The role of oxidative stress in the liver injury pathogenesis in patients with acute myeloid leukemia

Abstract

In patients with acute myeloid leukemia (AML), development of hepatotoxic reactions against the background of chemotherapy (CT) can be caused by either hematologic disease impact, or chemotherapy effects.Objective — to investigate the role of oxidative stress in the development of hepatotoxic reactions in patients with AML during CT.Materials and methods. The study involved 56 patients with AML, who underwent the first remission induction cycle. The ratio of women to men was 25 (44.6 %)/31 (55.4 %), age range 21 to 77 years. The examination was performed at baseline before treatment and on the 14th day of CT. Alanine (ALT) and asparagine (AST) aminotransferase, alkaline phosphatase (AP), gamaglutamyltranspeptidase (GGTP), total protein, total bilirubin and serum urea were evaluated. The concentration of TBA‑reactants and serum catalase activity were determined.Results. At baseline the abnormalities in biochemical liver tests were detected in 42.8 % (24/56) of patients. Prior to CT, the ALT activity in the blood serum of patients with AML was increased in 2.4 times, AST — in 1.3 times, GGTP — 2.3 times, AP — 1.7 times compared with almost healthy individuals (p < 0.05). The increased concentration of TBA‑reactants in 1.7 times (1.84 ± 0.1vs 1.1 ± 0.1) mmol/l and catalase activity in 1.9 times (25.8 ± 0.9 vs 13.07 ± 0.6) mkkat/l compared to norm was also revealed. After CT, the hepatotoxic reactions development was observed in 64.3 % (36/56) of patients with AML, whose risk factor was the primary impaired liver biochemical tests (RR = 2.66; 95 % СІ 1.7 — 4.17; р < 0.05).Conclusions. Liver injury in AML patients is characterized by the mixed‑type hepatotoxic reactions development, which are accompanied by the activation of free radical oxidation and antioxidant protection systems.