Thiol-Disulfide Homeostasis and Ischemia Modified Albumin as a New Oxidative Stress Marker in Patients with Polycythemia Vera

Abstract

P olycythemia Vera (PV) is a chronic myeloproliferative disease characterized by increased red blood cells or erythrocytosis originating from hematopoietic stem cells. [1][2][3] PV was first described in 1892 and its age-related incidence rate is 2.5-10/100,000 people. [4] The mean age at diagnosis is generally 60 years old in male patients. The diagnostic criteria of the World Health Organization (WHO) include elevated hemoglobin or hematocrit levels, abnormal results on bone marrow biopsy, and the presence of the JACK 2 genetic mutation, which is found in approximately 98% of cases. The majority of PV patients have a mutation in the Janus-type tyrosine kinase-2 (JAK2) gene. [3] A below-normal level of erythropoietin distinguishes PV from common secondary causes of erythrocytosis such as smoking, sleep apnea, and testosterone use. [5] The precise mechanism of uncontrolled cell growth in PV has not been clarified, although the consequences of tyrosine kinase activations due to JAK2-dependent mutation are known. In Objectives: The present study aims to indicate both thiol-disulfide hemostasis and ischemia-modified albumin (IMA) levels in patients with Polycythemia Vera (PV). Methods: In this prospective case-control study, 34 PV patients and 31 healthy control participants were included. Thiol levels were measured with a new modified colorimetric method. IMA levels were determined by cobalt binding test. Results: Thiol levels were statistically significant between the groups. (p<0.001). IMA levels were also significanlty higher in PV group than healthy control subjects (p<0.001). We revealed that thiol and IMA levels were significantly higher in patients with PV in respect to the control groups. Conclusion:The obtain results indicate that the oxidative balance is disturbed and changed towards the oxidant direction. The dynamic-thiol disulfide balance has moved to proliferation side in patients with PV, and may provide important contributions to the patient's follow-up and disease pathophysiology.