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Background Hand eczema (HE) is frequently associated with Staphylococcus aureus; however, its role in the pathogenesis of HE is poorly understood. Objective To investigate the temporal variation in S aureus subtypes, ie, clonal complex (CC) types, on the hands and relate it to S aureus colonization in the nose and severity in a cohort of HE patients. Methods S aureus from the hands and nose of 50 adult HE patients and 50 controls was prospectively identified at 5 visits over 3 weeks. Results S aureus was identified on the hands of 23 (46%) patients at 2 or more visits and on the hands of 1 control once. Of the HE patients with S aureus colonization, 78% had the same S aureus CC type over time. Twenty-one patients had the same S aureus CC type on the hands and in the nose. Persistent colonization was strongly related to an increased disease severity. Limitations A relatively small S aureus culture-positive population. Conclusion The temporal stability of S aureus CC type and high occurrence of the identical subtypes on the hands and in the nose imply that S aureus colonization in patients with HE is of a more permanent nature. Taken together with the finding that persistent colonization and HE severity are clearly related, our results indicate that S aureus may contribute to the perpetuating course of HE.

Ongoing investigations of the human skin microbiome strongly suggest a connection to skin diseases and skin health. This review provides an overview of recent literature on the skin microbiome in relation to skin diseases, with a specific focus on common inflammatory skin conditions, such as atopic dermatitis, psoriasis, hidradenitis suppurativa, acne, and rosacea. In healthy subjects, the skin microbiome mediates fundamental processes involving the immune response and epidermal development and differentiation. Microbiome characteristics in inflammatory skin diseases differ depending on disease, as both topography and disease severity and even host genetics seem to influence the microbiome composition. Not only the bacterial species are important but also different strains within the same species can act differently, where some can be commensal and protect against microbial dysbiosis, whereas others can induce skin inflammation and immune reactions in humans. The interplay between skin microbes, host genetics, and the immune system is anticipated to be of importance for both the development and severity of many skin diseases. However, the causality of specific pathogens and the effect on the pathogenesis in relation to inflammatory skin diseases is yet to be understood.

Investigation of changes in the skin microbiome following treatment of atopic dermatitis (AD) with dupilumab may provide valuable insights into the skin microbiome as a therapeutic target. The aim of this study is to assess changes in the AD skin microbiome following treatment of AD with dupilumab (n = 27). E-swabs were collected from nose, lesional, and nonlesional skin before and after 16 weeks of dupilumab therapy, and the microbiome was analyzed by 16S rRNA and tuf gene sequencing. Data for 17 patients with milder disease receiving treatment with non-targeted therapies are also presented. The results show that both groups experienced clinical improvement (p &lt, 0.001) following dupilumab therapy and that Shannon diversity increased and bacterial community structure changed. The relative abundance of the genus Staphylococcus (S.) and S. aureus decreased, while that of S. epidermidis and S. hominis increased. No significant changes were observed for patients receiving non-targeted treatments. The increases in S. epidermidis and S. hominis and the decrease in S. aureus correlated with clinical improvement. Furthermore, changes in S. hominis and S. epidermidis correlated inversely with S. aureus. In conclusion, treatment with dupilumab significantly changed the skin microbiome and decreased S. aureus. Our results suggest a favorable role of commensal staphylococci in AD.

We aimed to explore the association of key clinical characteristics with disease severity in atopic dermatitis (AD) and its relation to components of the atopic march in a large hospital cohort. Outpatients with AD referred to the Department of Dermatology, Bispebjerg Hospital, Copenhagen, Denmark, between January 2012 and December 2017, were compared based on disease severity (SCORAD); mild ( 50). A total of 470 AD patients were included: 122 small children ( 15 years of age). A significant difference between severity groups in small children was observed for FLG mutation carrier status (16.7 vs. 30.2 vs. 60.0% mutation carriers among patients with mild, moderate and severe AD, respectively, p = 0.012) and self-rated health (3.2 vs. 2.7 vs. 2.8 with 4 being excellent health, p = 0.022). A significant difference between severity groups in adults was observed for male sex (24.4 vs. 39.8 vs. 52.9%, p = 0.003), serum total IgE (577 vs. 1269 vs. 2379 × 103 IU/L, p

