Potmešil Petr, Szotkowská Radka
Third Faculty of Medicine, Department of Pharmacology, Charles University, Prague, Czech Republic and Faculty of Medicine, Department of Pharmacology and Toxicology, Charles University, Pilsen, Czech Republic.
2nd Department of Internal Medicine, University Hospital Královské Vinohrady and Third Faculty of Medicine, Charles University, Prague, Czech Republic.
Ther Adv Chronic Dis. 2020 Nov 16;11:2040622320964152. doi: 10.1177/2040622320964152. eCollection 2020.
Anastrozole is a selective non-steroidal aromatase inhibitor that blocks the conversion of androgens to estrogens in peripheral tissues. It is used as adjuvant therapy for early-stage hormone-sensitive breast cancer in postmenopausal women. Significant side effects of anastrozole include osteoporosis and increased levels of cholesterol. To date, seven case reports on anastrozole hepatotoxicity have been published. We report the case of an 81-year-old woman with a history of breast cancer, arterial hypertension, type 2 diabetes mellitus, hyperlipidemia, and chronic renal insufficiency. Four days after switching hormone therapy from tamoxifen to anastrozole, icterus developed along with a significant increase in liver enzymes (measured in the blood). The patient was admitted to hospital, where a differential diagnosis of jaundice was made and anastrozole was withdrawn. Subsequently, hepatic functions quickly normalized. The observed liver injury was attributed to anastrozole since other possible causes of jaundice were excluded. However, concomitant pharmacotherapy could have contributed to the development of jaundice and hepatotoxicity, after switching from tamoxifen to anastrozole since several the patient's medications were capable of inhibiting hepatobiliary transport of bilirubin, bile acids, and metabolized drugs through inhibition of ATP-binding cassette proteins. Telmisartan, tamoxifen, and metformin all block bile salt efflux pumps. The efflux function of multidrug resistance protein 2 is known to be reduced by telmisartan and tamoxifen and breast cancer resistance protein is known to be inhibited by telmisartan and amlodipine. Moreover, the activity of P-glycoprotein transporters are known to be decreased by telmisartan, amlodipine, gliquidone, as well as the previously administered tamoxifen. Finally, the role of genetic polymorphisms of cytochrome P450 enzymes and/or drug transporters cannot be ruled out since the patient was not tested for polymorphisms.
阿那曲唑是一种选择性非甾体芳香酶抑制剂,可阻断外周组织中雄激素向雌激素的转化。它被用作绝经后妇女早期激素敏感性乳腺癌的辅助治疗。阿那曲唑的显著副作用包括骨质疏松症和胆固醇水平升高。迄今为止,已发表了7例关于阿那曲唑肝毒性的病例报告。我们报告了一名81岁女性的病例,她有乳腺癌、动脉高血压、2型糖尿病、高脂血症和慢性肾功能不全病史。在将激素治疗从他莫昔芬改为阿那曲唑4天后,出现黄疸,同时肝酶(血液中测量)显著升高。患者入院后,进行了黄疸的鉴别诊断,并停用了阿那曲唑。随后,肝功能迅速恢复正常。观察到的肝损伤归因于阿那曲唑,因为排除了其他可能导致黄疸的原因。然而,从他莫昔芬改为阿那曲唑后,伴随的药物治疗可能导致了黄疸和肝毒性的发生,因为患者的几种药物能够通过抑制ATP结合盒蛋白来抑制胆红素、胆汁酸和代谢药物的肝胆转运。替米沙坦、他莫昔芬和二甲双胍均能阻断胆盐外排泵。已知替米沙坦和他莫昔芬可降低多药耐药蛋白2的外排功能,替米沙坦和氨氯地平可抑制乳腺癌耐药蛋白。此外,已知替米沙坦、氨氯地平、格列喹酮以及先前使用的他莫昔芬可降低P-糖蛋白转运体的活性。最后,由于未对患者进行细胞色素P450酶和/或药物转运体基因多态性检测,因此不能排除其作用。