Atopic dermatitis (eczema)

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Dermatitis cruris pustulosa et atrophicans–a frequent but poorly understood tropical skin condition–a case report from Burkina Faso.

Int J Dermatol. 2008 May;47(5):473-5

Authors: Bens G, Franck F, Diatto G, Preney L, Darie H, Géniaux M

Dermatitis cruris pustulosa et atrophicans (DCPA) is a benign inflammatory skin disease of the younger population in the tropics. Although this pustular skin condition of particular topography is frequently seen by dermatologists in tropical countries, its origin remains unknown. We report the case of a young woman with DCPA associated with prurigo nodularis. A bacterial origin has not been demonstrated in this case. Histology showed an intraepidermal neutrophilic pustule with dermal and subcutaneous infiltration by neutrophils and eosinophils forming flame figures. Different pathogenic hypotheses are discussed with special regard to a potential relationship between DCPA and eosinophilic cellulitis.

PMID: 18412864 [PubMed - indexed for MEDLINE]

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AhR ligands, malassezin, and indolo[3,2-b]carbazole are selectively produced by Malassezia furfur strains isolated from seborrheic dermatitis.

J Invest Dermatol. 2008 Jul;128(7):1620-5

Authors: Gaitanis G, Magiatis P, Stathopoulou K, Bassukas ID, Alexopoulos EC, Velegraki A, Skaltsounis AL

Malassezia yeasts are connected with seborrheic dermatitis (SD) whereas M. furfur pathogenicity is associated with the production of bioactive indoles. In this study, the production of indoles by M. furfur isolates from healthy and diseased skin was compared, the respective HPLC patterns were analyzed, and substances that are preferentially synthesized by strains isolated from SD lesions were isolated and characterized. Malassezin, pityriacitrin, indole-3-carbaldehyde, and indolo[3,2-b]carbazole (ICZ) were isolated by HPLC from extracts of M. furfur grown in L-tryptophan agar, and identified by nuclear magnetic resonance and mass spectroscopy. Of these, ICZ, a potent ligand of the aryl hydrocarbon receptor (AhR), is described for the first time to our knowledge as a M. furfur metabolite. HPLC-photodiode array detection analysis of strain extracts from 7 healthy subjects and 10 SD patients showed that M. furfur isolates from only SD patients consistently produce malassezin and ICZ. This discriminatory production of AhR agonists provides initial evidence for a previously unreported mechanism triggering development of SD and indicates that the variable pathogenicity patterns recorded for M. furfur-associated SD conditions may be attributed to selective production (P<0.001) of measurable bioactive indoles.

PMID: 18219281 [PubMed - indexed for MEDLINE]

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ADAM10-mediated E-cadherin release is regulated by proinflammatory cytokines and modulates keratinocyte cohesion in eczematous dermatitis.

J Invest Dermatol. 2008 Jul;128(7):1737-46

Authors: Maretzky T, Scholz F, Köten B, Proksch E, Saftig P, Reiss K

Acute eczema is an inflammatory skin disease characterized by the formation of small intraepidermal blisters, reduction of the adhesion molecule E-cadherin from the keratinocyte surface, and impaired keratinocyte cohesion. Here, we reveal that the disintegrin and metalloprotease ADAM10 is critically involved in regulating E-cadherin cell-surface expression in cultured primary human keratinocytes and in diseased human skin. Proinflammatory cytokines, transforming growth factor-beta, and lipopolysaccharide led to increased release of soluble E-cadherin by activating mitogen-activated protein kinase signaling in cultured keratinocytes. Moreover, these stimuli decreased the amount of pro-ADAM10 and increased the level of the active protease, leading to loss of E-cadherin from the cell surface and decreased keratinocyte cohesion. In situ examination and immunoblot analyses of E-cadherin and ADAM10 expression in lesional skin of eczema revealed that the reduction of E-cadherin expression in areas of blister formation closely correlated with increased level of ADAM10 expression and elevated E-cadherin shedding. Our data suggest that ADAM10-mediated E-cadherin proteolysis leads to the impaired cohesion of keratinocytes observed in eczematous dermatitis and provide previously unreported insights into the understanding of the molecular mechanisms involved in inflammatory diseases with loss in epithelial integrity.

PMID: 18200054 [PubMed - indexed for MEDLINE]

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Specific filaggrin mutations cause ichthyosis vulgaris and are significantly associated with atopic dermatitis in Japan.

