FEATURES OF PATHOHISTOLOGICAL CHANGES IN LUNG TISSUE IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND WITH COMORBIDITY WITH CHRONIC PANCREATITIS

In cases of comorbid acute and chronic pancreatitis (CP) and chronic obstructive pulmonary disease (COPD), pathological processes such as impaired lipid metabolism, chronic localized and systemic low-intensity inflammation, activation of oxidative and nitrosative stress and the onset of hypoxia contribute to the induction of fibrotic changes in lung and pancreatic tissues. Objective: To determine the pathological and morphological basis and patterns of progression of pulmonary insufficiency by comparing the morphological structure of the lungs in patients with isolated chronic obstructive pulmonary disease (COPD) and those with comorbid COPD and chronic pancreatitis (CP). Material and methods. A pathological study was carried out on cases of death where the clinical and pathological diagnoses included COPD with CP as well as COPD without pancreatic involvement. Results. In cases of combined COPD and CP, a more pronounced activation of pulmonary tissue fibrosis was observed compared to isolated COPD. This was evidenced by a 2.6 times increase (p < 0.05) in the specific volume of connective tissue in the lungs and a 1.5 times increase (p < 0.05) in its density due to collagen fibers in comparison with the control group. Combined COPD and CP were associated with a significant reduction in the specific volume of lipocytes and their average diameter in the lungs – 4.5 times and 1.4 times, respectively (p < 0.05), when compared to the control group. With isolated COPD, there was an 1.8 times increase (p < 0.05) in the specific volume of blood vessels in the peribronchial connective tissue, whereas COPD combined with CP showed a comparatively lower increase of 1.5 times (p < 0.05). Comorbid COPD and CP also showed a 1.2 times higher percentage (p < 0.05) of venous vessels with thrombosis in the peribronchial connective tissue compared to isolated COPD, and a 2.5 times increase (p < 0.05) in the percentage of venous vessels with thrombosis in the respiratory segments of the lungs. Additionally, the level of respiratory airway spaces occupied by desquamated cells increased significantly – by 9.3 times (p < 0.05) in cases of comorbid COPD and CP, compared to a 7.3 times increase (p < 0.05) in patients with isolated COPD. Conclusions. Comorbid COPD and CP displayed a higher activation of pulmonary tissue fibrosis compared to isolated COPD, as demonstrated by an increase in connective tissue volume and collagen density within the lungs. The combination of these conditions was accompanied by more severe structural damage to the lungs, characterized by reduced number and size of lipocytes, an elevated level of desquamation in respiratory segments, and pronounced microcirculatory dysfunctions. These factors may play a key role in the progression of pulmonary fibrosis.