Dermatitis drugs' mechanisms of action clarified

NEW YORK (Reuters Health) – Drugs used to treat atopic dermatitis and allergic contact dermatitis appear to work by interfering with T cell-mediated keratinocyte apoptosis, according to a recent report. "Monitoring keratinocyte apoptosis can therefore indicate the severity of the lesion and the effectiveness of any treatment," researchers suggest.

Dr. Axel Trautmann, from the Swiss Institute of Allergy and Asthma Research in Davos, and colleagues used an in vitro model of eczematous dermatitis to analyze the cellular actions of several dermatitis drugs. In addition, biopsy specimens from treated and untreated dermatitis patients were evaluated for keratinocyte apoptosis.

Dexamethasone, cyclosporine A, tacrolimus, rapamycine, and intravenous immunoglobulin inhibited T cell-mediated keratinocyte apoptosis, the researchers note in the November issue of The Journal of Allergy and Clinical Immunology.

Two major mechanisms of action were identified. The first, witnessed with dexamethasone, tacrolimus, cyclosporine A, and rapamycine, involved inhibition of T-cell activation. The second mechanism, seen with IVIG and high-dose dexamethasone, involved direct inhibition of Fas-mediated keratinocyte apoptosis.

In patients with eczematous dermatitis, a significant reduction in keratinocyte apoptosis was noted after successful topical treatment, the investigators note.

The extent of keratinocyte apoptosis appears to be a more reliable marker of disease severity than the magnitude of the T-cell response.

"These results demonstrate mechanisms of action of current treatment approaches and provide a future for more focused therapeutic applications," they conclude.

J Allergy Clin Immunol 2001;108:839-846.

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