Abstract
Lung transplantation is today a valid treatment for end-stage lung disorders, although long-term survival is still limited by chronic lung allograft dysfunction (CLAD). Repeat evidence has indicated gastroesophageal reflux and consequent retrograde chronic and silent microaspiration as a non-alloimmunogenic inflammatory risk factor for CLAD and/or bronchiolitis obliterans syndrome (BOS). Unfortunately, to date a gold standard methodology for detecting penetrance of refluxed duodenogastric secretions into the lung is lacking, and a definitive marker of retrograde microaspiration secondary to gastroesophageal reflux that identifies patients at risk for lung allograft dysfunction needs to be determined. Appropriately, designed clinical trials should be performed to understand better the role of gastroesophageal reflux in CLAD and/or BOS and to identify appropriate treatment algorithms.
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