureus. In turn, S. aureus can promote skin inflammation by a broad spectrum of virulence factors. Modulation of the skin microbiome by transferring beneficial skin commensals to the skin of AD patients may represent a promising strategy for the future management of AD.

Prevalence and Viral Loads of Cutaneous Human Polyomaviruses in the Skin of Patients With Chronic Inflammatory Skin Diseases.

Human skin microorganisms have been associated with various skin diseases. However, most studies have focused on bacterial communities, and little is known about normally resident skin viruses such as the Polyomaviridae and their association with cutaneous disorders. We investigated the infection levels of Merkel cell polyomavirus (MCPyV), human polyomavirus 6 (HPyV6), and human polyomavirus 7 (HPyV7), using triplet skin swabs collected from lesional and nonlesional skins of 86 Japanese patients with inflammatory skin diseases and mycosis fungoides, and from 149 healthy control individuals. This age-matched case-control study provides the first analyses of the loads of polyomaviruses in association with various skin diseases. The viral loads were significantly higher for HPyV6/HPyV7 and lower for MCPyV in patients with psoriasis. The viral load variation was observed not only at lesion sites, but also at clinically unaffected skin sites in most of the patients. The viral strains tested were all of the Asian/Japanese genotype. Our findings suggest a covariation in the infection levels of cutaneous polyomaviruses in certain inflammatory skin conditions. Worldwide prospective longitudinal studies are warranted to understand the influence of such alterations on the pathogenesis of inflammatory skin disorders.

Genetic Abnormalities in Large to Giant Congenital Nevi: Beyond NRAS Mutations

Large and giant congenital melanocytic nevi (CMN) are rare melanocytic lesions mostly caused by postzygotic NRAS alteration. Molecular characterization is usually focused on NRAS and BRAF genes in a unique biopsy sample of the CMN. However, large/giant CMN may exhibit phenotypic differences among distinct areas, and patients differ in features such as presence of multiple CMN or spilus-like lesions. Herein, we have characterized a series of 21 large/giant CMN including patients with spilus-type nevi (9/21 patients, 42.8%). Overall, 53 fresh frozen biopsy samples corresponding to 40 phenotypically characterized areas of large/giant CMNs and 13 satellite lesions were analyzed with a multigene panel and RNA sequencing. Mutational screening showed mutations in 76.2% (16/21) of large/giant CMNs. A NRAS mutation was found in 57.1% (12/21) of patients, and mutations in other genes such as BRAF, KRAS, APC, and MET were detected in 14.3% (3/21) of patients. RNA sequencing showed the fusion transcript ZEB2-ALK and SOX5-RAF1 in large/giant CMN from two patients without missense mutations. Both alterations were not detected in unaffected skin and were detected in different areas of affected skin. These findings suggest that large/giant CMN may result from distinct molecular events in addition to NRAS mutations, including point mutations and fusion transcripts.

Systemic and stratum corneum biomarkers of severity in infant atopic dermatitis include markers of innate and T helper cell-related immunity and angiogenesis.

SummaryBackgroundBiomarkers of atopic dermatitis (AD) are largely lacking, especially in infant AD. Those that have been examined to date have focused mostly on serum cytokines, with few on noninvasive biomarkers in the skin.ObjectivesWe aimed to explore biomarkers obtainable from noninvasive sampling of infant skin. We compared these with plasma biomarkers and structural and functional measures of the skin barrier.MethodsWe recruited 100 infants at first presentation with AD, who were treatment naive to topical or systemic anti‐inflammatory therapies, and 20 healthy children. We sampled clinically unaffected skin by tape stripping the stratum corneum (SC). Multiple cytokines and chemokines and natural moisturizing factor were measured in the SC and plasma. We recorded disease severity and skin barrier function.ResultsNineteen SC and 12 plasma biomarkers showed significant differences between healthy and AD skin. Some biomarkers were common to both the SC and plasma, and others were compartment specific. Identified biomarkers of AD severity included T helper 2‐skewed markers [interleukin (IL)‐13, CCL17, CCL22, IL‐5]; markers of innate activation (IL‐18, IL‐1α, IL1β, CXCL8) and angiogenesis (Flt‐1, vascular endothelial growth factor); and others (soluble intercellular adhesion molecule‐1, soluble vascular cell adhesion molecule‐1, IL‐16, IL‐17A).ConclusionsWe identified clinically relevant biomarkers of AD, including novel markers, easily sampled and typed in infants. These markers may provide objective assessment of disease severity and suggest new therapeutic targets, or response measurement targets for AD. Future studies will be required to determine whether these biomarkers, seen in very early AD, can predict disease outcomes or comorbidities.