Background Initially after tattooing, the skin barrier function is broken. However, the long-term impact of clinically healed tattoos on this has never been studied. The aim was to investigate the long-term effect on the skin barrier function in normal tattoos and examples of tattoos with chronic inflammatory complication. Methods Participants were recruited from the "Tattoo clinic" of the Dermatological Department on Bispebjerg Hospital in Denmark, where patients with complicated tattoo reactions are treated. Transepidermal water loss (TEWL), conductance, capacitance, and pH were measured in tattooed skin with regional control measurements in normal non-tattooed skin. Natural moisturizing factor (NMF) was measured in collected tape strips. Results Twenty six individuals with 28 tattoos were included, that is, 23 normal tattoos without any pathologic reaction and 5 tattoos with chronic inflammatory complications. No significant differences were found in tattooed versus non-tattooed skin with respect to TEWL (median values 6.6 vs 7.2 g/m2 /h), conductance (76 vs 78 a.u.), pH (5.94 vs 5.79), and NMF (0.58 vs 0.59 mmol/g protein). Capacitance (64 vs 57 a.u.) was higher in tattooed skin compared to non-tattooed skin (P = 0.006). Similar results were found in tattoos with inflammatory reactions. Conclusion Overall, skin tattoos do not affect the long-term skin barrier function markedly. The skin capacitance was, however, affected in tattooed skin areas compared to non-tattooed skin areas.

Background: Treatment of atopic dermatitis (AD) may be challenging, therefore some patients seek complementary and alternative medications (CAM). We determined prevalence and predictors for CAM use in a hospital cohort of AD patients. Material and Methods: Between January 1, 2012, and December 31, 2017, AD patients referred to the dermatological outpatient clinic at Bispebjerg Hospital were included in the study. Information on CAM use, demographics and disease characteristics were obtained by questionnaire, and associations were determined by χ2 and t test separately for children (< 16 years) and adults (≥16 years). Results: In total 441 filled in the questionnaire on AD, and 433 patients responded to the questions about CAM use: 198 children and 235 adults. A total of 137 (31.6%) had used one or more CAM. CAM use in children was significantly associated with prior use of ≥2 conventional treatments (p = 0.047) and topical calcineurin inhibitors (p = 0.021), a higher number of affected eczema sites (p < 0.001) including more frequent affection of the face and extremities, a higher SCORAD score (p = 0.045), and low mean overall self-rated health (p = 0.003). CAM use in adults was significantly associated with lower age of onset of AD (p = 0.004), comorbid allergic rhinoconjunctivitis (p = 0.039), frequent use of moisturizing cream (p = 0.024), facial and neck eczema (p = 0.005) and high educational level (p = 0.043). Conclusion: CAM use is frequent in both children and adult AD patients. CAM users are characterized by long disease duration, a significant disease burden and by having a longer education. The high prevalence of CAM may indicate that patients’ expectations regarding treatment of AD are not redeemed in the conventional health care system.

Background: A growing body of evidence links various biomarkers to atopic dermatitis (AD). Still, little is known about the association of specific biomarkers to disease characteristics and severity in AD. Objective: To explore the relationship between various immunological markers in the serum and disease severity in a hospital cohort of AD patients. Methods: Outpatients with AD referred to the Department of Dermatology, Bispebjerg Hospital, Copenhagen, Denmark, were divided into groups based on disease severity (SCORAD). Serum levels of a preselected panel of immunoinflammatory biomarkers were tested for association with disease characteristics. Two machine learning models were developed to predict SCORAD from the measured biomarkers. Results: A total of 160 patients with AD were included; 53 (33.1%) with mild, 73 (45.6%) with moderate, and 34 (21.3%) with severe disease. Mean age was 29.2 years (range 6–70 years) and 84 (52.5%) were females. Numerous biomarkers showed a statistically significant correlation with SCORAD, with the strongest correlations seen for CCL17/thymus and activation-regulated chemokine (chemokine ligand-17/TARC) and CCL27/cutaneous T cell-attracting-chemokine (CTACK; Spearman R of 0.50 and 0.43, respectively, p < 0.001). Extrinsic AD patients were more likely to have higher mean SCORAD (p < 0.001), CCL17 (p < 0.001), CCL26/eotaxin-3 (p < 0.001), and eosinophil count (p < 0.001) than intrinsic AD patients. Predictive models for SCORAD identified CCL17, CCL27, serum total IgE, IL-33, and IL-5 as the most important predictors for SCORAD, but with weaker associations than single cytokines. Conclusions: Specific immunoinflammatory biomarkers in the serum, mainly of the Th2 pathway, are correlated with disease severity in patients with AD. Predictive models identified biomarkers associated with disease severity but this finding warrants further investigation.

