Check Up: Drexel group finds cause of eczema itch

The eczema rash often appears after the itch. This patient has the skin irritation on his arm.
The eczema rash often appears after the itch. This patient has the skin irritation on his arm. (Drexel)
Posted: February 24, 2014

Patients with eczema tend to start itching before they see a rash, rather than the other way around, leading some to call it "the itch that rashes."

So what is this invisible agent that causes the itch?

Herbert B. Allen has been scratching his head over that one for years, but recently the Drexel University dermatologist achieved a measure of intellectual relief.

He and a team of colleagues at Drexel's College of Medicine report that the culprit is a slime-like substance called biofilm, produced by Staphylococcus bacteria on the skin.

The biofilm blocks sweat ducts, which in turn activates an immune response that leads to itching and inflammation, the team reported in the journal JAMA Dermatology.

Dermatologists have known for years that staph bacteria were somehow involved in the process, and they have known about the molecular pathways that lead to itching and inflammation.

What is new is the finding that the blocked sweat ducts lead to activation of the inflammatory response, said Allen, chairman of the medical school's dermatology department.

"This is kind of the missing puzzle piece," Allen said.

While estimates vary, physicians agree that eczema, which is marked by red, scaly patches on the skin, strikes tens of millions of Americans. It is also called atopic dermatitis.

Medicine is able to treat it fairly successfully, Allen said. The first line of defense is often topical steroids, which reduce the inflammation and give the body a chance to clear the bacteria on its own, Allen said.

The patient is then advised to change bathing habits to keep the ailment from coming back, Allen said. Cut back on soap and hot water, avoid scrubbing, and moisturize.

If the steroids do not work, some physicians advocate bathing in a mild bleach solution, but Allen urged that this be done only with physician guidance.

"If you do it too much, you can hurt the outer layer of the skin, and that just gets you into a vicious cycle," he said.

Still unclear is the role played by genetics. Past research has shown eczema sufferers tend to have a mutation in a gene called filaggrin - a variant that also predisposes the person to suffer from asthma.

Exactly how this mutation leads to eczema is unclear, but it contributes to the skin having a "faulty outer layer," Allen said.

In the study, the Drexel researchers found that a protein called "toll-like receptor 2" was activated in the skin of people suffering from eczema lesions, and not in the skin of people in a control group. This protein, which is involved in the part of the body's defenses called the innate immune system, was activated in the area of blocked sweat ducts, the authors reported.

Allen said the findings could theoretically lead to some sort of new drug treatment, but he said there was no reason to develop one because existing methods work well. His motivation for the research was simply to find out how the disease worked, he said.

"It seems so easy to cut back on soap and bathing, and to moisturize," Allen said. "And inexpensive, in this day when we're spending thousands on other drugs."


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