Exacerbation Of Atopic Dermatitis Research Articles

Nocturnal eczema: Review of sleep and circadian rhythms in children with atopic dermatitis and future research directions

Children with atopic dermatitis (AD) experience significant sleep disruption, and clinically, the disease is noted to worsen in a circadian manner at night. Epidemiologic findings highlight many negative consequences of AD, such as impaired linear growth, which is uniquely related to disturbed sleep. Clinical guidelines currently recommend assessing sleep in patients with AD as a crucial parameter of disease control with appropriate treatment. In this review we describe our current understanding of the roles of sleep cycles and circadian rhythms in the nighttime exacerbation of AD (nocturnal eczema). We present a schematic to explain the mechanism of nocturnal eczema. Treatment options for sleep disturbance and future directions for research are discussed in the context of AD.

Plasma α-defensins are elevated during exacerbation of atopic dermatitis.

There is no currently no information regarding the role of α-defensins in the pathophysiology of atopic dermatitis (AD). To investigate levels of plasma α-defensins at exacerbation and remission of AD, and to assess their association with clinical severity of AD. Patients with AD during exacerbation were recruited from the Dermatology department at the Chita Medical Academy (Chita, Russian Federation). SCORAD (SCORing Atopic Dermatitis), itch intensity, plasma concentrations of α-defensins, and serum total IgE, interleukin (IL)-1β, IL-8 and IL-10 levels were measured at study entry and after 4 months. In total, 82 patients with AD [35 (45.1%) female and 47 (54.9%) male patients, mean ± SD age 42.2 ± 11.5 years, range 15-40] and 30 healthy controls (HCs) were included. Mean objective SCORAD score was 48.8 ± 19.4 and 16.1 ± 8.3 during AD during exacerbation and remission, respectively (P < 0.01). Plasma α-defensin levels in patients with AD (1.41 ± 0.32 μg/L) were significantly higher than in HCs (0.91 ± 0.34 μg/L) (P < 0.001). Significant correlations were found between plasma α-defensin levels with objective SCORAD (r = 0.55, P < 0.001), itch severity (r = 0.25, P < 0.05) and serum IgE levels (r = 0.38, P < 0.001) during AD exacerbation. Serum concentrations of IL-1β, IL-4 and IL-8 were significantly higher and levels of IL-10 were lower at AD exacerbation in patients than in HCs, with a weak negative correlation between plasma α-defensin and serum IL-10 levels (r = -0.22; P < 0.05). During AD exacerbation, plasma α-defensin levels are elevated, and are positively correlated with AD clinical severity, itch intensity and serum IgE levels.

NOD2 and TLR2 ligands trigger the activation of basophils and eosinophils by interacting with dermal fibroblasts in atopic dermatitis-like skin inflammation.

The skin of patients with atopic dermatitis (AD) has a unique predisposition for colonization by Staphylococcus aureus (S. aureus), which contributes to the inflammation and grim prognosis of AD. Although the mechanism underlying the S. aureus-induced exacerbation of AD remains unclear, recent studies have found a pivotal role for pattern recognition receptors in regulating the inflammatory responses in S. aureus infection. In the present study, we used a typical mouse model of AD-like skin inflammation and found that S. aureus-associated nucleotide-binding oligomerization domain-containing protein 2 (NOD2) and toll-like receptor 2 (TLR2) ligands exacerbated AD-like symptoms, which were further deteriorated by the in vivo expansion of basophils and eosinophils. Subsequent histological analyses revealed that dermal fibroblasts were pervasive in the AD-like skin lesions. Co-culture of human dermal fibroblasts with basophils and eosinophils resulted in a vigorous cytokine/chemokine response to the NOD2/TLR2 ligands and the enhanced expression of intercellular adhesion molecule-1 on the dermal fibroblasts. Basophils and eosinophils were primarily responsible for the AD-related cytokine/chemokine expression in the co-cultures. Direct intercellular contact was necessary for the crosstalk between basophils and dermal fibroblasts, while soluble mediators were sufficient to mediate the eosinophil-fibroblast interactions. Moreover, the intracellular p38 mitogen-activated protein kinase, extracellular signal-regulated kinase, and nuclear factor-kappa B signaling pathways were essential for NOD2/TLR2 ligand-mediated activation of basophils, eosinophils, and dermal fibroblasts in AD-related inflammation. This study provides the evidence of NOD2/TLR2-mediated exacerbation of AD through activation of innate immune cells and therefore sheds light on a novel mechanistic pathway by which S. aureus contributes to the pathophysiology of AD.