We explored differences between lesional and non-lesional skin and anatomical variation in epidermal biomarker levels using stratum corneum (SC) tape strips in adult patients with atopic dermatitis (AD). SC tape strips from three distinct anatomical locations (upper extremity, trunk and lower extremity) and serum samples were collected from 25 adult patients with AD (mean age 34.8 years). Inflammatory cytokines in tape strips and serum, natural moisturizing factor (NMF), skin pH and trans-epidermal water loss (TEWL) were measured. Disease severity was assessed using SCORing of Atopic Dermatitis (SCORAD) scores, respectively, global (overall) and local (lesion specific based on objective signs) SCORAD. A clear differentiation between serum and epidermal biomarker levels was observed. Furthermore, a strong intrasample correlation between biomarker expression was observed.

Tape stripping is a promising technique for assessment of epidermal biomarkers in inflammatory skin diseases. However, to facilitate its implementation in the clinical practice, a thorough validation regarding sampling strategy is needed. Knowledge of biomarkers variation in concentration across stratum corneum is scarce. Therefore, this study aimed to assess the variability of cytokines across stratum corneum using tape stripping technique by consecutive application of 21 adhesive tapes (D-squame) to lesional and non-lesional skin from 15 patients with atopic dermatitis (AD) and 16 healthy controls. Concentration of cytokines (IL-1α, IL-1b, IL-5, IL-18, IFN-γ, CCL17, CCL22, CCL27, CXCL8, CXCL10, TNF-α, TSLP, VEGFA) was determined in five different depths, using multiplex immunoassay. Comparing tape 4 with tape 21, no cytokine changed significantly in concentration in AD lesional skin. In AD non-lesional skin a small decrease was found for CCL17, CXCL8 and CXCL10. For healthy controls, a decrease was found for IL-1a, IL-1b, VEGFA and an increase for IL-18. Differences were found between AD skin and healthy control skin. Concentration of cytokines was stable across stratum corneum, indicating that sampling of only one tape from the stratum corneum is reliable in reflecting the overall cytokine milieu. Differences between AD and healthy skin confirm robustness of tape stripping for measuring cytokine levels.

Tape-stripping is a minimally invasive approach for skin sampling that captures the cutaneous immune/barrier abnormalities in atopic dermatitis (AD). However, tape-strips have not been used to evaluate molecular changes with therapeutic targeting. In this study, we sought to characterize the proteomic signature of tape-strips from AD patients, before and after dupilumab therapy. Twenty-six AD patients were treated with every-other-week dupilumab 300 mg for 16 weeks. Tape-strips from lesional and non-lesional skin were collected before and after treatment, and analyzed with the Olink proteomic assay. Using criteria of fold-change>1.5 and FDR < 0.05, 136 proteins significantly decreased after dupilumab treatment, corresponding to an overall mean improvement of 66.2% in the lesional vs. non-lesional AD proteome. Significant decreases after dupilumab were observed in immune markers related to general inflammation (MMP12), Th2 (CCL13/CCL17), Th17/Th22 (IL-12B, CXCL1, S100A12), and innate immunity (IL-6, IL-8, IL-17C), while the Th1 chemokines CXCL9/CXCL10 remained elevated. Proteins related to atherosclerosis/cardiovascular risk (e.g., SELE/E-selectin, IGFBP7, CHIT1/ chitotriosidase-1, AXL) also significantly decreased after treatment. Dupilumab therapy suppressed AD-related immune biomarkers and atherosclerosis/cardiovascular risk proteins. Tape-strip proteomics may be useful for monitoring therapeutic response in real-life settings, clinical trials, and longitudinal studies for AD and beyond.

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.

Decreased levels of antimicrobial peptides (AMPs) in atopic dermatitis (AD) have previously been reported and have been linked to the increased susceptibility to skin infections found in AD patients. This study intents to identify AMPs: hBD-2, hBD-3, RNase7, psoriasin and LL-37 in AD patients and healthy controls, and determine concentrations in consecutive depths of the outer most skin layers. Tape stripping was used on lesional and non-lesional skin. From each skin site, 35 consecutive tape strips were collected and pooled in groups of 5. Commercially available ELISA kits were used to determine AMP concentration in stratum corneum samples. hBD-2, hBD-3, RNase7 and psoriasin were identified in stratum corneum samples. hBD-3-level was markedly higher in AD non-lesional skin compared to healthy controls, and a similar trend was observed for RNase7. Most AMPs were distributed evenly through 35 tape strips, implying a homogeneous distribution of antimicrobial defense in the outer most skin layers. The findings indicate that AD patients may not suffer from a general baseline deficiency in AMPs, and that the innate immune defense is present throughout the stratum corneum, both insights of importance for understanding the role of AMPs in AD.

