Koulisis Nicole, Moysidis Stavros N, Olmos de Koo Lisa C, Russell Christy A, Kashani Amir H
USC Roski Eye Institute, Department of Ophthalmology, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
University of Massachusetts Medical School, Worcester, MA, United States.
Am J Ophthalmol Case Rep. 2016 May 18;3:8-13. doi: 10.1016/j.ajoc.2016.05.004. eCollection 2016 Oct.
To describe a case of tamoxifen toxicity superimposed on central serous chorioretinopathy (CSCR). We review the role of estrogen and the effect of tamoxifen on ocular tissues.
A 32-year-old Hispanic female with infiltrating ductal carcinoma of the left breast (T2N1M0, triple-positive), status post chemotherapy and bilateral mastectomy, presented with complaint of a floater and decreased central vision of the right eye (OD). Symptoms began three weeks after initiating tamoxifen and five months after the last cycle of chemotherapy and dexamethasone. Visual acuity (VA) was 20/30 OD at presentation. Clinical examination and multimodal imaging revealed subretinal fluid (SRF) and pigment epithelial detachment (PED) suggestive of CSCR. After one month of monitoring, VA improved to 20/20; there was SRF resolution, small PED, and focal ellipsoid zone (EZ) band loss. Two weeks later, after undergoing surgery and starting a topical steroid, she returned with count fingers (CF) VA and large SRF OD. Steroid cessation improved SRF after one month, but VA was unchanged. Tamoxifen was discontinued, and VA improved to 20/100 with near-complete resolution of SRF at three weeks, and significant reduction in choroidal thickness at two months. At final follow-up, VA was 20/200, and there was focal EZ band loss sub-foveally, minimal SRF, and small PED.
Treatment with tamoxifen may lead to ocular toxicity and can complicate the recovery course of patients affected with CSCR. Variations in levels of the estrogen receptor-alpha (ER-α) and treatment with tamoxifen (ER-α partial agonist) may lead to loss of the protective effect of estrogen in the retinal pigment epithelial cells in premenopausal women. Furthermore, tamoxifen toxicity can lead to focal photoreceptor loss. Treatment in these cases should be coordinated together with the oncologist.
描述一例他莫昔芬毒性叠加在中心性浆液性脉络膜视网膜病变（CSCR）上的病例。我们回顾雌激素的作用以及他莫昔芬对眼组织的影响。
一名32岁的西班牙裔女性，患有左乳浸润性导管癌（T2N1M0，三阳性），化疗及双侧乳房切除术后，因右眼出现飞蚊症和中心视力下降前来就诊。症状在开始服用他莫昔芬三周后以及最后一轮化疗和地塞米松五个月后出现。就诊时右眼视力（VA）为20/30。临床检查和多模态成像显示视网膜下液（SRF）和色素上皮脱离（PED），提示CSCR。经过一个月的监测，视力提高到20/20；视网膜下液消退，有小的色素上皮脱离和局灶性椭圆体带（EZ）缺失。两周后，在接受手术并开始局部使用类固醇后，她右眼视力仅能数指（CF）且视网膜下液增多。停用类固醇一个月后视网膜下液有所改善，但视力未变。停用他莫昔芬后，三周时视力提高到20/100，视网膜下液几乎完全消退，两个月时脉络膜厚度显著降低。在最后一次随访时，视力为20/200，黄斑下有局灶性椭圆体带缺失，视网膜下液极少，色素上皮脱离较小。
他莫昔芬治疗可能导致眼部毒性，并可能使CSCR患者的恢复过程复杂化。雌激素受体-α（ER-α）水平的变化以及他莫昔芬（ER-α部分激动剂）治疗可能导致绝经前女性视网膜色素上皮细胞中雌激素的保护作用丧失。此外，他莫昔芬毒性可导致局灶性光感受器丧失。这些病例的治疗应与肿瘤学家共同协调。
