Division of Skin Surface Sensing, Kyushu University, Fukuoka, Japan ; Department of Dermatology, Kyushu University, Fukuoka, Japan.
Department of Dermatology, Kyushu University, Fukuoka, Japan.
Onco Targets Ther. 2015 Jan 28;8:259-63. doi: 10.2147/OTT.S76860. eCollection 2015.
It has recently been shown that patients treated with epidermal growth factor receptor (EGFR) inhibitors often develop various cutaneous adverse events. While the pathogenesis underlying these events remains unclear, the relationship between skin toxicity induced by EGFR inhibitors and the sebaceous glands that express EGFR has been previously reported.
The primary aim of this study was to determine the relationship between cutaneous sebum levels and acneiform rash, a typical skin toxicity of EGFR inhibitors, by measuring the sebum levels before and after EGFR inhibitor treatment.
Eight patients diagnosed with non-small cell lung cancer (NSCLC) (three men and five women with an average age of 69.3 years) who were initiated on treatment with EGFR inhibitors (either gefitinib [Iressa(®)] or erlotinib [Tarceva(®)]) were enrolled. Using a Sebumeter(®), sebum levels in the face, chest, and back of each patient were measured before and after EGFR inhibitor treatment. The development of acneiform rash in each skin region was also assessed.
Changes in sebum level along with the development of an acneiform rash were observed after patients were started on EGFR inhibitor treatment. Patients who developed an EGFR inhibitor-induced acneiform rash tended to have higher pretreatment sebum levels (baseline) than did patients who did not experience an acneiform rash. At each time point measurement, sebum levels were found to be significantly higher in patients who had developed an acneiform rash at that time. Patients who developed rash during treatment showed greater differences in sebum level compared with pretreatment baseline.
Patients who had increased levels of sebum or whose sebum levels showed greater change from pretreatment baseline developed an acneiform rash, suggesting that sebaceous gland activity may be involved in the mechanism underlying the development of acneiform rash, in patients treated with EGFR inhibitors.
最近的研究表明，接受表皮生长因子受体（EGFR）抑制剂治疗的患者常发生各种皮肤不良事件。虽然这些事件的发病机制尚不清楚，但已报道 EGFR 抑制剂诱导的皮肤毒性与表达 EGFR 的皮脂腺之间存在关系。
本研究的主要目的是通过测量 EGFR 抑制剂治疗前后的皮脂水平来确定皮脂水平与痤疮样皮疹（EGFR 抑制剂的一种典型皮肤毒性）之间的关系。
本研究纳入了 8 名被诊断患有非小细胞肺癌（NSCLC）的患者（3 名男性和 5 名女性，平均年龄 69.3 岁），他们开始接受 EGFR 抑制剂（吉非替尼[Iressa（®）]或厄洛替尼[Tarceva（®）]）治疗。使用 Sebumeter（®），在开始 EGFR 抑制剂治疗前后测量每位患者面部、胸部和背部的皮脂水平。还评估了每个皮肤区域痤疮样皮疹的发展情况。
在开始 EGFR 抑制剂治疗后，观察到皮脂水平随痤疮样皮疹的发展而变化。发生 EGFR 抑制剂诱导的痤疮样皮疹的患者在开始治疗前的皮脂水平（基线）往往高于未发生痤疮样皮疹的患者。在每个时间点测量时，当时发生痤疮样皮疹的患者的皮脂水平明显更高。在治疗过程中出现皮疹的患者的皮脂水平与治疗前基线相比差异更大。
皮脂水平升高或皮脂水平从治疗前基线变化较大的患者发生痤疮样皮疹，这表明皮脂腺活动可能参与了 EGFR 抑制剂治疗患者痤疮样皮疹的发生机制。
