Dermatology World

Can preservatives in personal care products trigger contact dermatitis in atopic patients?

Acta Eruditorum

Abby Van Voorhees

Dr. Van Voorhees is the physician editor of Dermatology World. She interviews the author of a recent study each month.

By Abby S. Van Voorhees, MD, May 1, 2014

In this month’s Acta Eruditorum column, Physician Editor Abby S. Van Voorhees, MD, talks with Donald V. Belsito, MD, about his recent Journal of the American Academy of Dermatology article, “Cutaneous delayed-type hypersensitivity in patients with atopic dermatitis: reactivity to topical preservatives.”

Dr. Van Voorhees: Atopic dermatitis (AD) and contact dermatitis — didn’t we used to think that these two conditions rarely occurred in the same person? Do you feel that the dry skin seen in these patients is contributory in some way?

Dr. Belsito: That’s an interesting question because when the whole notion was that AD was a Th2-mediated disease and contact dermatitis was Th1, the presumption was that people with AD could not develop contact dermatitis because their whole immune system is skewed toward Th2. And then there was data in the literature showing that in individuals who were having acute atopic flares, their ability to be sensitized to allergens such as dinitrochlorobenzene was reduced. However, that data also showed that once their AD quieted down, they were able to be sensitized about the same as the normal population. Then in 2004 Donald Leung wrote an interesting article (J Clin Invest. 2004;113(5):651-657) where he showed that acute AD starts off as a Th2 disease, but as it moves on in chronicity it actually is a Th1 disease, probably because barrier disruption and scratching lead to a lot of pro-inflammatory cytokines. So what starts off as a Th2 process in the acute phase will switch to Th1 in the chronic phase, or at least that’s what he postulated.

Beyond that what you’re dealing with in atopics is barrier dysfunction and people putting a lot of things on their skin. So you have more frequent exposure in terms of the types of products being put on the skin and the greater ability for those products to penetrate through skin to the antigen-presenting cells and create allergy. In fact when we looked at our numbers, atopics were significantly more likely to have at least one positive patch test than non-atopic patients. This was just based on patch testing; we didn’t look at the relevance of the patch test reaction but just whether they could mount a delayed-type cellular-mediated hypersensitity reaction to allergens.

Dr. Van Voorhees: Were atopics at increased risk for all contactants in your study? Were there certain ones where reactions occurred with an increased frequency? Were any at a lower frequency?