Atopic dermatitis (eczema)

Nickel earlobe dermatitis and clinical non-relevance of the oral exposure.

J Eur Acad Dermatol Venereol. 2008 May 20;

Authors: Di Berardino F, Alpini D, Cesarani A

Objective Nickel is the most common cause of allergic contact dermatitis (ACD). Because nickel restriction is commonly imposed on many patients with the only earlobe ACD to nickel hypersensitivity, the aim of this study was to identify the role of occasional and extended oral nickel exposure in these patients. Design This is a case-control study Subjects Thirty-four outpatients, previously diagnosed as monosensitized to nickel, suffering from earlobe dermatitis were enrolled; 11 of them showed active dermatitis. The control group consisted of six healthy (non-nickel-sensitive) subjects. Interventions High oral nickel challenge (20 mg) and protracted oral challenge (1 mg once a day). Observation period: 6 weeks. Results Clinical earlobe lesions were not affected by a high oral nickel intake nor by a protracted oral challenge. Conclusions Dietary nickel restriction seems to be useless in patients with earlobe ACD due to nickel hypersensitivity.

PMID: 18498338 [PubMed - as supplied by publisher]

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The efficacy of ‘0.05% Clobetasol + 2.5% zinc sulphate’ cream vs. ‘0.05% Clobetasol alone’ cream in the treatment of the chronic hand eczema: a double-blind study.

J Eur Acad Dermatol Venereol. 2008 May;22(5):531-6

Authors: Faghihi G, Iraji F, Shahingohar A, Saidat A

BACKGROUND: Many therapeutic modalities have been suggested for treatment of the chronic hand eczema. Despite good immediate efficacy of some of these treatments, there is high recurrence of the dermatitis following cessation of the treatment. AIM: Regarding the beneficial effects of the zinc sulfate on the skin, we designed a double blind study to evaluate the efficacy of the ‘0.05% Clobetasol + 2.5% zinc sulphate’ cream versus ‘0.05% Clobetasol alone’ cream in the treatment of the chronic hand eczema. SUBJECTS AND METHODS: This study was a double-blind, right to left, prospective, clinical trial. In total, 47 patients with chronic hand eczema admitted to dermatology center of Isfahan University of Medical Sciences were selected and their right hand or left hand were selected at random to be treated with either the ‘0.05% Clobetasol + 2.5% zinc sulphate’ cream or ‘0.05% Clobetasol alone’ cream twice daily for 2 weeks. All of the patients were treated for 2 weeks and were followed up at weeks 2, 4, 6 and 8 after starting the treatment. For determining the severity of chronic hand eczema, we assessed and scored 4 different characteristics of the lesions including redness; scaling; lichenification and pruritus. The data were analyzed using SPSS program (release 13) and statistical tests including Mann-Whitney test. RESULTS: Overall, 47 patients (94 samples) were evaluated. All of these patients had similar and symmetrical lesions on their right and left hands. Out of them, 35 patients were females and 12 patients were male. In all of the evaluated characterisitics, the ‘0.05% Clobetasol + 2.5% zinc sulphate’ cream was more effective than ‘0.05% Clobetasol alone’ cream (P < 0.05). The recurrence rate of eczema was significantly lower in the group treated with this combination treatment (P < 0.05). CONCLUSION: With regard to the encouraging results of the combination treatment with Clobetasol + zinc sulphate, we suggest that in a more extensive clinical trial, the efficacy of this treatment against chronic hand dermatitis be evaluated. In addition, evaluation of this combination therapy against other inflammatory dermatosis seems to be logical.

PMID: 18284511 [PubMed - indexed for MEDLINE]

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Development of atopic dermatitis in mice transgenic for human apolipoprotein C1.

