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一名接受芳香化酶抑制剂治疗乳腺癌的患者出现红细胞增多症的病例。

A case of erythrocytosis in a patient treated with an aromatase inhibitor for breast cancer.

作者信息

Iyengar Abhinav, Sheppard Dawn

机构信息

Hematology Division, Department of Medicine, The Ottawa Hospital, 501 Smyth Road, Ottawa, ON, Canada K1H 8L6.

出版信息

Case Rep Hematol. 2013;2013:615189. doi: 10.1155/2013/615189. Epub 2013 Nov 7.

DOI:10.1155/2013/615189
PMID:24312736
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3838821/
Abstract

A previously healthy 79-year-old female was referred to hematology for further evaluation of erythrocytosis. Two years earlier she had been diagnosed with ER/PR-positive ductal carcinoma of the breast and was receiving hormonal therapy with exemestane. No secondary cause of erythrocytosis was identified. Serum erythropoietin (EPO) level was normal, and molecular testing for the JAK2 V617F and exon 12 mutations was negative. A bone marrow biopsy showed a mild increase in erythropoiesis, and no spontaneous erythroid colonies were demonstrated. Erythrocytosis is common reason for referral to a hematologist. The myeloproliferative disorder, polycythemia vera, and the rare congenital polycythemias represent primary erythrocytosis. Common secondary causes include smoking, obstructive sleep apnea, and other pulmonary diseases. Erythrocytosis is well described with certain classes of drugs, including androgens. We hypothesize that exemestane contributed to the development of erythrocytosis in our patient. To our knowledge, erythrocytosis has not been previously described in association with aromatase inhibitors. These drugs prevent the conversion of androstenedione and testosterone to estrogen; thus the physiologic mechanisms may be similar to those responsible for erythrocytosis seen with exogenous androgens. These mechanisms are not well understood, but may include altered iron metabolism by a reduction in hepcidin levels.

摘要

一名既往健康的79岁女性因红细胞增多症被转诊至血液科进行进一步评估。两年前,她被诊断为雌激素受体/孕激素受体(ER/PR)阳性的乳腺导管癌,正在接受依西美坦激素治疗。未发现红细胞增多症的继发原因。血清促红细胞生成素(EPO)水平正常,JAK2 V617F和第12外显子突变的分子检测为阴性。骨髓活检显示红细胞生成轻度增加,未发现自发红系集落。红细胞增多症是转诊至血液科医生的常见原因。骨髓增殖性疾病、真性红细胞增多症和罕见的先天性红细胞增多症代表原发性红细胞增多症。常见的继发原因包括吸烟、阻塞性睡眠呼吸暂停和其他肺部疾病。某些类别的药物(包括雄激素)也会导致红细胞增多症。我们推测依西美坦导致了我们患者红细胞增多症的发生。据我们所知,以前尚未有过依西美坦与红细胞增多症相关的报道。这些药物可阻止雄烯二酮和睾酮转化为雌激素;因此其生理机制可能与外源性雄激素导致红细胞增多症的机制相似。这些机制尚不完全清楚,但可能包括通过降低铁调素水平改变铁代谢。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6855/3838821/4a44879896fd/CRIM.HEMATOLOGY2013-615189.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6855/3838821/4a44879896fd/CRIM.HEMATOLOGY2013-615189.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6855/3838821/4a44879896fd/CRIM.HEMATOLOGY2013-615189.001.jpg

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引用本文的文献

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Aromatase Inhibitor-Induced Erythrocytosis in a Patient Undergoing Hormonal Treatment for Breast Cancer.一名接受乳腺癌激素治疗的患者出现芳香化酶抑制剂诱导的红细胞增多症。
Case Rep Hematol. 2015;2015:784783. doi: 10.1155/2015/784783. Epub 2015 Jun 2.

本文引用的文献

1
Testosterone suppresses hepcidin in men: a potential mechanism for testosterone-induced erythrocytosis.睾酮抑制男性的铁调素:睾酮诱导红细胞增多症的一个潜在机制。
J Clin Endocrinol Metab. 2010 Oct;95(10):4743-7. doi: 10.1210/jc.2010-0864. Epub 2010 Jul 21.
2
JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis.真性红细胞增多症和特发性红细胞增多症中的JAK2外显子12突变
N Engl J Med. 2007 Feb 1;356(5):459-68. doi: 10.1056/NEJMoa065202.
3
JAK2 associates with the erythropoietin receptor and is tyrosine phosphorylated and activated following stimulation with erythropoietin.
JAK2与促红细胞生成素受体结合,并在促红细胞生成素刺激后发生酪氨酸磷酸化并被激活。
Cell. 1993 Jul 30;74(2):227-36. doi: 10.1016/0092-8674(93)90414-l.
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A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietin gene enhancer at a site required for transcriptional activation.一种通过从头合成蛋白质由缺氧诱导的核因子,在转录激活所需的位点与人类促红细胞生成素基因增强子结合。
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