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Case Reports in Hematology
Volume 2013, Article ID 615189, 3 pages
http://dx.doi.org/10.1155/2013/615189
Case Report

A Case of Erythrocytosis in a Patient Treated with an Aromatase Inhibitor for Breast Cancer

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

Received 2 September 2013; Accepted 22 September 2013

Academic Editors: U. Dasgupta, C. Imai, K. Khair, and D. Rund

Copyright © 2013 Abhinav Iyengar and Dawn Sheppard. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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.