J Invest Dermatol. 2008 May;128(5):1165-72

Authors: Nagelkerken L, Verzaal P, Lagerweij T, Persoon-Deen C, Berbee JF, Prens EP, Havekes LM, Oranje AP

Mice with transgenic expression of human apolipoprotein C1 (APOC1) in liver and skin have strongly increased serum levels of cholesterol, triglycerides, and free fatty acids, indicative of a disturbed lipid metabolism. Importantly, these mice display a disturbed skin barrier function, evident from increased transepidermal water loss, and spontaneously develop symptoms of dermatitis including scaling, lichenification, excoriations, and pruritus. Histological analysis shows increased epidermal thickening and spongiosis in conjunction with elevated numbers of inflammatory cells (eosinophils, neutrophils, mast cells, macrophages, and CD4+ T cells) in the dermis. In addition, affected mice have increased serum levels of IgE and show abundant IgE(+) mast cells in the dermis. Partial inhibition of disease could be achieved by restoration of the skin barrier function with topical application of a lipophilic ointment. Furthermore, the development of atopic dermatitis in these mice was suppressed by corticosteroid treatment. These findings in APOC1(+/+) mice underscore the role of skin barrier integrity in the pathogenesis of atopic dermatitis.

PMID: 18049452 [PubMed - indexed for MEDLINE]

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Efalizumab therapy for atopic dermatitis causes marked increases in circulating effector memory CD4+ T cells that express cutaneous lymphocyte antigen.

J Invest Dermatol. 2008 May;128(5):1173-81

Authors: Harper EG, Simpson EL, Takiguchi RH, Boyd MD, Kurtz SE, Bakke AC, Blauvelt A

Efalizumab is an mAb directed against CD11a, a molecule involved in T-cell activation and extravasation from blood into tissue. Ten patients with severe atopic dermatitis were treated with efalizumab for 84 days, and peripheral blood mononuclear cells were analyzed for expression of activation and adhesion markers. Efalizumab treatment led to decreases in CD11a mean fluorescence intensity (MFI) on naive, central memory, and effector memory CD4+ and CD8+ T cell subsets. MFI for CD18 was decreased in both CD4+ and CD8+ T cells. Percentages of cells positive for cutaneous lymphocyte antigen (CLA) were increased fourfold in all CD4+ and CD8+ T cell subsets. Increases in the percentages of CD4+ and CD8+ T cells expressing beta7 and CD49d were also observed. No significant changes were observed in the percentages of CD4+ and CD8+ T cells that produced either IFN-gamma or IL-4. In summary, efalizumab treatment resulted in (i) decreases in CD11a and CD18 expression in all circulating T-cell subsets and (ii) increases in the percentages of blood T cells expressing tissue homing markers (CLA, beta7, CD49d). These data suggest that blockade of T-cell extravasation into tissue is the major pathway by which efalizumab leads to improvement in cutaneous inflammation.

PMID: 18007580 [PubMed - indexed for MEDLINE]

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Modeling atopic dermatitis with increasingly complex mouse models.

J Invest Dermatol. 2008 May;128(5):1061-4

Authors: Scharschmidt TC, Segre JA

Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disorder that affects approximately 15% of children in the United States. A complex disorder, AD is characterized by both skin barrier impairment and immunologic abnormalities, including decreased innate immune function and a polarized adaptive immune response. Mouse models have demonstrated the complex interdependence of immune cell-keratinocyte interactions and teased apart gene-environment relationships in a controlled setting. In this issue, Nagelkerken et al. present a mouse model with transgenic expression of apolipoprotein C1 that disrupts the skin lipid barrier and manifests many hallmark features of AD.

PMID: 18408744 [PubMed - indexed for MEDLINE]

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“Outside-to-inside” (and now back to “outside”) pathogenic mechanisms in atopic dermatitis.

J Invest Dermatol. 2008 May;128(5):1067-70

Authors: Elias PM, Steinhoff M

The pathogenesis of atopic dermatitis (AD) has been attributed largely to abnormalities in the adaptive immune system, with key roles played by T-helper 1(Th1)/Th2 cell dysregulation, IgE production, dendritic cell signaling, and mast-cell hyperactivity, resulting in the pruritic, inflammatory dermatosis that characterizes AD (Leung et al., 2004). Accordingly, therapy has been focused on ameliorating Th2-mediated inflammation and pruritus (eg, Leung, 2000). Indeed, there is emerging evidence that inflammation in AD results first from inherited and acquired insults that converge to alter epidermal structure and function, followed by immune system activation, which in turn has negative consequences for skin-barrier homeostasis. This cycle comprises an “outside-inside-outside” model of AD pathogenesis (Elias et al., in press).

