K Eishi1, J-B Lee, S-J Bae, M Takenaka, I Katayama. 1. Department of Dermatology, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Japan. kumeishi-ngs@umin.ac.jp
Abstract
BACKGROUND: Impaired sweating is thought to be a cause of barrier dysfunction in atopic dermatitis (AD). OBJECTIVES: To examine the sweating function in AD in a quantitative manner. METHODS: We investigated the sweating response of lesional and non-lesional skin of adult patients with AD by a quantitative sudomotor axon reflex test in which the axon reflex is stimulated by acetylcholine iontophoresis. Sweat volume on the volar aspect of the forearm was measured in 18 adult patients with AD and in 40 non-atopic controls; five patients with Sjögren's syndrome were also studied as disease comparators. We also evaluated the sweating function in four AD patients after topical corticosteroid therapy. Latency time, direct (DIR) sweat volume and axon reflex-mediated indirect (AXR) sweat volume were the variables studied. RESULTS: The latency time in AD patients was significantly prolonged and AXR sweat volume significantly reduced compared with those in non-atopic control subjects. The latency time and AXR sweat volume of lesional AD skin were significantly more prolonged and reduced, respectively, than those of non-lesional skin. In contrast, the DIR sweat volume of lesional or non-lesional AD skin induced by direct stimulation with acetylcholine was only slightly reduced when compared with that in non-atopic controls. Latency time and sweat volumes of lesional and non-lesional AD skin improved after topical corticosteroid therapy. CONCLUSIONS: These results suggest that the impaired sweat response in AD is attributable to an abnormal sudomotor axon reflex, which is reversed by topical corticosteroid administration.
BACKGROUND: Impaired sweating is thought to be a cause of barrier dysfunction in atopic dermatitis (AD). OBJECTIVES: To examine the sweating function in AD in a quantitative manner. METHODS: We investigated the sweating response of lesional and non-lesional skin of adult patients with AD by a quantitative sudomotor axon reflex test in which the axon reflex is stimulated by acetylcholine iontophoresis. Sweat volume on the volar aspect of the forearm was measured in 18 adult patients with AD and in 40 non-atopic controls; five patients with Sjögren's syndrome were also studied as disease comparators. We also evaluated the sweating function in four ADpatients after topical corticosteroid therapy. Latency time, direct (DIR) sweat volume and axon reflex-mediated indirect (AXR) sweat volume were the variables studied. RESULTS: The latency time in ADpatients was significantly prolonged and AXR sweat volume significantly reduced compared with those in non-atopic control subjects. The latency time and AXR sweat volume of lesional AD skin were significantly more prolonged and reduced, respectively, than those of non-lesional skin. In contrast, the DIR sweat volume of lesional or non-lesional AD skin induced by direct stimulation with acetylcholine was only slightly reduced when compared with that in non-atopic controls. Latency time and sweat volumes of lesional and non-lesional AD skin improved after topical corticosteroid therapy. CONCLUSIONS: These results suggest that the impaired sweat response in AD is attributable to an abnormal sudomotor axon reflex, which is reversed by topical corticosteroid administration.
Authors: L A Nattkemper; H G Lee; R Valdes-Rodriguez; N K Mollanazar; K M Sanders; G Yosipovitch Journal: Br J Dermatol Date: 2015-05-18 Impact factor: 9.302