Dysregulation of the Wnt signaling pathway in South African patients with diffuse systemic sclerosis.

The objectivewas to explore changes in gene expression in Wnt pathway genes in skin samples of black South Africans with diffuse cutaneous systemic sclerosis (dcSSc). Affected (forearm) and unaffected (upper back) skin samples of eight Black South Africans with active early dcSSc were compared to skin samples from seven ethnically matched control subjects. The Wnt Pathway Plus RT2 Profiler qPCR Array was used to determine gene expression and analyzed for differential expression between cases and controls. Selective validation was done using single-gene TaqMan assays. Several genes were similarly upregulated in both affected and unaffected skin of the dcSSc patients compared to controls. These included the Wnt ligands WNT7A and WNT10A, the frizzled receptors FZD8 and FZD9, intracellular signaling proteins AXIN1 and AXIN2, and the pathway target genes FGF4 and MMP7. Principal component analysis revealed patients clustering into two groups, which co-segregated with clinical features of interstitial lung disease and/or inflammatory myopathy, or the absence of an inflammation phenotype. These two groups showed paradoxical gene expression of the genes TCF7, SOX17, and FRZB in affected and unaffected skin. This study provides further evidence of dysregulation of gene expression at various levels of the Wnt signaling pathway in dcSSc. Moreover, principal component analysis showed two distinct patient clusters of gene expression, which co-segregated with the presence or absence of clinical inflammatory features, and may reflect different pathological pathways in dcSSc.

SENSITIVITY OF MULTI-RESISTANT PSEUDOMONAS AERUGINOSA STRAINS DEPENDING ON LOCALIZATION OF INFECTIOUS PROCESS

Objective of work was study of antibiotic resistance peculiarities and isolation localization of multi-resistant Pseudomonas aeruginosa strains.&#x0D; Materials and methods. The objects of investigation were multi-resistant P. aeruginosa strains isolated from pleural exudate, bronchial flushing fluid, blood, samples of wound surface and unaffected skin. Identification of the obtained cultures was carried out for morphological, tinctorial and cultural properties as well as using an automatic microbiological analyzer Vitek 32 (BioMerieux). The selected cultures were tested for sensitivity to a wide range of antibiotics using Vitek 32 (BioMerieux).&#x0D; Results. 18 cultures were selected among P. aeruginosa strains isolated from patients. Correspondingly to antibiotic resistance level, these strains were divided into three groups. The first group includes 7 strains (39%) with maximum resistance, representatives of the second group – 5 isolates (28%) were characterized by high resistance, and 6 cultures (33%) were referred to microorganisms with moderate resistance – the third group. Among 12 strains from the first and second groups, only two cultures were isolated in the intensive care unit. But, four cultures were isolated in the burn department, three – in orthopedics and traumatology, two – in surgery, and one – in proctology. It was found that in 50% of cases (9 strains) the cultures studied were isolated from the wound surface in patients with skin burns and after surgical intervention. At the same time, 3 strains (16% of all microorganisms) were localized in the composition of bronchial washings, as well as 2 strains (11% of all cultures) from pleural exudate and blood. From the abscess and skin of the ear, there was isolated one by one strain (6%).&#x0D; Conclusions. More often P. aeruginosa multi-resistant strains were isolated from the wound surface, however, the microorganisms isolated from pleural exudate were characterized the highest resistance to antibiotics, incl. to meropenem. All studied P. aeruginosa cultures retained sensitivity only to colistin and phosphomycin. The activity of other antibiotics was significantly limited, as only the netilmicin (43% of the sensitive strains), meropenem (41%), amikacin (33%), ciprofloxacin (28%) and norfloxacin (28%) influenced the isolated microorganisms.

Treatment of Pityriasis Rubra Pilaris with Adalimumab: A Case Report

Pityriasis Rubra Pilaris (PRP) is a rare inflammatory dermatosis of unknown etiology and variable presentation. Common clinical features include hyperkeratotic follicular papules, palmoplantar hyperkeratosis and well-demarcated red-orange scaly plaques interspersed with islands of unaffected skin. A limited body of anecdotal evidence predominantly supports the use of systemic retinoids and/or methotrexate in treating the disease. In a subset of these patients, there has been a documented role for biologic tumor necrosis factor (TNF) inhibitors, especially in patients who have failed retinoid or antimetabolite therapy. We present a case of a woman whose PRP responded favorably to adalimumab, highlighting the role of TNF inhibitors and the need for their continued exploration in the treatment of PRP.

