Doelker Laurence, Tran Christian, Gkomouzas Angelos, Grand Denise, Sorg Olivier, Saurat Jean-Hilaire, Lübbe Jann
Department of Dermatology, University Hospital, Geneva, Switzerland.
Exp Dermatol. 2006 May;15(5):342-6. doi: 10.1111/j.0906-6705.2006.00413.x.
Ultraviolet (UV)-induced pyrimidine dimers are an early step in skin carcinogenesis, which is accelerated in the setting of long-term immunosuppression with systemic calcineurin inhibitors. It is not known whether topical application of calcineurin inhibitors exposes to a similar risk.
To assess the formation and clearance of UV-induced dipyrimidine dimers in human epidermis treated with topical pimecrolimus as compared to topical steroid, vehicle and untreated control.
Pretreated buttock skin of 20 human volunteers with (10) or without (10) atopic dermatitis was exposed to two minimal erythema doses (MED) of simulated solar radiation. DNA was extracted from epidermis 1 and 24 h postirradiation. Pyrimidine dimers were visualized by immuno slot blots and quantified by chemoluminescence image analysis.
One-hour postirradiation, pimecrolimus-treated epidermis contains less DNA damage as compared to untreated control, but there were no statistically significant differences between pimecrolimus, triamcinolone acetonide and vehicle. Dimer levels at 24 h postirradiation showed no significant differences between different treatments.
Treatment with pimecrolimus cream, triamcinolone acetonide cream and vehicle is not associated with increased epidermal DNA damage at 1 and 24 h post-UV exposure.
紫外线（UV）诱导的嘧啶二聚体是皮肤癌发生的早期步骤，在长期使用全身钙调神经磷酸酶抑制剂导致免疫抑制的情况下，这一过程会加速。尚不清楚局部应用钙调神经磷酸酶抑制剂是否会带来类似风险。
与局部用类固醇、赋形剂及未治疗的对照相比，评估局部应用吡美莫司治疗的人表皮中紫外线诱导的二嘧啶二聚体的形成和清除情况。
20名有（10名）或无（10名）特应性皮炎的人类志愿者的预处理臀部皮肤接受两次最小红斑量（MED）的模拟太阳辐射。在照射后1小时和24小时从表皮提取DNA。通过免疫斑点印迹观察嘧啶二聚体，并通过化学发光图像分析进行定量。
照射后1小时，与未治疗的对照相比，吡美莫司治疗的表皮DNA损伤较少，但吡美莫司、曲安奈德和赋形剂之间无统计学显著差异。照射后24小时的二聚体水平在不同治疗之间无显著差异。
在紫外线照射后1小时和24小时，使用吡美莫司乳膏、曲安奈德乳膏和赋形剂治疗与表皮DNA损伤增加无关。