J Invest Dermatol. 2008 Jun;128(6):1436-41

Authors: Nomura T, Akiyama M, Sandilands A, Nemoto-Hasebe I, Sakai K, Nagasaki A, Ota M, Hata H, Evans AT, Palmer CN, Shimizu H, McLean WH

Mutations in the gene encoding filaggrin (FLG) have been identified as the cause of ichthyosis vulgaris (IV) and shown to be major predisposing factors for atopic dermatitis (AD). However, these studies have been mainly carried out in European populations. In early 2007, we identified two Oriental-specific FLG mutations in four Japanese families with IV and reported that filaggrin mutations were also significant predisposing factors for AD in Japan. However, the frequency of FLG mutations observed in our Japanese AD cohort (5.6%), was much lower than that seen in Europeans (up to 48%). Here, we studied a further seven Japanese families with IV and identified two additional nonsense mutations in FLG, S2889X, and S3296X. We found that more than 20% of patients in our Japanese AD case series carry FLG mutations, and there is significant statistical association between the four mutations and AD (chi(2) P=8.4 x 10(-6); heterozygote odds ratio 7.57, 95% CI 2.84-23.03). These data emphasize that skin-barrier impairment due to reduced filaggrin expression plays an important role in the pathogenesis of AD and sheds further light on the genetic architecture of atopy in Japan.

PMID: 18200065 [PubMed - indexed for MEDLINE]

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Human natural killer T cells infiltrate into the skin at elicitation sites of allergic contact dermatitis.

J Invest Dermatol. 2008 Jun;128(6):1460-9

Authors: Gober MD, Fishelevich R, Zhao Y, Unutmaz D, Gaspari AA

The purpose of this study is to identify invariant natural killer T cells (NKT cells) in cellular infiltrate of human allergic contact dermatitis (ACD) skin challenge sites. Skin biopsy specimens were taken from positive patch test reactions from 10 different patients (9 different allergens) and studied by immunochemistry, real-time PCR, nested PCR, and in situ hybridization to identify NKT cells and the cytokines associated with this cell type. Invariant NKT cells were identified in all the 10 skin biopsy specimens studied, ranging from 1.72 to 33% of the cellular infiltrate. These NKT cells were activated in all cases, as they expressed cytokine transcripts for IFN-gamma and IL-4. Invariant NKT cells are present in ACD, regardless of the allergen that triggers the reaction, and are in an activated state. We conclude that innate immunity plays a role in late phases of type IV hypersensitivity reactions and may be responding to self-lipids released during allergic inflammation. These data complement the previous work by other investigators that suggest that NKT cells are important in the early cellular response during primary immune responses to allergens. Herein, it is demonstrated that NKT cells are constantly present during the late elicitation phase of human type IV hypersensitivity reactions.

PMID: 18079745 [PubMed - indexed for MEDLINE]

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Morbidity and cost of atopic eczema in Australia.

Australas J Dermatol. 2004 Feb;45(1):16-22

Authors: Jenner N, Campbell J, Marks R

The severity, morbidity and financial costs of atopic eczema (AE) were assessed during a 1-year prospective study of a cohort of 85 people aged 14-63 years (mean 36 years) with the disease. A dermatologist examined each participant using the Six Area Six Sign Atopic Dermatitis severity scoring system to classify severity. Participants completed a Dermatology Life Quality Index (DLQI), a Nottingham Eczema Severity Score (NESS) and an ongoing diary of health-care consultations and treatment costs. Follow up by mail to each participant was conducted every 2 months and participants completed a NESS, a DLQI and a diary of costs incurred. The DLQI data revealed that 36% spent over 10 min per day applying treatments, 28% indicated that AE influenced the clothes they wore, 21% felt embarrassed by their skin and 15% reported problems with treatments. There appeared to be a relationship between increased morbidity and increased severity. The average annual out-of-pocket cost for products used for treatment was A$425, ranging from A$13.50 to over A$2000 per individual. The average out-of-pocket cost for medical consultations was A$120, ranging from zero to over A$800 per individual. Although there were concerns about the reproducibility of the severity and morbidity measures, the data showed that AE can have substantial effects both financially and from a personal perspective for those affected.

PMID: 14961903 [PubMed - indexed for MEDLINE]

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Allergic contact dermatitis caused by the clothing dye, disperse blue 106, an important contact allergen that may be frequently missed.

