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The magnitude of contact allergy responses can be quantified with imaged perfusion
Author(s) -
Bjarnason Bolli,
Xu H,
Elmets CA
Publication year - 2004
Publication title -
contact dermatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.524
H-Index - 96
eISSN - 1600-0536
pISSN - 0105-1873
DOI - 10.1111/j.0105-1873.2004.00309hc.x
Subject(s) - perfusion , contact allergy , blisters , delayed hypersensitivity , medicine , contact dermatitis , forearm , allergy , laser doppler velocimetry , immunology , pathology , immune system , blood flow
Objective: The objective of this study was to determine whether the magnitude of the perfusion of the contact hypersensitivity response as measured by the laser Doppler perfusion imaging (LDPI) technique was associated with immunological parameters implicated in the pathogenesis of the disease. Methods: Urushiol was applied on one of the forearms of volunteers for 48 hours while the other forearm served as a control. Twenty‐four hours later, measurements of perfusion of the patch test sites were performed with the LDPI technique. To determine whether there was a correlation with immunological parameters associated with human contact hypersensitivity, suction blisters were produced at the test sites. Blister fluid was removed and examined for the cytokine interleukin‐8 (IL‐8). Results: There was an extremely close correlation between the magnitude of the contact hypersensitivity response as measured by the imaged perfusion and the level of IL‐8 in the blister fluid (r = 1.00). Compared to subjects with visually positive urushiol reactions, patients who failed to develop urushiol contact hypersensitivity despite repeated exposures to that substance had both greatly diminished perfusion and blister fluid IL‐8 levels. Conclusion: The results indicate that LDPI is a sensitive method of quantifying contact hypersensitivity reactions in humans and that the magnitude of the measurements with this technique correlates extremely well with cutaneous cytokine levels that have been implicated in the immunopathogenesis of contact hypersensitivity.