Staphylococcus aureus overinfection in atopic dermatitis

The skin of patients affected by atopic dermatitis (AD) is extremely susceptible to colonization by Staphylococcus aureus , which plays an important role in AD exacerbations and is correlated with AD extent and severity. The mechanisms by which the bacterium colonizes and infects the skin of patients with AD can be summarized by three different and subsequent steps: 1) a defective skin barrier, on which 2) S. aureus is able to adhere and proliferate thanks to 3) the defective immune response of the skin. Several S. aureus strains can secrete enterotoxins, which can act as superantigens thus contributing to disease severity by inducing a polyclonal T-cell activation and the release of proinflammatory cytokines such as TNFα, IL-1β, IL-2. The production of immunoglobulin E antibodies against staphylococcal exotoxins has also been demonstrated, and the staphylococcal wall protein A has been suggested to act as a “superallergen”. Therapeutical actions against S. aureus skin overinfection include both pharmacological (antimicrobial and/or anti-inflammatory therapy and the newer topical calcineurin inhibitors) and nonpharmacological treatments (silk fabric textiles), and are aimed at minimizing skin colonization in order to reduce clinical exacerbations and AD severity.

Plasma endothelin-1 levels during exacerbation of atopic dermatitis.

Endothelin (ET) -1 was found to participate in the pathogenesis of bronchial asthma. At present, there is no information regarding the role of ET-1 in the pathophysiology of atopic dermatitis (AD). We assessed blood ET-1 levels during the exacerbation of AD and during the 4 months postexacerbation period, to assess the relationships between blood ET-1 levels and clinical severity of AD and pruritus. Patients with AD and during exacerbation were recruited from the dermatology department at the Chita Medical Academy (Chita, Russia). Objective Severity Scoring of Atopic Dermatitis index, itch intensity, plasma concentrations of ET-1, and serum total immunoglobulin E levels were measured at study entry and after 4 months. Eighty-two patients with AD, 35 women (45.1%) and 47 men (54.9%), mean (SD) age of 42.2 ± 11.5 years were included. Thirty healthy volunteers served as controls. The mean (SD) objective Severity Scoring of Atopic Dermatitis index score during AD exacerbation was 48.8 ± 19.4 and at the 4 months postexacerbation period was 16.1 ± 8.3 (p < 0.01). Mean (SD) itch score during AD exacerbation was 6.9 ± 1.9 and, at 4 months postexacerbation was 2.6 ± 0.7 (p < 0.01). Mean (SD) plasma levels of ET-1 in patients with AD (0.74 ± 0.45 fmol/mL) were significantly higher than in healthy subjects (0.43 ± 0.24 fmol/mL) (p < 0.001). Significant correlations were found between plasma ET-1 levels with the objective Severity Scoring of Atopic Dermatitis index (r = 0.51; p < 0.001), Itch severity (r = 0.62; p < 0.001), and with serum immunoglobulin E levels (r = 0.63; p < 0.001) at the exacerbation time point in patients with AD. During AD exacerbation, plasma ET-1 levels were elevated and were positively correlated with AD clinical severity, itch intensity, and serum IgE levels.

Exacerbation of atopic dermatitis on grass pollen exposure in an environmental challenge chamber

It has frequently been speculated that pruritus and skin lesions develop after topical exposure to aeroallergens in sensitized patients with atopic dermatitis (AD). We sought to study cutaneous reactions to grass pollen in adult patients with AD with accompanying clear IgE sensitization to grass allergen in an environmental challenge chamber using a monocenter, double-blind, placebo-controlled study design. Subjects were challenged on 2 consecutive days with either 4000 pollen grains/m(3) of Dactylis glomerata pollen or clean air. The severity of AD was assessed at each study visit up to 5 days after challenge by (objective) scoring of AD (SCORAD). Additionally, air-exposed and non-air-exposed skin areas were each scored using local SCORAD scoring and investigator global assessments. Levels of a series of serum cytokines and chemokines were determined by using a Luminex-based immunoassay. The primary end point of the study was the change in objective SCORAD scores between prechallenge and postchallenge values. Exposure to grass pollen induced a significant worsening of AD. A pronounced eczema flare-up of air-exposed rather than covered skin areas occurred. In grass pollen-exposed subjects a significantly higher increase in CCL17, CCL22, and IL-4 serum levels was observed. This study demonstrates that controlled exposure to airborne allergens of patients with a so-called extrinsic IgE-mediated form of AD induced a worsening of cutaneous symptoms.

