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Genetic Screening for Filaggrin Mutation in Atopic Dermatitis and Ichthyosis Vulgaris in the African American Population

2014-08-27 03:17:55 | BioPortfolio

Summary

The investigators' primary objective is to identify common and rare mutations in the filaggrin gene in African American patients with a diagnosis of atopic dermatitis and ichthyosis vulgaris. Atopic dermatitis, or eczema, is a common, chronic, relapsing and remitting problem in many children and affects 10-20% of the pediatric population. Itch is a predominant feature of this disease and is quite disruptive to daily activities of life. In addition to itch, it is characterized by markedly dry skin, small red bumps that may have fluid. Ichthyosis vulgaris is characterized by extremely dry, scaly skin with a fine white scale and increased amounts of lines noted on the palms. Filaggrin is a protein that is essential for the skin to function properly as a barrier and found to be mutated in some European patients with ichthyosis vulgaris and atopic dermatitis. This association has not been looked at in the African American population. Genomic DNA (gDNA) will be purified from buccal swabs using commercially available kits and analyzed.

Study Design

Allocation: Non-Randomized, Control: Active Control, Intervention Model: Single Group Assignment, Primary Purpose: Diagnostic

Conditions

Atopic Dermatitis

Intervention

Buccal Swab

Location

Children's Memorial Hospital
Chicago
Illinois
United States
60614

Status

Not yet recruiting

Source

Northwestern University

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:17:55-0400

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Medical and Biotech [MESH] Definitions

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A STEROID with GLUCOCORTICOID RECEPTOR activity that is used to manage the symptoms of ASTHMA; ALLERGIC RHINITIS, and ATOPIC DERMATITIS.

Rare autosomal recessive disease with variable expressions. Clinical features of the disease include variable ICHTHYOSIFORM ERYTHRODERMA, CONGENITAL; bamboo hair (trichorrhexis invaginata); and ATOPIC DERMATITIS. The disease is caused by mutations in the SPINK5 gene.

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