Patch-Test Results of the North American Contact Dermatitis Group 2005-2006

Ka, Zug; Em, Warshaw; Jf, Fowler; Hi, Maibach; Dl, Belsito; Pratt,; Sasseville, Denis; Fj, Storrs; Js, Taylor; Cg, Mathias; Va, DeLeo; Rl, Rietschel; Marks, James G.

doi:10.2310/6620.2009.08097

Cited by 272 publications

(193 citation statements)

References 25 publications

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“…It accounts for approximately 30% of all cases of occupational disease (Clark and Zirwas 2009), it aff ects between 7 and 19% of the general population, and it remains prevalent in the general population (Mortz et al 2001, Nielsen et al 2001, Thyssen et al 2009). ACD can result from exposure to chemicals such as metals (nickel, chromium), formaldehyde, corticosteroids or ingredients in personal care products such as cosmetics and hair dyes (Zug et al 2009, Warshaw et al 2009a, 2009b, Hamilton and de Gannes 2011, Mortz and Andersen 2008). ACD is characterized by epidermal spongiosis, vesicle formation, and infl ammatory cell infi ltration.…”

Section: Introductionmentioning

confidence: 99%

Anchoring molecular mechanisms to the adverse outcome pathway for skin sensitization: Analysis of existing data

Veen

Soeteman‐Hernández

Ezendam

et al. 2014

Critical Reviews in Toxicology

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Allergic contact dermatitis (ACD) is a hypersensitivity immune response induced by small protein-reactive chemicals. Currently, the murine local lymph node assay (LLNA) provides hazard identification and quantitative estimation of sensitizing potency. Given the complexity of ACD, a single alternative method cannot replace the LLNA, but it is necessary to combine methods through an integrated testing strategy (ITS). In the development of an ITS, information regarding mechanisms and molecular processes involved in skin sensitization is crucial. The recently published adverse outcome pathway (AOP) for skin sensitization captures mechanistic knowledge into key events that lead to ACD. To understand the molecular processes in ACD, a systematic review of murine in vivo studies was performed and an ACD molecular map was constructed. In addition, comparing the molecular map to the limited human in vivo toxicogenomic data available suggests that certain processes are similarly triggered in mice and humans, but additional human data will be needed to confirm these findings and identify differences. To gain insight in the molecular mechanisms represented by various human in vitro systems, the map was compared to in vitro toxicogenomic data. This analysis allows for comparison of emerging in vitro methods on a molecular basis, in addition to mathematical predictive value. Finally, a survey of the current in silico, in chemico, and in vitro methods was used to indicate which AOP key event is modeled by each method. By anchoring emerging classification methods to the AOP and the ACD molecular map, complementing methods can be identified, which provides a cornerstone for the development of a testing strategy that accurately reflects the key events in skin sensitization.

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Section: Introductionmentioning

confidence: 99%

Anchoring molecular mechanisms to the adverse outcome pathway for skin sensitization: Analysis of existing data

Veen

Soeteman‐Hernández

Ezendam

et al. 2014

Critical Reviews in Toxicology

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“…Nickel is one of the most common contact allergens, causing ACD in about 4% to 8% of male subjects and 18% to 30% of female subjects in the industrialized world. 15,16 …”

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confidence: 99%

Atopic dermatitis results in intrinsic barrier and immune abnormalities: Implications for contact dermatitis

Gittler

Krueger

Guttman‐Yassky

2013

Journal of Allergy and Clinical Immunology

191

130

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Atopic dermatitis (AD), as well as irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD), are common skin diseases. These diseases are characterized by skin inflammation mediated by activated innate immunity or acquired immune mechanisms. Although AD, ICD, and ACD can be encountered in pure forms by allergists and dermatologists, patients with AD often present with increased frequency of ICD and ACD. Although a disturbed barrier alone could potentiate immune reactivity in patients with AD through increased antigen penetration, additional immune mechanisms might explain the increased susceptibility of atopic patients to ICD and ACD. This review discusses cellular pathways associated with increased skin inflammation in all 3 conditions and presents mechanisms that might contribute to the increased rate of ICD and ACD in patients with AD.

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“…For example, the patch test results of the North American Contact Dermatitis Group in 2005-2006 found 19% positive patch test results to nickel, 11.5% to fragrance, and 4.4% to cinnamic alcohol. 13 Results on the gallates are less widely published, but one center reported 7% prevalence to dodecyl gallate and 3% to octyl gallate. 14 It is important to identify and educate the patient as to the source of the allergen identified.…”

Section: Discussionmentioning

confidence: 99%

Burning Mouth Syndrome

2014

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Background: Burning mouth syndrome (BMS) is a burning or sore mouth in the absence of changes in the oral mucosa. It is often difficult to diagnose and treat. Numerous theories of the etiology have been suggested, including contact allergy.Objective: To determine the clinical utility of patch testing in patients with BMS. Methods: We retrospectively reviewed the charts of patients diagnosed with BMS who had patch testing performed between January 1, 2008, and July 31, 2012.Results: Of 142 consecutive patients with BMS, 132 consented to patch testing; 89 (67%) had allergic patch test reactions. Of the patients with positive results, 66 (74%) had results that were deemed to have possible relevance. The most common allergens detected were nickel sulfate 2.5%, dodecyl gallate 0.3%, octyl gallate 0.3%, fragrance mix 8%, benzoyl peroxide 1%, and cinnamic alcohol 1%.Conclusions: Our findings suggest that contact allergy may be an etiologic factor in some patients with BMS. Patch testing is a useful investigation for BMS patients.Contexte: Le «syndrome de la bouche brû lante (SBB)», ou stomatodynie, se manifeste par une sensation de brû lure ou de la douleur dans la bouche, sans qu'il y ait modification de la muqueuse buccale. Le syndrome est souvent difficile à diagnostiquer et à traiter. De nombreuses thé ories, dont celle de l'allergie de contact, ont é té avancé es sur la cause du syndrome.Objectif: L'é tude visait à dé terminer l'utilité clinique des tests é picutané s chez les personnes souffrant du SBB. Mé thode: Nous avons procé dé à un examen ré trospectif des dossiers mé dicaux de patients atteints du SBB, qui ont é té soumis à des tests é picutané s entre le 1 er janvier 2008 et le 31 juillet 2012. Ré sultats: Sur 142 patients consé cutifs, souffrant du SBB, 132 ont accepté de subir des tests é picutané s; sur ce nombre, 89 (67%) ont fait une ré action allergique. Dans 66 (74%) cas positifs, il semblait y avoir un lien pertinent possible. Les allergè nes le plus souvent incriminé s é taient le sulfate de nickel: 2.5%; le gallate de dodé cyle: 0.3%; le gallate d'octyle: 0.3%; le mé lange de composants de parfum (fragrance mix): 8%; le peroxyde de dibenzoyle: 1% et l'alcool cinnamique: 1%.Conclusions: Les ré sultats de l'é tude donnent à penser que l'allergie de contact est un facteur possible du SBB chez certaines personnes, et les tests é picutané s se ré vè lent des outils utiles d'exploration.

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Patch-Test Results of the North American Contact Dermatitis Group 2005-2006

Cited by 272 publications

References 25 publications

Anchoring molecular mechanisms to the adverse outcome pathway for skin sensitization: Analysis of existing data

Anchoring molecular mechanisms to the adverse outcome pathway for skin sensitization: Analysis of existing data

Atopic dermatitis results in intrinsic barrier and immune abnormalities: Implications for contact dermatitis

Burning Mouth Syndrome

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