CLINICAL LABORATORY PARALLELS DURING ULCER BLEEDING

Hemostatic therapy of ulcer bleeding (UB) is based on activation of the coagulation system and depression of the fibrinolytic one. However, not so much attention is paid to the oxidation-reduction system. Aim of the study. To elaborate the recommendations on optimization of hemostatic therapy. Materials and methods. 25 patients with UB. 4 pa-tients were evaluated by Forrest classification, type ІВ, 5 – type ІІА, 6 – type ІІВ, and 10 – type ІІІС. Patients with type ІВ had endoscopic hemostasis procedures. All patients got a standard complex of haemostatic therapy. Two patients who were evalu-ated by Forrest classification type ІІА had bleeding recurrence. The following data was determined in blood plasma: fibrinolytic and proteolytic activity, fibrinase, antithrombin ІІІ, prothrombin index, isolated double bonds, diene conjugates, cetodienes and conjugated trienes, oxidation of neutral and alkaline proteins, malonic aldehyde, renew glutathione, catalase. Results of the study. Patients who were evaluated by Forrest classification type ІІА had both a disorder of redox system and hemostasis system balance, caused by a violation of synthesis of its factors. This contributes to the occurrence of bleeding recurrence. The results of redox system together with the criteria for hemostasis condition can be used to predict the recurrence of ulcer bleeding. Medicinal measures need to be adjusted, and antioxidants together with hepatic protectors to be prescribed. Conclusions: 1. Patients with UB recurrence have an excessive activation of lipoperoxidation, low level of basic proteins, decrease in functional capacity of antioxidant mecha-nisms and hemostasis system imbalance, caused by a violation of synthesis of its factors. 2. Characteristic measurement of peroxidation activity, antioxidant mechanisms and criteria of hemostasis system is essential to take into account while predicting UB recurrence. 3. In case of UB one should add to the medication management those means that inhibit the activity of lipid oxidation and contribute to the restoration of synthesis processes of hemostasis factors.