INVESTIGATION OF EXTERNAL RESPIRATORY FUNCTION AND HEMOSTASIS SYSTEM’S STATUS IN PATIENTS WITH CHRONIC OBSTRUCTIVE LUNG DISEASE WITH CONCOMITANT CHRONIC PANCREATITIS

Abstract

INTRODUCTION: It can be assumed that the comorbidity course of сhronic obstructive pulmonary disease (COPD) and chronic pancreatitis (CP) can enhance the clinical symptoms of both diseases and lead to frequent relapses of the pathological process due to changes in the proteolysis intensity of high and low molecular weight plasma proteins and the state of the hemocoagulation.
 OBJECTIVE: To establish the features of hemocoagulation and proteolytic hemostasis at COPD with concomitant CP.
 METHODS: 120 patients with COPD and CP were examined. The function of external respiration, total coagulation potential of blood plasma, the state of enzymatic and non-enzymatic fibrinolysis, total fibrinolytic activity were investigated.
 RESULTS: CP contributes to the development of broncho-obstructive syndrome, and the maximum indicators of reduction of FEV1 relative to the proper values are observed in patients with a comorbid course of COPD and CP. Reducing the intensity of collagenolysis in patients of groups 1-2 contributed to the development of diffuse pulmonary fibrosis in response to chronic inflammation. The imbalanced increase in the intensity of proteolysis due to reduced expression of its inhibitors in COPD patients with CP led to progressive destruction of the cell membranes of alveolocytes, acinar epithelium of pancreas and epithelium of the bronchial mucosa, acceleration of their apoptosis and development of desquamation, atrophic changes, metaplasia, and the like. The above factors are active as inducers of inflammation, and the formation of pulmonary fibrosis and fibrosis of the pancreas.
 CONCLUSIONS: In COPD patients with accompanying CP are an increase in the lysis rate of low and high molecular weight proteins and a decrease in blood collagenolytic activity on the background of a significant imbalance in the activity of plasma proteinase inhibitors. Defined suppression of the activity of the anti-coagulation system factors and enzymatic, Hageman-factor-dependent fibrinolysis indicates the formation of hypercoagulation syndrome in these patients.