PMID: 18408746 [PubMed - indexed for MEDLINE]

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Treatment of mild to moderate seborrhoeic dermatitis with MAS064D (Sebclair), a novel topical medical device: results of a pilot, randomized, double-blind, controlled trial.

J Eur Acad Dermatol Venereol. 2008 Mar;22(3):290-6

Authors: Veraldi S, Menter A, Innocenti M

AIM: MAS064D (Sebclair) is a novel steroid-free cream containing multiple active ingredients. Objective of this pilot study was to evaluate the efficacy and safety of MAS064D in the treatment of mild to moderate SD of the face. METHODS: Patients (n = 60) with SD were randomized to receive MAS064D (n = 40) or a matching vehicle (n = 20). The primary study endpoint was investigators’ global assessment (IGA) score at day 28, compared with baseline. Secondary endpoints included: IGA score at day 14; investigators’ assessment of erythema and scaling; patients’ assessment of burning/stinging, pruritus and global response to MAS064D; resort to rescue medication; quality of life. RESULTS: Use of MAS064D for 4 weeks was associated with a higher percentage of success in the MAS064D group than in the vehicle group (approximately 68% vs 11%, P < 0.0001). The effects of MAS064D were significantly better than those of vehicle for investigator-assessed erythema and scaling, and patients’ assessed pruritus and global response to MAS064D (P 0.01). No patient in the MAS064D group required rescue medication, compared with two patients in the vehicle group. Four patients (two each in the MAS064D and vehicle groups) reported a total of six non-serious adverse events. CONCLUSIONS: MAS064D appears to be an effective and well tolerated cream for the treatment of mild to moderate SD of the face. Further clinical evaluation of MAS064D in SD is warranted.

PMID: 18269596 [PubMed - indexed for MEDLINE]

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Prevalence and risk factors for atopic dermatitis in preschool children.

Br J Dermatol. 2008 Mar;158(3):539-43

Authors: Peroni DG, Piacentini GL, Bodini A, Rigotti E, Pigozzi R, Boner AL

BACKGROUND: Atopic dermatitis (AD) is a common condition in infancy which usually disappears by 3 years of age in a significant proportion of children. The prognosis is mostly determined by severity and presence of atopic sensitization. OBJECTIVES: To investigate prevalence of AD, comorbidities and risk factors in a population of preschool children aged 3-5 years. METHODS: Children in kindergartens were evaluated. The International Study of Asthma and Allergies in Childhood written questionnaire (WQ) was used, with additional questions on risk factors. Atopy was investigated by skin prick tests. RESULTS: One thousand, four hundred and two valid WQs (92% response rate) were returned for evaluation. The prevalence of AD symptoms in the last 12 months in the whole population was 18.1% (254 cases). Seventy-two per cent of these children presented AD-specific localizations. The prevalence of eczema as a doctor’s diagnosis in the total population was 15.4%. Positive atopic sensitization was present in 18.6% of the total and in 32.2% of the AD study population, respectively. Multiple sensitivities were observed in 58.2% of sensitized children. The prevalence of sensitization demonstrated that the most common sensitizing allergens in children with AD were mites and grass pollen. Rhinitis symptoms and wheezing were present in 32.2% and 24.2%, respectively, of children with AD. Allergic sensitization to egg, cat, grass pollen and mites, as well as the presence of symptoms of rhinitis, and a positive family history of atopy were all significant risk factors for AD. CONCLUSIONS: The study demonstrates a high prevalence of AD and a close relationship with rhinitis symptoms. Significant risk factors for AD were sensitization to food or inhalant allergens as well as parental history of atopy.

PMID: 18067476 [PubMed - indexed for MEDLINE]

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