Lerche Catharina M, Philipsen Peter A, Poulsen Thomas, Wulf Hans Christian
Department of Dermatology, Copenhagen University Hospital, Bispebjerg, Copenhagen, Denmark.
Exp Dermatol. 2010 Nov;19(11):973-9. doi: 10.1111/j.1600-0625.2009.01034.x.
Topical corticosteroids such as hydrocortisone-17-butyrate (HCB) and clobetasol-17-propionate (CP) and vitamin D(3) derivatives such as calcipotriol (CAL) are widely used to treat psoriasis. The immunosuppressive effects of corticosteroids make their topical use a concern for skin carcinogenicity. Few studies have assessed the effect of topical corticosteroids and topical vitamin D(3) derivatives on photocarcinogenesis induced by ultraviolet radiation. We investigated whether HCB, CP, or CAL can accelerate photocarcinogenesis using simulated solar radiation (SSR). HCB, CP, or CAL was applied topically to the backs of hairless, female, C3.Cg/TifBomTac-immunocompetent mice in 16 groups of 25 mice each. The drugs were applied three times weekly followed by 0, 2, 4, or 6 standard erythema doses (SED) of SSR for 365 days or until death. No change was observed in the time required for tumor development in mice treated with HCB and 2 SED (HCB-2SED) and HCB-6SED. However, the time required for tumor development increased with HCB-4SED treatment. Treatment with CP-2SED did not change the time to onset of the first and second tumor, but all other CP treatments in combination with SSR increased the time. CAL-2SED decreased the time to onset of the first tumor but not of the second and third tumor. CAL-4SED and CAL-6 SED did not change or increased the time to tumor development. Our data indicated that topical administration of HCB and CAL did not alter the photocarcinogenesis of SSR and that topical CP administration had a photoprotective effect. Thus, HCB, CP, and CAL do not increase photocarcinogenesis induced by SSR.
外用皮质类固醇如丁酸氢化可的松（HCB）和丙酸氯倍他索（CP）以及维生素D(3)衍生物如卡泊三醇（CAL）被广泛用于治疗银屑病。皮质类固醇的免疫抑制作用使其外用引发了对皮肤致癌性的担忧。很少有研究评估外用皮质类固醇和外用维生素D(3)衍生物对紫外线诱导的光致癌作用的影响。我们使用模拟太阳辐射（SSR）研究了HCB、CP或CAL是否会加速光致癌作用。将HCB、CP或CAL局部应用于16组每组25只的无毛雌性C3.Cg/TifBomTac免疫活性小鼠的背部。每周给药三次，随后给予0、2、4或6个标准红斑剂量（SED）的SSR，持续365天或直至死亡。在用HCB和2 SED（HCB - 2SED）以及HCB - 6SED处理的小鼠中，未观察到肿瘤发生时间的变化。然而，HCB - 4SED处理使肿瘤发生时间增加。CP - 2SED处理并未改变第一和第二个肿瘤出现的时间，但与SSR联合的所有其他CP处理均增加了时间。CAL - 2SED缩短了第一个肿瘤出现的时间，但未缩短第二个和第三个肿瘤出现的时间。CAL - 4SED和CAL - 6 SED未改变或增加肿瘤发生时间。我们的数据表明，局部应用HCB和CAL不会改变SSR的光致癌作用，局部应用CP具有光保护作用。因此，HCB、CP和CAL不会增加SSR诱导的光致癌作用。
