Prospects in non-invasive diagnosis of bronchial asthma-related gastroesophageal reflux disease: a single-stage open uncontrolled non-randomised observational study

Background. Respiratory symptoms of bronchial asthma (BA) comorbid with gastroesophageal reflux disease (GERD) may provoke duodenogastroesophageal reflux (DGER) via aggressive agents like pepsinogens and bilirubin.

Objectives. A clinical and functional study of the saliva pepsinogen and bilirubin-associated BA-comorbid GERD for non-invasive DGER diagnosis.

Methods. A total of 29 patients with an allergic BA phenotype, comorbid GERD and 50,2 ± 2,4 years mean age have been examined. Biochemical blood panel included bilirubin, C-reactive protein and allergen-specific IgE. Saliva bilirubin was estimated in colorimetry, and the pepsinogen-1, -2 content — in immunological tests. Grade A–D reflux oesophagitis (RO) in oesophagoscopy was assigned to erosive reflux disease, and grade N–M oesophageal mucosa (OM) lesions — to non-erosive reflux disease. External respiratory function (ERF) was assessed with forced expiratory volume (FEV1, L/s), forced vital capacity (FVC), Tiffeneau index (FEV1/FVC), pre- and post-berodual FEF1 and FVC dynamics.

Results. The BA–GERD patients were markedly polymorbid. Cough and chest tightness associated with age, and the tight chest rate — with a higher body mass index and lower FEV1/FVC. The association between higher pepsinogen-I and lower FEV1/FVC–FVC in response to inhaled berodual, as well as between higher saliva bilirubin and lower FVC–FEV1 after berodual intake reflects a significant high-DGER effect on BA representation.

Conclusion. In BA–GERD patients, saliva pepsinogen and bilirubin are biomarkers of both DGER and respiratory inflammation with bronchospasm.