New insight into the pathogenesis of atopic dermatitis from analysis of the mutual association between permeability barrier dysfunction and allergic inflammation

The mutual association between permeability barrier dysfunction and allergic inflammation is one of the most important issues in the pathogenesis of atopic dermatitis (AD). Permeability barrier abrogation not only induces cutaneous inflammation, but is also involved in the induction of T helper 2 (Th2)-type immunological reactions. Conversely, Th2 or other cytokines abrogate permeability barrier homeostasis. Some molecules and/or pathogenic factors have been found to be simultaneously involved in both aspects of AD. Decreases in filaggrin or peroxisome proliferator-activated receptor α, which are observed in AD lesions, not only disturb the permeability barrier function but could also directly augment cutaneous inflammation via the upregulation of proinflammatory cytokines. Elevation of the stratum corneum (SC) pH, which is also observed in AD lesions, could initiate and/or drive many of the pathogenic features including both the permeability barrier disturbance and induction of Th2-type inflammation via protease-activated receptor-2-dependent and -independent mechanisms, leading to the emergence and/or exacerbation of AD. Disturbance of the SC pH recovery function is observed in flaky tail mice and might be involved in the susceptibility to AD-like dermatitis of mice with genetic abnormalities associated with permeability barrier function. Disturbed SC acidity maintenance could be regarded as a missing link that connects genetic abnormalities associated with permeability barrier dysfunction and environmental factors in the pathogenesis of AD.

The Clinical Relevance of Various Hypersensitivity Tests in Patients with Atopic Dermatitis as Assessed by Their History, SCORAD Changes, and Number of Days with Need of Anti-Inflammatory Treatment.

Immediate and delayed hypersensitivity reactions can play a role in the pathogenesis of atopic dermatitis (AD). We tested 71 patients (median age 5 years) with AD for hypersensitivity to grass and birch pollen, Dermatophagoides pteronyssinus, and Dermatophagoides farinae using atopy patch test (APT), skin prick test (SPT), and specific IgE measurement. The sensitivity (SE) and specificity (SP) of the tests were calculated on the basis of personal history of AD exacerbation, clinical AD score (SCORAD) changes, and the number of days with need for topical anti-inflammatory treatment (AITD) in relation to exposure to the allergens being tested. APT was positive in 45 patients, mostly to D. farinae (n=37). SPT and/or specific IgE were positive in 42 subjects, in most cases to grass and birch pollen (n=29). SE of APT reached 33%-56% for history, 33% for SCORAD, and 0%-60% for AITD; SP of APT was comparable for all three assessment standards (history, SCORAD, and AITD) (48%-67%). SE of SPT/specific IgE was higher for history (26%-63%) than for the other two standards of assessment (0%-67%); SP of SPT/specific IgE was also highest for history (69%-91%), and lower for SCORAD (59%-87%) and AITD (65%-80%). AD is often associated with hypersensitivity; its influence on AD, however, is clinically significant only in a minor group of patients. While personal history and SCORAD changes present themselves as possible standards in the evaluation of clinically relevant hypersensitivity in AD patients, the anti-inflammatory treatment days (AITD) appears to be unsuitable for this purpose.

Review: The role of antibodies, autoantigens and food allergens in canine atopic dermatitis.

