Published online Nov 26, 2020. doi: 10.12998/wjcc.v8.i22.5657
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
Processing time: 175 Days and 9.6 Hours
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.
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.
Azacitidine therapy can improve hematopoiesis and decrease ROS and d-ROM production.
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.