Розлади системи гемостазу на тлі порушення функції зовнішнього дихання при коморбідному перебігу хронічного обструктивного захворювання легень та хронічного панкреатиту

The comorbidity course of chronic obstructive pulmonary disease (COPD) and chronic pancreatitis (CP) can exacerbate the clinical manifestations of both diseases and increases the frequency of relapses of the pathological process due to disturbances of hemocoagulation. The objective: to establish the features of the external respiratory function and the state of selected hemostasis factors and fibrinolytic activity in patients with COPD and concomitant CP. Materials and methods. 144 patients with COPD and CP were examined. The external respiratory function, total coagulation potential of blood plasma, enzymatic and non-enzymatic fibrinolysis, total fibrinolytic activity were investigated. Results. CP contributes to the progression of bronchial obstructive syndrome with a maximum reduction in forced expiratory volume in the first second compared to the normal values (1.4 times, p < 0.05) and vital capacity (1.2 times, p < 0.05) observed in patients with comorbid COPD and CP. The prothrombin time was significantly shortened in all patient groups compared with the practically healthy individuals (PHI): in patients of group 1 – by 20.1%, in group 2 – by 26.3%, in group 3 – by 38.8% (p1–3 < 0.05). Plasma concentration of fibrinogen was significantly reduced across all patient groups in group 1 – by 12.3%, in group 2 – by 18.6%, in group 3 – by 29.2% (p1–3 < 0.05). Thrombin time was also reduced in all groups of patients with the greatest decline in group 3 – by 36.3% (p < 0.05) compared with group of PHI. Activation of systemic proteolysis was confirmed by changes in the activity of antithrombin III (AT III), the activity of which in patients of group 3 was reduced compared to the normative values by 29% (p < 0.05). Plasma total fibrinolytic activity in patients of all groups was significantly lower than the control indicators: in group 1 – by 12.8%, in group 2 – by 14.3% and in group 3 – by 21.7% (p1–3 < 0.05). The activity of Hageman-factor-dependent fibrinolysis (HFDF) was decreased in all groups: in group 1 – by 1.6 times, in group 2 – by 1.7 times, in group 3 – by 1.8 times (p1–3 < 0.05) compared with PHI with no significant difference between patient groups (p > 0.05). The activity of blood coagulation factor XIII in patients of group 1 was decreased by 24.3%, in group 2 – by 20.1%, in group 3 – by 32.6% (p1–3 < 0.05). In COPD patients with comorbid CP exacerbation, a significant decrease in plasminogen activity was found: in patients of group 1 – by 21.9%, in group 2 – by 32.2%, and in group 3 – by 42.6%, respectively (p1–3 < 0.05). Conclusions. The factors that worse the course of CP with hypoxia caused by COPD include a decrease in AT III activity by 29%; a decrease in enzymatic fibrinolytic activity by 21.7% and a decrease in HFDF activity by 1.8 times compared to normal values. Suppression of the anticoagulant potential of blood (decrease in AT III activity and blood coagulation factor XIII), decreased overall fibrinolytic activity due to inhibition HFDF and enzymatic fibrinolysis, a compensatory increase in the activity of non-enzymatic fibrinolysis and an increase in the proteolytic activity of blood plasma indicate the formation of a hypercoagulable syndrome, which is aggravated by dysfunction of external respiration in patients with CP and comorbid COPD. This leads to disorders in microcirculation processes in the pancreas in patients with COPD, which is one of the risk factors for exacerbation of CP.