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. 2011 Oct;150(4):598-606.
doi: 10.1016/j.surg.2011.07.053.

The protective role of laparoscopic antireflux surgery against aspiration of pepsin after lung transplantation

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The protective role of laparoscopic antireflux surgery against aspiration of pepsin after lung transplantation

P Marco Fisichella et al. Surgery. 2011 Oct.

Abstract

Background: The goal of this study was to determine, in lung transplant patients, if laparoscopic antireflux surgery (LARS) is an effective means to prevent aspiration as defined by the presence of pepsin in the bronchoalveolar lavage fluid (BALF).

Methods: Between September 2009 and November 2010, we collected BALF from 64 lung transplant patients at multiple routine surveillance assessments for acute cellular rejection, or when clinically indicated for diagnostic purposes. The BALF was tested for pepsin by enzyme-linked immunosorbent assay (ELISA). We then compared pepsin concentrations in the BALF of healthy controls (n = 11) and lung transplant patients with and without gastroesophageal reflux disease (GERD) on pH-monitoring (n = 8 and n = 12, respectively), and after treatment of GERD by LARS (n = 19). Time to the development of bronchiolitis obliterans syndrome was contrasted between groups based on GERD status or the presence of pepsin in the BALF.

Results: We found that lung transplant patients with GERD had more pepsin in their BALF than lung transplant patients who underwent LARS (P = .029), and that pepsin was undetectable in the BALF of controls. Moreover, those with more pepsin had quicker progression to BOS and more acute rejection episodes.

Conclusion: This study compared pepsin in the BALF from lung transplant patients with and without LARS. Our data show that: (1) the detection of pepsin in the BALF proves aspiration because it is not present in healthy volunteers, and (2) LARS appears effective as a measure to prevent the aspiration of gastroesophageal refluxate in the lung transplant population. We believe that these findings provide a mechanism for those studies suggesting that LARS may prevent nonallogenic injury to the transplanted lungs from aspiration of gastroesophageal contents.

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Figures

Fig 1
Fig 1
Comparison of the pepsin levels in the BALF among patients who are GERD (+), GERD (−), patients who underwent LARS, and controls shows that pepsin was not detectable in the BALF of controls, and that pepsin levels were less after LARS than in those GERD (+) patients who did not undergo LARS (P = .029). GERD, Gastroesophageal reflux disease; LARS, laparoscopic antireflux surgery.
Fig 2
Fig 2
The actuarial curves comparing recipients based on GERD status or treatment by early or late LARS shows that the percentage of patients who did not develop BOS over time after their transplant was similar among those with or without GERD or who had early or late LARS (P = .818). Complete FEV1 data to generate actuarial curves were available in 38 patients. BOS, Bronchiolitis obliterans syndrome; GERD, gastroesophageal reflux disease; LARS, laparoscopic antireflux surgery.
Fig 3
Fig 3
The actuarial curves show a decreased time since lung transplant to development of BOS in patients with any detectable pepsin than in those without pepsin (P = .058). Two patients whose FEV1 data were incomplete were excluded from the analysis. BOS, Bronchiolitis obliterans syndrome.

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