Multiphotonic staging of chronic wounds and evaluation of sterile, optical transparent bacterial nanocellulose covering: A diagnostic window into human skin.

Diagnostics of healing, infection, and inflammation in chronic wounds in comparison with physiological wound healing in acute wounds may help for therapy decisions toward individualized therapy management. With emerging new optical techniques the coupling of optical diagnostic devices with tissue provides a great challenge. Traditional coupling with cover slips is used since the early days of microscopy. In modern health care, hygienic covering of surfaces is necessary to avoid infections and cross-contaminations. Measurements in chronic wounds were performed at three different areas including the center of the wound, the border of the wound and healthy skin as comparison area. For each measurement area, three vertical stacks were taken by MPT. Additionally, three different optical measuring procedures (MPT, OCT, CLSM) were used for the examination of BNC foil. Examinations of BNC foil were carried out at two different areas of healthy skin compared to a standard setup as control. The MPT evaluation revealed a distinct difference in the second harmonic generation-to-autofluorescence aging index of dermis (SAAID) behavior between the vertical stacks taken at central wound areas and wound margins as well as unaffected skin. Through BNC foil covers, MPT CLSM and OCT images were captured with good quantitative and qualitative results. Phases in chronic wounds could be matched with physiologically healing in acute wounds according to SAAID and MPT imaging. BNC provided an alternative covering for MPT, OCT, and CLSM with clear morphological images.

Psoriasis and Microbiota: A Systematic Review.

Background: Recent advances have highlighted the crucial role of microbiota in the pathophysiology of chronic inflammatory diseases as well as its impact on the efficacy of therapeutic agents. Psoriasis is a chronic, multifactorial inflammatory skin disorder, which has a microbiota distinct from healthy, unaffected skin. Aim: Through an extensive review of the literature, we aim to discuss the skin and gut microbiota and redefine their role in the pathogenesis of psoriasis. Conclusions: Unfortunately, the direct link between the skin microbiota and the pathogenesis of psoriasis remains to be clearly established. Apart from improving the course of psoriasis, selective modulation of the microbiota may increase the efficacy of medical treatments as well as attenuate their side effects.

Characterizing the tissue dielectric constant of skin basal cell cancer lesions

Measuring tissue dielectric constant (TDC) of cancer tissues to distinguish them from normal or non-cancerous tissues has been an active area of research that has targeted several different cancer types usually using in vitro specimens. The goal of this study was to determine if and to what extent TDC values measured in vivo at 300MHz using a simple hand-held measuring device might differentiate between skin cancer lesions and non-cancerous skin. Triplicate TDC measurements were made in 32 patients who were subsequently diagnosed with skin basal cell carcinoma (BCC) and in 14 patients subsequently diagnosed as having non-cancerous lesions. Lesion TDC values were compared to contralateral unaffected skin and between lesion types. A significantly lower TDC value (mean±SD) of BCC lesions (TDCL ) vs TDC values of contralateral non-affected skin (TDCC ) was found (22.4±16.2 vs 38.1±15.2, P<.00001). A similar pattern was found for non-cancerous lesions with lesion TDC values less than non-affected skin (14.5±9.0 vs 29.1±9.0, P<.0001). However, TDC values were not statistically different between BCC lesions and non-cancerous lesions (22.4±16.2 vs 14.5±9.0, P=.096) and calculated TDCL /TDCC ratios between BCC lesions and non-cancerous lesions also were not significantly different (0.596±0.345 vs 0.501±0.261, P=.364). (1) Main results do not support using TDC measurements to differentiate in vivo skin cancer lesions from non-cancerous lesions. (2) TDC values strongly suggest reduced water content of both cancerous and non-cancerous lesions. (3) Lesion TDC measurements provide reference values for future studies.

1096 Non-invasive tape sampling reveals a type I interferon RNA signature in cutaneous lupus erythematosus that distinguishes affected from unaffected and healthy volunteer skin

1096 Non-invasive tape sampling reveals a type I interferon RNA signature in cutaneous lupus erythematosus that distinguishes affected from unaffected and healthy volunteer skin