SummaryBackground Atopic dermatitis (AD) is a prevalent disease with significant impact on physical health and quality of life. Staphylococcus aureus has been directly correlated to disease severity, and may also be a contributing causal factor in the pathogenesis of AD. Objectives The primary aim was to assess differences in S. aureus colonization in patients with AD with and without filaggrin gene mutations. The secondary aim was to assess disease severity in relation to S. aureus colonization. Exploratory analyses were performed to investigate S. aureus genetic lineages in relation to filaggrin gene (FLG) mutations and disease severity. Methods Adult patients with AD (n = 101) were included in the study. Bacterial swabs were taken from lesional skin, nonlesional skin and the nose. Swabs positive for S. aureus were characterized by spa and the respective clonal complex (CC) type assigned. Patients were characterized with respect to disease severity (Scoring Atopic Dermatitis) and FLG mutations (n = 88). Fisher's exact test was used to analyse differences in S. aureus colonization in relation to FLG mutations. Results Of the 101 patients included, 74 (73%) were colonized with S. aureus. Of the colonized patients, 70 (95%) carried only one CC type in all three different sampling sites. In lesional skin, S. aureus was found in 24 of 31 patients with FLG mutations vs. 24 of 54 wild-type patients (P = 0·0004). Staphylococcus aureusCC1 clonal lineage was more prevalent in patients with FLG mutations (n = 10) than in wild-type patients (n = 2) (P = 0·003). No specific bacterial lineage was linked to disease severity. Conclusions Increased S. aureus colonization in patients with AD with FLG mutations, and increased prevalence of CC1 in patients with FLG mutations, suggest that host–microbe interactions and clonal differences in S. aureus are important for colonization of AD skin.

Background A strong link between disease severity and Staphylococcus aureus colonization of the skin has been reported in patients with atopic dermatitis (AD). Objectives To examine temporal variations in S. aureus colonization and S. aureus CC type in patients with AD, and to investigate links to disease severity, skin barrier properties and filaggrin gene (FLG) mutations. Methods This was a follow-up study of a cohort of 101 adult patients with AD recruited from an outpatient clinic. Bacterial swabs were taken at baseline and follow-up from lesional skin, nonlesional skin and the nose. Swabs positive for S. aureus were characterized by spa and the respective clonal complex (CC) type was assigned. Patients were characterized with respect to disease severity [Scoring Atopic Dermatitis (SCORAD)], skin barrier properties [transepidermal water loss (TEWL), pH] and FLG mutations. Results In total, 63 patients participated in a follow-up visit. Twenty-seven patients (43%) were colonized at both visits, 27 were colonized at only one visit and nine (14%) were not colonized at either visit. Of patients colonized at both visits, 52% remained colonized with the same CC type at follow-up. Change in CC type was related to an increase in SCORAD of 10·7 points; patients who carried the same CC type had a reduction in SCORAD of 4·4 points. Significantly higher skin pH was found in patients colonized at both visits, while change in CC type was not related to TEWL, pH or FLG mutations. Conclusions The data indicate that temporal variation in S. aureus CC type is linked to flares of the disease.

Background Staphylococcus aureus skin colonization is common in patients with atopic dermatitis (AD) and is associated with risk of skin infections. AD patients therefore often receive antibiotic treatments, including topical treatment with fusidic acid, which have been associated with resistance development. Objectives To examine the prevalence of antibiotic resistance in S. aureus isolated from Danish AD patients, with a primary focus on fusidic acid resistance and the genetic mechanisms that underlie it. Methods One hundred and thirty-eight S. aureus isolates collected from lesional skin (n = 54), non-lesional skin (n = 27) and anterior nares (n = 57) from 71 adult AD patients were included in the study. Isolates were tested for susceptibility to 17 selected antibiotics. S. aureus whole-genome sequences were used to examine the genetic determinants of fusidic acid resistance (fusA or fusE mutations or carriage of fusB or fusC genes). Results One hundred and nine isolates (79%) were resistant to at least one of the tested antibiotics, with the most prevalent resistances being to penicillin (55%), fusidic acid (41%) and erythromycin (11%). The primary genetic mechanisms of fusidic acid resistance were carriage of fusC (57%) or mutations in fusA (38%). The most prevalent S. aureus lineage was ST1 (23%). All ST1 isolates carried fusC. Conclusions S. aureus fusidic acid resistance, caused by either fusA mutations or fusC gene carriage, is a major concern among AD patients. Resistant S. aureus might spread from the patients to the community, indicating the need to reduce the use of fusidic acid in the treatment of AD.