Australas J Dermatol. 2004 Feb;45(1):64-6

Authors: Dawes-Higgs E, Freeman S

A 43-year-old woman presented with a history of dermatitis in a somewhat linear pattern under her breasts, across her back and around her waist. This dermatitis occurred after wearing a new blue dress with a blue lining. Patch testing showed an allergy to disperse blue 106 dye and also to her dress lining. However, she was not positive to p-phenylene-diamine, a dye in the standard patch test series. We recommend that any patient even slightly suspected of having an allergy to a textile dye should be tested with disperse blue, in addition to the standard series.

PMID: 14961913 [PubMed - indexed for MEDLINE]

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Severe contact dermatitis as a result of an antiseptic bath oil.

Australas J Dermatol. 2004 Feb;45(1):73-5

Authors: Storer E, Koh KJ, Warren L

Siblings aged 7 and 5 years developed extensive truncal and flexural inflammation and desquamation unresponsive to standard eczema therapy. After delays in diagnosis, subsequent history revealed prior use of an antiseptic bath oil in a much stronger concentration than recommended. The case illustrates the severe irritant contact dermatitis that can arise following inadequate dilution of antiseptic bath oils, presumably as a result of skin contact with benzalkonium chloride and triclosan. Features that may direct attention to such irritant dermatitis are flexural predominance with superficial desquamation and rapid improvement after avoidance of exposure to the antiseptic solution.

PMID: 14961916 [PubMed - indexed for MEDLINE]

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StabiEL: Stabilization of skin condition with Elidel - a patients’ satisfaction observational study addressing the treatment, with pimecrolimus cream, of atopic dermatitis pretreated with topical corticosteroid.

J Eur Acad Dermatol Venereol. 2008 Jun 6;

Authors: Gollnick H, Luger T, Freytag S, Bräutigam M,

Background The objective of this 4-month multicentre observational study was to evaluate safety and efficacy of intermittent long-term treatment of patients with atopic dermatitis (AD) with pimecrolimus cream 1% in the daily practice and to compare it with the preceding topical corticosteroid-based therapy in retrospective. Patients and methods Overall severity of AD and individual symptoms were assessed in 3200 patients by the physician, whereas acceptance of treatment and satisfaction of patients was investigated using a patient questionnaire. Results The percentage of patients clear or almost clear of symptoms increased from 12% to 82%. Seventy-four per cent of physician rated the treatment better than the preceding therapy, and 21% noted no difference. Seventy-seven per cent of the patients asserted that long-term intermittent treatment with pimecrolimus reduces the frequency of flares as opposed to less than 27% for topical corticosteroids. Patients also felt that pimecrolimus results in a higher improvement in quality of life; 84% stated that pimecrolimus stabilized the skin compared with 27% for topical steroids. Conclusion Intermittent treatment of AD patients with pimecrolimus cream 1% is effective and well tolerated, and results in higher patient satisfaction compared with topical corticosteroids in retrospective.

PMID: 18540990 [PubMed - as supplied by publisher]

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CD30 expression on CD1a+ and CD8+ cells in atopic dermatitis and correlation with disease severity.

Eur J Dermatol. 2008 Jan-Feb;18(1):41-9

Authors: Oflazoglu E, Simpson EL, Takiguchi R, Grewal IS, Hanifin JM, Gerber HP

Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with cutaneous hyperreactivity to environmental stimuli, resulting in increased infiltration of inflammatory cells, IgE production and enhanced expression of costimulatory molecules, cytokines and chemokines. CD30, a TNF receptor superfamily member, is a costimulatory molecule expressed on activated T and B cells. A positive correlation between soluble CD30 (sCD30) levels in patient serum and AD disease severity has been described previously. However, the relative frequencies and identities of cells expressing CD30 in AD patients and the relationship between the frequency of CD30 positive cells and serum sCD30 levels with disease severity remained unknown. To address these questions, immunofluorescence analysis of AD skin lesions representing different disease stages, was conducted. In addition to the CD4+ T cells, CD1a+ Langerhans cells and CD8+ T cells were found to express CD30 in AD lesions and the cell numbers correlated with disease severity. FACS analysis of AD patient blood samples revealed expression of CD30 on memory T-cells and a correlation with disease severity was identified. Finally, serum analysis of soluble mediators revealed positive correlations between sCD30, IgE, MDC, TARC and PARC levels with disease severity. Combined, our data provide correlative evidence that CD30+ cells, including Langerhans cells and CD8+ T-cells, may contribute to AD disease severity and that therapeutic strategies targeting CD30+ cells may provide benefit to AD patients.

PMID: 18086588 [PubMed - indexed for MEDLINE]

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