Canine atopic dermatitis (AD) is considered to be an immunoglobulinE (IgE)-mediated hypersensitivity response to environmental allergens. The role of other antibody isotypes and nonenvironmental allergens in disease pathogenesis remains unclear. The objective of this review is to provide an update on advances in the understanding of the relevance of specific antibody isotypes, autoallergens and nonenvironmental allergens in the pathogenesis of canine AD. Citation databases, abstracts and proceedings from international meetings published between 2001 and 2013 were reviewed. Where necessary, older articles were included for background information. Neither total nor allergen-specific IgE necessarily correlates with clinical disease in canine AD. Some dogs exhibit clinical signs that are indistinguishable from AD but have no demonstrable allergen-specific IgE (atopic-like dermatitis). Allergen-specific immunoglobulinG may be demonstrated in canine AD, but there is no evidence that this isotype plays a role in disease development. Although humans with AD may develop serum IgE against autoallergens, this finding has not been substantiated in the dog. In contrast, adverse food reactions are frequently co-associated with AD in the dog. Ingestion of food and environmental allergens may trigger exacerbations of AD. Determination of the role of IgE in the pathogenesis of canine AD still requires clarification. Clinical trials and research studies must distinguish atopic dogs with allergen-specific IgE orskin test reactivity from those without. There is no convincing evidence demonstrating a pathogenic role for either allergen-specific immunoglobulinG or autoallergens in canine AD, but food items may be triggers for disease flares in certain individuals.

Disseminated coxsackievirus A6 affecting children with atopic dermatitis

Coxsackievirus A6 (CV-A6) is an emerging pathogen that has in recent years been associated with atypical hand, foot and mouth disease. This manifests as a generalized papular or vesicular eruption, which may be associated with fever and systemic disturbance. We report a series of six children presenting to a single centre in the UK with disseminated CV-A6 infection on a background of atopic dermatitis (AD). Our patients exhibited a widespread papular or vesicular eruption in association with exacerbation of AD. Several of our cases mimicked eczema herpeticum, but the extent was more generalized, and individual lesions were discrete rather than clustered and were less circumscribed in character. This series highlights that CV-A6 infection may be encountered in the UK, and should be considered in the differential diagnosis of an acute exacerbation of AD, particularly in children.

Severe Food Allergy to Cow's Milk Treated with Oral Immunotherapy Along with Omalizumab

E S D A Y 842 Successful Specific Oral Tolerance Induction with Hake in an Allergic Child Detecting Fish in Cooking Steam Carmen M. Damelio, MD; Departament of Allergy Clinica Universidad de Navarra, PAMPLONA, Spain. RATIONALE: To describe a specific oral tolerance induction (SOTI) protocol with hake in a child suffering urticaria/angioedema upon fish cooking steam exposure. METHODS: A 6-year old girl who presented at 9 month of age acute urticaria after eating different types of fish (i.e. hake, sole). Skin prick test rendered positive results and since then she avoided fish. Subsequently she suffered several acute urticaria episodes after accidental intakes and even when exposed to tuna fish cooking steam. Comorbidities: mild and controlled atopic dermatitis, no bronchial asthma. A SOTI protocol was decided to apply. Sensitization was evaluated by Prick-to-prick (T1), specific IgE (sIgE) and IgG4 (sIgG4) to hake during the induction phase (T2) and when finalized (T3). SOTI to hake was performed using frozen hake loin, starting with lyophilized hake and when 20gr. were tolerated, we used cooked hake until reaching 40gr. RESULTS: The induction phase of the SOTI lasted 11 months until 40gr of hake were reached suffering one anaphylaxis, related to an infectious process and 5 episodes of abdominal pain requiring antihistamines in only 2 of them. After one month in maintenance-phase, eating 40gr of hake daily without reactions, she tolerated 50gr of bass, 50gr. of tuna, 50gr. of monkfish uneventfully. No atopic dermatitis exacerbation was observed. sIgE against hake (T1:3.31kUA/L; T2: 3.98kUA/L; T3: 2.02kUA/L) and wheal size for hake prick-to-prick (T1: 13x11mm; T2: 10x6mm; T3: 7x5mm) decreased during induction phase whereas hake sIgG4 levels increased (T2: 12.7kU/L, T3: 39.2kU/L). CONCLUSIONS: In our case, SOTI with hake induces tolerance to bass, tuna and monkfish.

The role of antiseptic agents in atopic dermatitis.

