Le T K, De Mon P, Schalkwijk J, van der Valk P G
Department of Dermatology, University Hospital Nijmegen, The Netherlands.
Contact Dermatitis. 1997 Jul;37(1):19-26. doi: 10.1111/j.1600-0536.1997.tb00369.x.
Exposure of the skin to sodium dodecyl sulfate (SDS) leads to disruption of barrier and skin irritation. We used repetitive short exposure to a low molarity SDS solution as an in vivo model to mimic the development of irritant contact dermatitis. In this model, we studied clinical (erythema), functional (transepidermal water loss(TEWL)) and cell biological changes. 24 healthy volunteers were patch tested with SDS (0.2%) for 4 h a day for 5 consecutive days. After removal of the patches, the exposed sites were treated 1 X daily either with a topical corticosteroid (triamcinolon acetonide cream 0.05%), a retinoid (tretinoin cream 0.025%), or a vitamin D3 derivative (calcipotriol ointment 50 micrograms/g). Irritant reactions were assessed by erythema scoring and measurement of barrier function with TEWL up to 14 days after the first challenge. Skin biopsies were taken for cell biological changes at day 4. Vehicle-treated sites served as controls. Repetitive exposure of human skin to SDS resulted in a gradual increase in erythema scoring and TEWL associated with the upregulation of proliferative cells as measured by the expression of Ki-67-antigen and of differentiation markers, visualized by increased expression of involucrin and epidermal-fatty-acid binding protein (E-FABP). Skin irritation as assessed by erythema scoring and TEWL was not significantly suppressed by triamcinolone cream. However, a significant reduction of the number of cycling keratinocytes and a decrease in involucrin positive cell layers was observed in this group. Neither treatment with calcipotriol ointment nor with tretinoin cream induced improvement of skin irritation as judged by visual scoring and TEWL. In contrast to steroid treatment, no significant effect of calcipotriol ointment or tretinoin cream treatment was observed with regard to the number of cycling cells and differentiation markers. Further studies are needed to assess whether treatment with topical corticosteroids is an effective modality in skin irritation and irritant contact dermatitis.
皮肤暴露于十二烷基硫酸钠（SDS）会导致屏障破坏和皮肤刺激。我们使用低摩尔浓度SDS溶液的重复短时间暴露作为体内模型，以模拟刺激性接触性皮炎的发展。在此模型中，我们研究了临床（红斑）、功能（经表皮水分流失（TEWL））和细胞生物学变化。24名健康志愿者连续5天每天用0.2%的SDS进行4小时的斑贴试验。去除斑贴后，暴露部位每天用一种局部皮质类固醇（0.05%曲安奈德乳膏）、一种维甲酸（0.025%维甲酸乳膏）或一种维生素D3衍生物（50微克/克卡泊三醇软膏）治疗1次。通过红斑评分和TEWL测量屏障功能，在首次激发后长达14天评估刺激性反应。在第4天取皮肤活检样本进行细胞生物学变化研究。用赋形剂处理的部位作为对照。人体皮肤重复暴露于SDS导致红斑评分和TEWL逐渐增加，这与通过Ki-67抗原表达测量的增殖细胞上调以及通过内聚蛋白和表皮脂肪酸结合蛋白（E-FABP）表达增加而可视化的分化标志物有关。通过红斑评分和TEWL评估的皮肤刺激未被曲安奈德乳膏显著抑制。然而，在该组中观察到循环角质形成细胞数量显著减少以及内聚蛋白阳性细胞层数减少。根据视觉评分和TEWL判断，卡泊三醇软膏或维甲酸乳膏治疗均未引起皮肤刺激改善。与类固醇治疗相反，卡泊三醇软膏或维甲酸乳膏治疗对循环细胞数量和分化标志物没有显著影响。需要进一步研究以评估局部皮质类固醇治疗是否是皮肤刺激和刺激性接触性皮炎的有效治疗方式。
