IMPAIRED COAGULATION HEMOSTASIS IN VITAMIN B 12-DEFICIENCY ANEMIAS

Aim. To reveal the presence of hemostatic disturbances in vitamin B 12-deficient anemias. Materials and methods. Coagulation hemostasis, lipid oxidation and epithelial vasodilating function indices were studied in 22 patients with vitamin B 12-deficient anemia. The control indices were assessed in 25 practically healthy persons. The examined group of patients and the control group were comparable by sex and age. Results. Lipid peroxidation parameters estimated in patients with megaloblastic anemias confirmed reliable increase in plasma malonic dialdehyde (MDA) content ( p =0,0041). Simultaneously, significant decrease in antioxidant activity (AOA) of both plasma ( p =0,00041) and erythrocytes ( p =0,0006) was detected. Reliable shortening of activated partially thromboplastin time (APTT) and lengthening of XIIa-kallikrein-dependent fibrinolysis (XDF) in long-ailing patients ( p =0,040 and p =0,023) indicated aggravation of disturbances in coagulation and fibrinolytic components of hemostasis sytem in case of B 12-DA while the disease is progressing. Analysis of the obtained data shows that the parameter characterizing the activity of lipid (plasmа.MDA) free-radical oxidation (FRO) is negatively connected with duration of autocoagulation test (ACT) and APTT ( r =0,53, p =0,026 and r =0,56, p =0,009). Plasma AOA directly correlates with duration of prothrombin time (PTT) ( r =0,42, p =0,039). Conclusions. Hemic hypoxia conditioned by the degree of severity of anemia is accompanied by activation of free-radical lipid oxidation and development of oxidative stress. Decline in blood antioxidant potential and increase in malonic dialdehyde concentration in plasma and erythrocytes leads to endothelial dysfunction, development of hypocoagulation, inhibition of fibrinolysis and appearance of laboratory signs of chronic DIVC syndrome.

Vitamin B -deficiency anemia, hemic hypoxia, prooxidant stress, endothelial dysfunction, impaired coagulation hemostasis