Wet work tasks are the most common exposures leading to occupational irritant contact dermatitis. Use of liquid-proof gloves is recommended when performing wet work, however, gloves may also contribute to impairment of the skin barrier and development of irritant contact dermatitis. The aim of this study is to review the literature on the effects of glove occlusion on skin barrier function. The PubMed database was searched up to 1 February 2015 for articles on the association between glove occlusion and skin barrier function, including human studies only and in English. Only experimental studies including assessment of the skin barrier function were included in the data analysis. Thirteen articles were identified, 8 with focus on occlusion alone, 7 with focus on occlusion in combination with irritant exposure (some overlapping), and 2 field studies. In conclusion, data from the literature showed that the negative effect of occlusion in itself is limited, and that only extensive and long-term occlusion will cause barrier impairment. However, studies investigating combined effect of occlusion and exposure to soaps/detergents indicate that occlusion significantly enhances the skin barrier damage caused by detergents/soaps in a dose-response fashion.

The atopic diseases: atopic dermatitis, asthma and allergic rhinoconjunctivitis are frequent diseases in the population occurring sequentially in the young (the atopic march). The discovery of filaggrin gene (FLG) mutations and impairments in the skin barrier as predisposing factors for atopic dermatitis and subsequent asthma and atopic sensitization in the context of eczema has improved our understanding of the atopic march. The atopic diseases can now be viewed upon as causally related conditions—rather than sequentially occurring manifestations of the same underlying atopic disease state—with atopic dermatitis and FLG mutations being a prerequisite for the development of the other atopic diseases, particularly asthma. This review discusses the role of the skin barrier function, particularly the role of FLG mutations, in the atopic march.

Contact sensitization is common and affects up to 20% of the general population. The clinical manifestation of contact sensitization is allergic contact dermatitis. This is a clinical expression that is sometimes difficult to distinguish from other types of dermatitis, for example irritant and atopic dermatitis. Several studies have examined the pathogenesis and severity of allergic contact dermatitis by measuring the absence or presence of various biomarkers. In this review, we provide a non-systematic overview of biomarkers that have been studied in allergic contact dermatitis. These include genetic variations and mutations, inflammatory mediators, alarmins, proteases, immunoproteomics, lipids, natural moisturizing factors, tight junctions, and antimicrobial peptides. We conclude that, despite the enormous amount of data, convincing specific biomarkers for allergic contact dermatitis are yet to be described.

Probiotic supplementation is a promising preventive strategy for atopic dermatitis (AD). To help clarifying the significance of timing with respect to prevention of AD, we here evaluate the benefit of prophylactic use of probiotic supplementation in neonates younger than 30 weeks of gestation. Preterm children from the Department of Neonatology, Rigshospitalet, Denmark from two different admission periods were included in a historically controlled cohort study. Neonates from January 2007 to February 2010, not treated with and neonates from March 2010 to February 2013 treated with probiotic were enrolled. Main outcome was prevalence of AD, and secondary outcomes were use of topical corticosteroids, and number of skin-related visits to GPs and dermatologists. 527 preterm neonates were included in the study, 249 treated and 278 not treated with probiotics. Response rate for the two cohorts was 76.7 and 77.7% respectively. The prevalence of AD was similar in the two groups (20.9% in the probiotic treated group versus 17.1% in the not treated group, p = 0.33). No significant differences were found between the groups with respect to treatment with topical corticosteroids, or visits at GPs or dermatologist. We found no indication that probiotics may prevent AD when administered to neonates

