Correction of systemic inflammation in patients with exacerbation of chronic pancreatitis and chronic obstructive pulmonary disease.

Abstract

A significant increase in the incidence of chronic pancreatitis (CP) and its progression against the background of various comorbid conditions indicates the relevance of studying the mechanisms of their mutual burden. CP progresses with the development of exocrine pancreatic insufficiency (EPI), which occurs when the active area of the acinar epithelium decreases as a result of the inflammatory process and fibrosis of the organ. The factors contributing to the pancreas fibrosis in CP under the conditions of chronic obstructive pulmonary disease (COPD) against the background of systemic inflammation are the activation of lipid peroxidation (LPO), oxidative modification of proteins (OMP), processes of apoptosis of pancreatocytes, endogenous intoxication (EI), hyperproduction of pro-inflammatory cytokines: TNF-α, IL-1β and growth factors: TGF-β1, IGF-1, etc. The aim of the study. To study the features of the systemic inflammatory response and the processes of fibrosis of the pancreas tissue in patients with chronic pancreatitis with comorbidity with chronic obstructive pulmonary disease (COPD).