Gastro-oesophageal reflux and gastric aspiration in lung transplant patients with or without chronic rejection

Abstract

Acid gastro-oesophageal reflux (GOR) and gastric aspiration have been labelled as risk factors for chronic rejection bronchiolitis obliterans syndrome (BOS) after lung transplantation (LTx). The present study aimed to further characterise GOR (both acid and nonacid) and the degree of gastric aspiration in LTx recipients both with and without BOS.Impedance-pH recordings were used for GOR detection. Pepsin and bile acid levels were measured in bronchoalveolar lavage fluid (BALF).A total of 48% of patients had increased GOR, of which 27% had exclusively increased nonacid reflux. Cystic fibrosis patients had the highest prevalence of GOR. Pepsin was found in BALF of all patients and bile acids in BALF of 50% of the patients. Patients with BOS had neither increased GOR nor elevated pepsin in BALF. However, 70% of the patients with BOS had bile in BALF compared with 31% of stable patients. Proton pump inhibitor (PPI) treatment reduced acid reflux but did not affect nonacid reflux. Moreover, pepsin and bile levels in BALF were not reduced by PPI.One-half of the lung transplant patients had increased reflux, and nonacid reflux was common. Gastric aspiration occurred in most lung transplant patients. Pepsin was a more general marker and bile acids a more specific marker that might be associated with bronchiolitis obliterans syndrome. Proton pump inhibitor treatment did not prevent nonacid reflux and gastric aspiration.

International practical guidelines on diagnosis, prevention and treatment of bronchiolitis obliterans syndrome

“…К дополни тельным факторам риска относятся вирусные [29,31,32,[56][57][58][59][60][61][62][63][64], бактериальные [65][66][67][68] и грибковые инфекции [69][70][71]. Цитомегаловирусной инфекцией поражаются как врожденный, так и адаптивный компоненты иммунитета и стимулируется выработ ка антигенов HLA I и II классов на эпителиальных клетках [72,73], а также стимулируется и усиливает ся аллогенный иммунный ответ и синтез провоспа лительных цитокинов [72,74].…”

Cough and gastroesophageal reflux: From the gastroenterologist end

“…Pepsin is found in BALF of almost all lung transplant patients and bile acids in half of the lung transplant patients. [24] It is not yet known which component of the refluxate is the most harmful to bronchial epithelial damage.…”

Gastro-oesophageal reflux disease and non-asthma lung disease

“…In contrast, patients with severe lung disease often have unrecognised pathological reflux. In one study of 65 consecutive IPF patients, 87% had pathological gastro-oesophageal reflux (GER) [12], another study reported GERD in 48-76% of patients following lung transplantation [13][14][15]. Microaspiration is more likely in the setting of impaired swallowing mechanism and depressed alertness, conditions more prevalent in the elderly, as suggested by one study [16] which showed an association of bilateral chest radiography scarring with pH probe-proven GERD in elderly patients referred for evaluation of gastrointestinal symptoms.…”

“…Factors predisposing to GERD-related lung disease in this population include gastroparesis [81], vagus nerve dysfunction, a high incidence of post-operative oropharyngeal dysphagia [82], and depressed cough reflex due to the lack of innervation of the allograft [83]. Most lung transplant patients with GERD lack classic symptoms [14], and although acid suppression therapy is frequently given to this patient group, non-acid reflux is present in up to 50% as documented by the finding of bile acids in lung lavage samples [13], a finding associated with BOS in one study [84]. Supporting the aetiological role of GERD in a subset of BOS patients, DAVIS et al [85] NTM infection NTM infection of the lung may produce a clinical picture of nodular bronchiectasis in nonsmokers [86], and this disease has been associated with oesophageal disorders [87][88][89].…”

“…BOS manifests clinically as progressive dyspnoea, cough and recurrent infection, with the characteristic finding of progressive airflow limitation on pulmonary function testing. It has been increasingly recognised that GERD, present in 48-76% of patients post-transplantation [13][14][15], may be a key factor in the development and progression of BOS [80]. Factors predisposing to GERD-related lung disease in this population include gastroparesis [81], vagus nerve dysfunction, a high incidence of post-operative oropharyngeal dysphagia [82], and depressed cough reflex due to the lack of innervation of the allograft [83].…”