Eishi K, Lee J-B, Bae S-J, Takenaka M, Katayama I
Department of Dermatology, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Japan.
Br J Dermatol. 2002 Oct;147(4):683-8. doi: 10.1046/j.1365-2133.2002.04765.x.
Impaired sweating is thought to be a cause of barrier dysfunction in atopic dermatitis (AD).
To examine the sweating function in AD in a quantitative manner.
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.
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.
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.
出汗功能受损被认为是特应性皮炎(AD)屏障功能障碍的一个原因。
以定量方式研究AD患者的出汗功能。
我们通过定量汗腺轴突反射试验,对成年AD患者的皮损和非皮损皮肤的出汗反应进行了研究,该试验中轴突反射由乙酰胆碱离子导入刺激。测量了18例成年AD患者和40例非特应性对照者前臂掌侧的出汗量;还研究了5例干燥综合征患者作为疾病对照。我们还评估了4例AD患者局部使用皮质类固醇治疗后的出汗功能。研究的变量包括潜伏期、直接(DIR)出汗量和轴突反射介导的间接(AXR)出汗量。
与非特应性对照受试者相比,AD患者的潜伏期显著延长,AXR出汗量显著减少。皮损AD皮肤的潜伏期和AXR出汗量分别比非皮损皮肤显著延长和减少。相比之下,与非特应性对照相比,乙酰胆碱直接刺激引起的皮损或非皮损AD皮肤的DIR出汗量仅略有减少。局部使用皮质类固醇治疗后,皮损和非皮损AD皮肤的潜伏期和出汗量有所改善。
这些结果表明,AD患者出汗反应受损归因于异常的汗腺轴突反射,局部使用皮质类固醇可使其逆转。