Case Report
Copyright ©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Nov 26, 2020; 8(22): 5657-5662
Published online Nov 26, 2020. doi: 10.12998/wjcc.v8.i22.5657
Azacitidine decreases reactive oxygen species production in peripheral white blood cells: A case report
Hidekazu Hasunuma, Naomi Shimizu, Hiromitsu Yokota, Ichiro Tatsuno
Hidekazu Hasunuma, Department of Blood Transfusion, Toho University Medical Center Sakura Hospital, Sakura 2858741, Japan
Naomi Shimizu, Department of Hematology, Toho University Medical Center Sakura Hospital, Sakura 2858741, Japan
Hiromitsu Yokota, Clinical Laboratory Program, Education Development Center, Faculty of Science Toho University, Funabashi 2748510, Japan
Ichiro Tatsuno, Center for Diabetes, Metabolism and Endocrinology, Toho University Medical Center Sakura Hospital, Sakura 2858741, Japan
Author contributions: Hasunuma H carried out basic experiments; Shimizu N collected clinical data and drafted the manuscript; Yokota H and Tatsuno I checked the manuscript.
Informed consent statement: Written informed consent was obtained from the patient for publication of this report.
Conflict-of-interest statement: The authors declare no conflict of interests for this manuscript.
CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Naomi Shimizu, MD, PhD, Assistant Professor, Department of Hematology, Toho University Medical Center Sakura Hospital, No. 564-1, Shimoshizu, Sakura 2858741, Japan. naomis-cib@umin.ac.jp
Received: June 3, 2020
Peer-review started: June 3, 2020
First decision: September 13, 2020
Revised: September 22, 2020
Accepted: October 13, 2020
Article in press: October 13, 2020
Published online: November 26, 2020
Abstract
BACKGROUND

In myelodysplastic syndrome (MDS), oxidative stress is closely related to iron overload and DNA damage. A recent study suggested the possibility that increased oxidative stress causes not only iron overload but also disease progression of MDS with DNA damage. We present a case of MDS with decreased reactive oxygen species (ROS) production in peripheral white blood cells (WBCs) and decreased diacron-reactive oxygen metabolites (d-ROMs) in serum after azacitidine therapy.

CASE SUMMARY

A 74-year-old man presented to the hematological department with the chief complaint of anemia. His vital signs were within normal limits at admission with a heart rate of 80 bpm and blood pressure of 135/60 mmHg. Laboratory tests indicated pancytopenia, a WBC count of 2190 cells/µL, a hemoglobin level of 6.2 g/dL and a platelet count of 7.4 × 104/µL. The patient was diagnosed with MDS with fibrosis after a bone marrow examination. This case showed decreased ROS production in WBCs, d-ROMs in serum and Wilms’ tumor 1 after azacitidine therapy, after which his hematopoiesis recovered.

CONCLUSION

Azacitidine therapy can improve hematopoiesis and decrease ROS and d-ROM production.

Keywords: Myelodysplastic syndrome, Reactive oxygen species, Diacron-reactive oxygen metabolites, Ferritin, Azacitidine, Case report

Core Tip: Accumulation of reactive oxygen species (ROS) contributes to the development and progression of cancer. We reported a case of myelodysplastic syndrome that showed decreased ROS production by white blood cells, decreased diacron-reactive oxygen metabolites (d-ROMs) in serum and decreased Wilms’ tumor 1 after azacitidine therapy, which can improve hematopoiesis by decreasing ROS and d-ROMs production.