The skin of individuals with atopic dermatitis has a susceptibility to be colonized with Staphylococcus aureus. This has been associated with increased frequency and severity of exacerbations of atopic dermatitis. Therefore, there is a growing interest in the use of antiseptic agents to target primary bacterial colonization and infection. Antiseptic agents have been found to be better tolerated and less likely to induce bacterial resistance as compared to antibiotics. There is also a wide variety of antiseptic agents available. The efficacy of antiseptic agents has yet to be established as the studies reviewed previously have been small and of suboptimal quality. This review discusses the rationale behind targeting S. aureus with antiseptic agents and presents findings from a review of studies assessing the efficacy of antiseptics in atopic dermatitis in the last five years. Four studies were found, including a bleach bath study which has already been reviewed elsewhere. The remaining 3 studies assessed the efficacy of sodium hypochlorite containing cleansing body wash, sodium hypochlorite baths and 1% triclosan in leave on emollient. These studies suggested some benefit for the inclusion of antiseptic use with the mainstay management of atopic dermatitis, including a potential steroid sparring effect. However, there are many limitations to these studies which therefore warrant further investigation on the impact of antiseptic use in atopic dermatitis.

Feasibility of actigraphy wristband monitoring of atopic dermatitis in children

Actigraphy monitors are used to monitor sleep and scratching. Previous studies have implemented these monitors to evaluate behavior in adult patients with atopic dermatitis. However, such monitoring devices have been implemented in a paucity of studies involving pediatric patients with atopic dermatitis. The purpose of this study was to assess the feasibility of actigraphy monitoring in children with mild-to-severe atopic dermatitis. A total of six pediatric subjects were recruited. The severity of atopic dermatitis at the wrist area was assessed prior to placement of the wristband monitor. After wearing the wristbands for 7days, subjects returned to clinic to undergo reassessment of the wrist area to determine if atopic dermatitis was exacerbated by the wrist-worn device. Data on sleep quality and how often patients wore the wristband monitors were also collected. No subjective data from the subjects or parents/caregivers were collected on tolerability of the monitors. None of the subjects exhibited exacerbation of atopic dermatitis at the wrist area after wearing the actigraphy monitors for 7days. No adverse events were reported. Pediatric patients with atopic dermatitis exhibited less total sleep time compared with children evaluated in previous actigraphy studies. Actigraphy wristband monitoring can be used to continuously assess disease severity in children with atopic dermatitis.

Dynamic Analysis of Histamine-Mediated Attenuation of Acetylcholine-Induced Sweating via GSK3β Activation

Sweating has been associated with the exacerbation of atopic dermatitis (AD) in diverse ways. Acetylcholine (ACh)-mediated sweating is known to be attenuated in AD, but its cause remains obscure. To address this issue, the impact of histamine on ACh-induced sweating was evaluated. Sweating was measured by counting the number of active sweat pores by the starch-iodine reaction and dynamic optical coherence tomography; sweat was visualized using two-photon excitation fluorescence microscopy in mice and the quantitative sudomotor axon reflex test in humans. Both histamine receptor antagonists and H1 receptor (H1R)-knockout (KO) mice were used to determine methodological specificity. Histamine demonstrably inhibited ACh-induced sweating in both mice and humans via H1R-mediated signaling. In sweat glands, ACh inactivated glycogen synthase kinase 3β (GSK3β), a kinase involved in endocytosis and secretion, whereas simultaneous stimulation with histamine activated GSK3β. Results of two-photon excitation fluorescence microscopy confirmed the dynamic motion of sweat and sweat glands after ACh treatment, showing that simultaneous stimulation with histamine altered their dynamic properties. These results indicate that histamine inhibits sweat gland secretions by blocking ACh-induced inactivation of GSK3β. Histamine-mediated hypohidrosis might be involved in the mechanism of abnormal skin dryness in patients with AD.

