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Dermatitis (Eczema)

»	What is dermatitis and why is it so important?
»	What is atopy?
»	Why is atopic dermatitis becoming more common?
»	What are the diagnostic criteria for atopic dermatitis?
»	What is the underlying defect in patients with atopic dermatitis?
»	In atopic dermatitis, which comes first - the itch or the rash?
»	Why does atopic dermatitis itch?
»	Why do people like to scratch an itch?
»	Does psychological stress worsen atopic dermatitis?
»	Did John Phillip Sousa write the “Atopic March?”
»	How does atopic dermatitis present at different ages?
»	What physical findings are associated with atopic dermatitis?
»	What factors provoke or exacerbate atopic dermatitis?
»	How can your atopic patients relieve their pruritic agony and discomfort?
»	What is the role of antihistamines in atopic dermatitis?
»	Describe the “two-pajamas treatment.”
»	Is “hand dermatitis” a specific entity?
»	What is pompholyx?
»	How can pompholyx be managed?
»	Describe the typical presentation of nummular eczema.
»	What causes nummular eczema?
»	Is there a cure for nummular eczema?
»	How does seborrheic dermatitis present in children?
»	How does seborrheic dermatitis present in adults?
»	What causes seborrheic dermatitis, and with what disease states is it commonly found?
»	Discuss the treatment approaches to seborrheic dermatitis.
»	What is an “id” reaction, and what does it have to do with Sigmund Freud?
»	What are the most common settings for an id reaction and how should you treat it?
»	What do you call dermatitis that covers virtually the whole cutaneous surface?
»	How can you determine the cause of a patient’s exfoliative dermatitis?
»	What general treatment measures are used to treat patients with exfoliative dermatitis?

What is the underlying defect in patients with atopic dermatitis?

At least 50% of patients with moderate to severe atopic dermatitis have a defect in the gene coding for filaggrin, a protein essential to maintaining the barrier function of the stratum corneum. The stratum corneum then allows various irritants, microbes, or allergens to penetrate the skin surface, elicit cytokine release from keratinocytes, and initiate a Th2 immune response acutely that leads to the clinical manifestations of disease and increased IgE levels. In chronic cases of atopic dermatitis, the Th2 response is replaced by a Th1 response. A primary immune defect, at least in some atopic patients, cannot yet be ruled out because bone marrow stem cell transplants from atopic patients have transferred atopic dermatitis to recipients.

Terui T: Analysis of the mechanism for the development of allergic skin inflammation and the application for its treatment: overview of the pathophysiology of atopic dermatitis, J Pharmacol Sci 110:232–236, 2009.