Importance Skin microbiome correlates with disease severity for lesional and nonlesional skin, indicating a global influence of atopic dermatitis (AD). A relation between skin microbiome and filaggrin gene (FLG) mutations proposes a possible association between skin microbiome and host genetics. Objectives To assess skin and nasal microbiome diversity and composition in patients with AD and compare with healthy controls, and to investigate the microbiome in relation to disease severity and FLG mutations in patients with AD. Design, Setting, and Participants An observational case-control study of 45 adult healthy controls and 56 adult patients with AD was carried out from January 2015 to June 2015 in a tertiary referral center, Department of Dermatology, Bispebjerg Hospital, Denmark. Exposures Bacterial swabs were taken from patients with AD (lesional skin, nonlesional skin, and anterior nares) and from healthy controls (nonlesional skin and anterior nares). Eczema severity was assessed and FLG mutations noted. Bacterial DNA was extracted from swabs, and V3-V4 16S rDNA regions amplified with PCR. Samples were analyzed at Statens Serum Institut September 2015 to September 2016. Bioinformatics analyses of the microbiome were analyzed using R statistical software (version 3.3.1, R Foundation Inc). Main Outcomes and Measures Skin microbiomes were investigated using next-generation sequencing targeting 16S ribosomal RNA. Results Microbiome alpha diversity was lower in patients with AD compared with healthy controls in nonlesional skin (effect size, 0.710; 95% CI, 0.27-1.15; P = .002), lesional skin (effect size, 0.728; 95% CI, 0.35-1.33; P = .001), and nose (effect size, 1.111; 95% CI, 0.48-0.94; P P = .02) and nonlesional skin (effect size, 0.451; 95% CI, 0.04-2.44; P = .04) in patients with AD. Microbiome composition in AD nonlesional skin was linked to FLG mutations. Conclusions and Relevance An altered microbiome composition in patients with AD in nonlesional skin, lesional skin, as well as nose, suggests a global influence of AD. Microbiome composition in AD nonlesional skin is associated with FLG mutations, proposing a possible association between the skin microbiome and host genetics.

Surface scanning of the face of a suspect is presented as a way to better match the facial features with those of a perpetrator from CCTV footage. We performed a simple pilot study where we obtained facial surface scans of volunteers and then in blind trials tried to match these scans with 2D photographs of the faces of the volunteers. Fifteen male volunteers were surface scanned using a Polhemus FastSCAN Cobra Handheld Laser Scanner. Three photographs were taken of each volunteer's face in full frontal, profile and from above at an angle of 45 degrees and also 45 degrees laterally. Via special software (MIMICS and Photoshop) the surface scans were matched with the photographs in blind trials. The matches were graded as: a good fit; possible fit; and no fit. All the surface scans and photos were matched correctly, although one surface scan could be matched with two angled photographs, meaning that the discriminatory value was 86.7%. We also tested the surface scanner in terms of reliability in establishing point measures on skulls, and compared with physical measurements performed by calipers. The variation was on average 1 mm for five cranial measures. We suggest how surface scanning might be applied in forensic facial identification.

Atopic dermatitis is a multifactorial chronic disease that poses a great burden for patients and society. In recent decades the prevalence has increased substantially in many countries, notably in Western societies, and the causes for this increase are not completely understood. There are still many unanswered questions regarding atopic dermatitis with respect to aetiology, pathophysiology, co-morbidity as well as subgrouping and treatment of the disease. Establishment of the Danish Atopy Database (DAD), a cohort with ongoing inclusion of outpatients with atopic dermatitis from a tertiary referral centre, allows the study of these aspects of the disease. Herein we present our methodological considerations in regards to establishment of this cohort.

SummaryBackground Skin infections related to disrupted antimicrobial defence are a common problem in atopic dermatitis (AD). Altered levels of antimicrobial peptides, including human β-defensin (hBD)-2, have been reported in AD skin, and a link to impaired barrier function has been suggested. Objectives To study hBD-2 in relation to skin barrier function in patients with AD and controls, and to study hBD-2 in relation to disease severity. Methods Twenty-five patients with AD and 11 controls were enrolled. hBD-2 peptide concentration was determined in stratum corneum samples collected by a minimally invasive tape-stripping method. Disease severity was assessed by SCORing Atopic Dermatitis (SCORAD), and skin barrier function was evaluated by measurement of transepidermal water loss (TEWL) and skin pH. Patients with AD were characterized according to filaggrin mutations. Results hBD-2 concentrations in the stratum corneum were found to differ between lesional and nonlesional AD skin and controls, with the highest values in lesional skin (P