EGFR Signaling Blunts Allergen-Induced IL-6 Production and Th17 Responses in the Skin and Attenuates Development and Relapse of Atopic Dermatitis

Despite the important role for epidermal growth factor (EGF) in epithelial homeostasis and wound healing, it has not been investigated in atopic dermatitis (AD). We used AD animal models to explore the role of EGF in AD. In an acute AD model, skin transepidermal water loss was significantly attenuated in EGF-treated mice. Blockade of EGFR signaling genetically or pharmacologically confirms a protective role for EGFR signaling in AD. In a chronic/relapsing AD model, EGF treatment of mice with established AD resulted in an attenuation of AD exacerbation (skin epithelial thickness, cutaneous inflammation, and total and allergen specific IgE) following cutaneous allergen rechallenge. EGF treatment did not alter expression of skin barrier junction proteins or antimicrobial peptides in the AD model. However, EGF treatment attenuated allergen-induced expression of IL-17A, CXCL1, and CXCL2 and neutrophil accumulation in AD skin following cutaneous allergen exposure. IL-17A production was decreased in the in vitro restimulated skin-draining lymph node cells from the EGF-treated mice. Similarly, IL-17A was increased in waved-2 mice skin following allergen exposure. Whereas IL-6 and IL-1β expression was attenuated in the skin of EGF-treated mice, EGF treatment also suppressed allergen-induced IL-6 production by keratinocytes. Given the central role of IL-6 in priming Th17 differentiation in the skin, this effect of EGF on keratinocytes may contribute to the protective roles for EGFR in AD pathogenesis. In conclusion, our study provides evidence for a previously unrecognized protective role for EGF in AD and a new role for EGF in modulating IL-17 responses in the skin.

ROLE OF ENVIRONMENTAL ALLERGENS ON ATOPIC DERMATITIS

Background: Atopic dermatitis (AD) is a chronic eczematous skin disease that develops in a patient with atopic diathesis, which is characterized by an increased liability to produce IgE antibodies for allergens mostly derived from environmental or inhalant allergens and food allergens. They are produced by cell-mediated allergic contact reactions, and recently contact sensitivity to various environmental allergens has been demonstrated in patients with AD. Atopic patients are recognized by their ability to produce large amounts of specific IgE antibodies to common substances as environmental allergens, i.e. house dust mites, grass pollens, animal danders, molds, food, etc. These antibodies can be detected by skin prick test. The aim of this study was to identify the sensitization against environmental or inhalants allergens through skin prick tests in the patients with atopic dermatitis. Material and Methods: This is a retrospective, descriptive study. We revised all medical records of patients with AD since January 2002 to December 2004 in the Out Patients Unit of Sanglah General Hospital, Bali-Indonesia. The variables studied were: gender, age, work related, diagnosis associates to AD, and prick test of environmental allergens. Results: In 3 years periods we had revised 46 of patients with AD that was done skin prick tests. The median age was 38 years (range 29-54 years), 34/46 (73.9 %) of these were male and 12 (26.1 %) female. Twenty nine patients presented pure AD, and 17 patients had AD with asthma and allergic rhinitis. Only 16 (34.7%) of patients had no history of allergic disease. Thirsty six of 46 (78.20%) of all tested AD patients had a positive skin prick tests against inhalant (aeroallergens) 16 patients and food allergens 21 patients. Sixteen patients with positive of skin test include; dust mite in 12 patients, animal dander in 10 patients, grass pollen in 9 patients and cockroach in 6 patients. Conclusion: We concluded that Environmental work related particularly dust-mite were significant that contributed to symptoms exacerbation and positive skin prick test. The skin prick tests are important methods to determine inhalant allergens in work related that exacerbation of AD patients.Â

IL-10 suppresses IL-17-mediated dermal inflammation and reduces the systemic burden of Vaccinia virus in a mouse model of eczema vaccinatum

Individuals with atopic dermatitis (AD) are susceptible to a severe, potentially fatal, systemic infection and inflammatory response following exposure to Vaccinia virus (VV). IL-10 acts both as an inducer of Th2 responses and as a regulator of T cell activation. It has been shown to limit skin inflammation elicited by contact sensitizers. AD exacerbations have been associated with decreased IL-10 function. We used IL-10(-/-) mice to test the role of the cytokine in VV immunity. They exhibited larger primary lesions and increased cutaneous neutrophil infiltration compared to wild-type (WT) counterparts. This was associated with enhanced production of IL-17A, IL-17F and CXCL2. Paradoxically, despite intact adaptive immune responses, tissue viral burdens were increased in IL-10(-/-) mice. These findings suggest that IL-10 is important in limiting skin inflammation induced by VV and that abnormal IL-17-driven neutrophil recruitment at the primary infection site in the skin results in increased systemic viral dissemination.

