Buschke-Lowenstein 肿瘤 (BLT) 是人乳头瘤病毒 (HPV) 的良性皮肤病表现。它们起源于免疫系统受损的个体中长期存在的尖锐湿疣。在本病例报告中，我们介绍了一位免疫功能正常的 68 岁女性，患有 HPV 尖锐湿疣，她的右侧腹股沟已转变为大型真菌性 BLT。患者的免疫能力取决于是否存在糖尿病、皮质类固醇治疗、器官移植、细胞毒治疗或任何已知的原发性或其他继发性免疫缺陷。值得注意的是，该患者有乳腺癌病史，通过肿瘤切除术、局部放疗、两年芳香酶抑制剂和选择性雌激素受体调节剂 (SERM) 联合治疗以及随后三年的进一步 SERM 治疗进行治疗。我们认为，她之前接受的 SERM 治疗将辅助性 T (Th)1 免疫反应转变为 Th2 反应。这可能损害了患者的 HPV 特异性细胞介导的免疫，有利于非保护性 Th2 主导效应。因此，它有可能实现免疫逃避，转变为 BLT 表型。此外，SERM 的免疫偏差最初可能会受到芳香酶抑制剂增强 Th1 反应的已知能力的阻碍。事实上，在 SERM 的无对抗影响下，随着芳香酶抑制剂治疗的停止，患者首先注意到 HPV 尖锐湿疣进展为 BLT 表型。由此产生的细胞因子环境可能导致了这名免疫功能正常的患者 BLT 表型的异常进展。版权所有 © 2023，Stratton 等人。

Buschke-Lowenstein tumors (BLTs) are benign dermatologic manifestations of human papillomavirus (HPV). They originate from longstanding condylomata in individuals with compromised immune systems. In this case report, we present a 68-year-old immunocompetent female with HPV condylomata that had transitioned to a large, fungated BLT in her right groin. The patient's immunocompetency was determined by the absence of diabetes, corticosteroid therapy, organ transplant, cytotoxic therapy, or any known primary or other secondary immunodeficiencies. Notably, the patient had a history of breast cancer, managed through lumpectomy, local radiation, and two years of combined aromatase inhibitor and selective estrogen receptor modulator (SERM) therapy, followed by three years of further SERM therapy. We propose that the effect of her previously received SERM therapy shifted the T helper (Th)1 immune response to a Th2 response. This may have compromised the patient's HPV-specific cell-mediated immunity, favoring a non-protective Th2-dominant effect. Thus, it potentially enabled immune evasion, transitioning to a BLT phenotype. Additionally, the immune skewing of the SERM may have been initially opposed by the known ability of aromatase inhibitors to potentiate Th1 responses. Indeed, the patient first noticed the appearance of HPV condylomata progressing to the BLT phenotype with the cessation of the aromatase inhibitor therapy under the unopposed influence of the SERM. The resultant cytokine milieu may have contributed to the unusual progression to the BLT phenotype in this otherwise immunocompetent patient.Copyright © 2023, Stratton et al.