Nonalloimmune mechanisms contributing to lung allograft dysfunction: A potential role for gastroesophageal reflux disease

Purpose of review: Lung allograft dysfunction and bronchiolitis obliterans syndrome remain the primary impediment to long-term survival after lung transplantation. Chronic aspiration resulting from gastroesophageal reflux disease is particularly common in lung transplant recipients and represents an important form of nonalloimmune injury that may initiate or exacerbate lung allograft dysfunction. Recent findings: New evidence from large retrospective studies not only corroborates that nonalloimmune injury in the form of gastroesophageal reflux disease is associated with acute rejection, bronchiolitis obliterans syndrome, and mortality, but also suggests that these sequelae can be prevented or reversed with fundoplication. More important, however, is that it is becoming clear that fundoplication is less advantageous when delayed (i.e. more than 90 days after transplant), suggesting a dose-dependent relation. Preliminary data from in-vitro studies suggest that nonalloimmune injury in lung transplant recipients with chronic aspiration involves the interaction of innate and acquired immune pathways. The details of these pathways and the extent of interaction between them have yet to be elucidated. Summary: Increasing evidence supports an important association between chronic aspiration in the context of gastroesophageal reflux disease and lung allograft dysfunction. In the future, more extensive studies in animal models and the development of prospective clinical trials will be necessary to fully elucidate this relation. © 2005 Lippincott Williams & Wilkins.

Duke Scholars

Author Matthew Hartwig Surgery, Cardiovascular and Thoracic Surgery