Chemokine Expression in Nummular Dermatitis and Atopic Dermatitis
Recruitment status was: Active, not recruiting
|Atopic Dermatitis Nummular Eczema|
|Study Design:||Observational Model: Case Control
Time Perspective: Prospective
|Official Title:||Chemokine Expression in Nummular Dermatitis and Atopic Dermatitis|
|Study Start Date:||November 2010|
|Estimated Study Completion Date:||March 2012|
|Estimated Primary Completion Date:||October 2011 (Final data collection date for primary outcome measure)|
|Patients with atopic dermatitis|
|Patients with nummular eczema|
Atopic dermatitis(AD) is a common cutaneous inflammatory disease. The pathogenesis of atopic dermatitis involves a complex interaction between atopy and environmental protein allergens which produces Th2 immune responses with IgE formation, Th2 cells dominate in lesions of atopic dermatitis, whereas Th1 and Th2 cells co-dominate in late eczematus lesions.
Nummular dermatitis(ND) is another common cutaneous inflammatory disease. The nummular patches and papules disseminated over four extremities and less over trunk . The serum levels of Th2 chemokines(CCL17, CCL22, CCL27) are elevated in AD patients. The expression levels of these chemokines in lesional epidermis are also increased. CCL18 which is derived from APC is also increased in the serum as well as lesional skin of AD patients. In contrast, there are very few reports regarding the chemokine expression profiles in ND patients. Because erosis is a remarkable exacerbating factor for ND. The investigators hypothesize that ND is a specialized contact dermatitis induced by environmental substances. It has been known, CCL17 and CXCL10 were highly expressed in lesion of allergic contant dermatitis, whereas almost no expression of these chemokines could be detected in lesions of irritant contact dermatitis.
The aim of this study is to measure the serum levels of CCL17, CCL18, CCL22 and CXCL10 and their expression levels in epidermis in AD and ND patients. The investigators hope that the results of this study will provide useful information for clinical differential diagnosis for AD and ND as well as understanding the pathogenesis of ND.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01311986
|National Taiwan University Hospital|
|Taipei, Taiwan, 100|
|Principal Investigator:||Hsien-Ching Chiu, MD||Department of Dermatology, National Taiwan University Hospital|