Calmodulin‐like skin protein level increases in the differentiated epidermal layers in atopic dermatitis

In atopic dermatitis (AD), the skin barrier is disturbed, and the expression of calcium-dependent S100 proteins and the calcium gradient is also altered in the epidermis. The calmodulin-like skin protein (CLSP), which is expressed in the differentiated epidermis, is believed to modulate the function of calcium-dependent proteins involved in barrier formation and is significantly increased in the epidermis of psoriatic patients. We, therefore, investigated the CLSP level in skin biopsies taken from patients with acute exacerbated and non-exacerbated AD as well as from healthy control subjects. Immunohistochemical, Western blot and ELISA analyses showed significant increases (P < 0.03) in CLSP level in the epidermis from patients with acute exacerbated AD as compared to that from patients with non-exacerbated AD and from control subjects. Such increased expression of CLSP may help re-establish a functional epidermal barrier in acute AD.

Late Breaking Poster Sessions

Background: Atopic dermatitis (AD) and food allergy frequently co-exist in children. Both immediate and late reactions have been reported after oral food challenge. The aim of this study was to investigate the reactions occurring in children with AD during double blind, placebo-controlled food challenges (DBPCFC). Also, the frequency of positive DBPCFCs in children reporting exacerbations of eczema as their only symptom to foods was studied. Method: Between 2001 and 2011, children underwent DBPCFCs for one or more suspected food allergies as part of regular care. The history relating to the suspected food was obtained. Children and/or parents were questioned about current AD. Immediate symptoms were defined as symptoms occurring during the challenge, or within 2 h after the last dose. Symptoms were considered 'intermediate' when they occurred between 2 and 6 h and 'late' between 6 and 48 h after the last challenge dose. McNemar's test was used to test for statistical differences between frequencies on verum and placebo days. Results: Of the 682 children undergoing DBPCFC, 381 children (55.9%) had a current history of AD, of which 317 had a history of reactions to foods and 64 had no known ingestion of the food previously. Immediate reactions consisting of exacerbations of AD only occurred rarely [two patients out of 326 (0.6%) on verum days vs one patient on a placebo day (0.3%), not significant (n.s.)]. Comparing verum to placebo days, immediate symptoms other than AD were seen more frequently (39.6% vs 8.0% respectively, P <0.01), as was the combination of AD with other symptoms (4.3% vs 0% respectively, P <0.01). Intermediate reactions of exacerbations of AD, were seen rarely either on verum or placebo days (4.0% vs 3.1% respectively, n.s.). Late eczematous reactions were also rarely seen on either verum or placebo days (1.5% vs 1.2% respectively, n.s.). Of all 317 children with a history relating to the suspected food, 19 children had a history of only an exacerbation of AD. In these children 4 verum reactions and 8 placebo reactions occurred. Conclusion: In our population of children with AD and a history suggestive of food allergy, isolated eczematous reactions were seen rarely at any time point. When AD exacerbations occurred, they almost always occurred in combination with other symptoms. Our results thus suggest that children with an exacerbation of AD in the absence of other symptoms in their history are unlikely to be food allergic.

Chemical atopy

Although atopic disease is associated with protein allergy, its relationship with chemicals (haptens/contact allergens and irritants) is less clearly defined. The 'hapten-atopy' hypothesis, whereby significant hapten and irritant exposure during times of natural T helper (Th)2 bias (pregnancy and first year of life) promotes the development of atopy and atopic disease in the resulting child, has been previously proposed. Supporting evidence includes the practice of repeated cutaneous application of haptens in generating animal models of atopic dermatitis, and the observation of a significant increase in atopic disease in children born to mothers with occupations associated with high chemical exposure during pregnancy. To observe the relationship between personal chemical exposure and atopic disease in a particular case series. We report a case series of exacerbation of atopic dermatitis after repeated cutaneous chemical exposure. Most of the patients had atopic dermatitis in young childhood that had resolved. However, after repeated chemical exposure, either occupationally as an adult or after starting to use cosmetics as a teenager, there was clear exacerbation of atopic dermatitis. Patch tests gave negative results in most cases. We propose that repeated exposure to chemicals in patients with an atopic background can occasionally lead to reactivation of atopic dermatitis.