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Akihiko Ikoma, MD; Roman Rukwied, PhD; Sonja Ständer, MD; Martin Steinhoff, MD, PhD; Yoshiki Miyachi, MD, PhD; Martin Schmelz, MD, PhD

Arch Dermatol. 2003;139:1455-1458.

Objective  Lowered threshold of neurons (ie, neuronal sensitization) in atopic dermatitis was investigated by testing sensitivity to histamine.

Design  Comparative study.

Setting  A dermatological clinic and a research laboratory.

Participants  Eighteen patients with atopic dermatitis (AD) and 6 patients with chronic plaque-type psoriasis as well as 14 healthy control subjects.

Interventions  Histamine prick was performed in lesional and nonlesional skin of patients and in control subjects.

Main Outcome Measures  Axon reflex flare and wheal were measured planimetrically, and the itch intensity was rated on a numerical scale (0-10).

Results  In nonlesional skin of patients with AD, itch intensity and axon reflex flare were both significantly smaller compared with controls (mean ± SEM maximum itch, 1.5 ± 0.3 vs 3.1 ± 0.2 [P<.05]; mean ± SEM diameter, 12.3 ± 2.0 vs 25.3 ± 2.5 mm [P<.01]). In lesional skin of patients with AD, on the contrary, massive itch was provoked (maximum itch, 4.4 ± 0.3), although flare was relatively small (diameter, 16.1 ± 3.4 mm). Itch ratings in patients with psoriasis were low both in lesional and nonlesional skin (maximum itch, 1.3 ± 0.6 and 1.0 ± 0.4, respectively).

Conclusion  As the area of axon reflex flare is an indirect measure of activity in primary afferent neurons, our results suggest a decreased activation of peripheral pruriceptors in patients with AD. The massively increased itch in lesional skin of patients with AD might therefore be based on sensitization for itch in the spinal cord rather than in primary afferent neurons. This sensitization does not appear to be simply based on skin inflammation because histamine-induced itch was not augmented in lesional skin of psoriasis.

From the Departments of Dermatology, Kyoto University, Kyoto, Japan (Drs Ikoma and Miyachi), and University of Muenster, Muenster, Germany (Drs Ständer and Steinhoff); Department of Physiology and Experimental Pathophysiology, University of Erlangen-Nuremberg, Erlangen, Germany (Dr Schmelz); and Department of Anesthesiology–Mannheim, University of Heidelberg, Mannheim, Germany (Drs Rukwied and Schmelz). The authors have no relevant financial interest in this article.

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