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Clinical Investigations: TRANSPLANTS |

Lung Transplantation Exacerbates Gastroesophageal Reflux Disease*

Lisa R. Young; Denis Hadjiliadis; R. Duane Davis; Scott M. Palmer
Author and Funding Information

*From the Division of Medicine and Pediatrics (Dr. Young), University of Cincinnati, Cincinnati, OH; Toronto Lung Transplant Program (Dr. Hadjiliadis), University of Toronto, Toronto, Canada; and Divisions of Thoracic Surgery (Dr. Davis) and Pulmonary and Critical Care Medicine (Dr. Palmer), Duke University Medical Center, Durham, NC.

Correspondence to: Denis Hadjiliadis, MD, MHS, 200 Elizabeth St, 10-Eaton North, Room 240, Toronto, ON, M5G 2C4, Canada; e-mail: Denis.Hadjiliadis@utoronto.ca



Chest. 2003;124(5):1689-1693. doi:10.1378/chest.124.5.1689
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Introduction: A high prevalence of gastroesophageal reflux (GER) has been reported in lung transplant recipients and is possibly linked to the development of bronchiolitis obliterans syndrome. The etiology of posttransplant GER remains unknown but may occur due to the transplant operation or posttransplant medications, or represent preexisting GER disease. We evaluated these possibilities by studying the nature and severity of GER in a cohort of patients before and after lung transplantation.

Methods: Total, upright, and supine acid contact times were recorded in lung transplant recipients who underwent 24-h pH studies before and after transplantation. Patients also underwent esophageal manometry and gastric-emptying studies. Medications for acid suppression and gastric motility were discontinued before testing. Paired comparison between pretransplant and posttransplant results was performed using a paired t test.

Results: Twenty-three patients were included in the analysis. The mean age was 51.5 years, and native diseases included emphysema (n = 11), cystic fibrosis (n = 4), pulmonary fibrosis (n = 3), and others (n = 5). Posttransplant studies occurred a median of 100 days after transplantation. After lung transplantation, the total acid contact time increased a mean of 3.7% (p = 0.03) and the supine acid contact time increased a mean of 6.4% (p = 0.019). Thirty-five percent (8 of 23 patients) had abnormal acid contact times before transplant, and 65% (15 of 23 patients) had abnormal acid contact after transplant. Changes in acid contact times were not explained by changes in esophageal or gastric motility. Only 20% (3 of 15 patients) with abnormal posttransplant pH studies were symptomatic.

Conclusions: There is a significant increase in GER after lung transplantation, as measured objectively by 24-h pH studies, despite a lack of symptoms in most patients. Further research is needed to determine the physiologic mechanisms of posttransplant GER and its impact on long-term allograft function.

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