The article presents data on the role of pepsinogen-1 and -2 and bilirubin in the formation of gastroesophageal reflux disease (GERD) in patients with chronic obstructive pulmonary disease (COPD). Clinical, biochemical, immunological research methods were used in the work. The activity of pepsinogens 1 and 2 and bilirubin in saliva was determined in all patients with combined pathology. It has been established that the presence of concomitant GERD in patients is an independent aggravating factor for the function of external respiration. In patients with concomitant GERD, a significant increase in acute phase parameters in the serum, indicating active systemic inflammation. Increased activity of the cytokine IL-6 and IFNγ indicates the activation of the cellular immune system, with an unregulated immune response that supports chronic inflammation in the bronchi even in remission. Increased levels of IL-4 are compensatory in nature, as IL-4 inhibits the production of macrophages of proinflammatory cytokines, including IL-6. Detection of correlations between the concentration of total bilirubin in saliva with a decrease in external respiration, namely FVC, FEV-1, as well as the presence of shortness of breath allows us to consider bilirubin as a possible marker of reflux and respiratory inflammation in the bronchi, until obstruction. The positive correlation of pepsinogen-1 in saliva with an allergic history, and pepsinogen-2 in saliva with cough, shortness of breath and smoking, and a negative correlation of pepsinogen-1 with the value of FEV1 / FVC, allows to consider pepsinogen-1 and pepsinogen-2 as markers of non-acid reflux and respiratory inflammation with bronchoobstruction