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Ann Thorac Surg 2006;82:1570
© 2006 The Society of Thoracic Surgeons
Departments of Surgery and Pulmonary Medicine, University of California San Francisco, 513 Parnassus, S-321, San Francisco, CA 94143
(Email: mswe04{at}yahoo.com).
We read with interest D'Ovidio and colleagues' [1] article describing the prevalence of reflux disease in the patients referred for lung transplantation at the University of Toronto. The pathogenesis of gastroesophageal reflux disease (GERD) in patients with end-stage lung disease remains unclear. Whether this is primarily an esophageal process, a gastric process, or a consequence of thoracoabdominal pressure gradients has yet to be determined.
There are two questions that have interested our group. (1) What role does delayed gastric emptying play in the pathogenesis of reflux? (2) How do or how should pre-transplant esophageal studies inform subsequent management?
It is known that about one third of patients with GERD have a component of delayed gastric emptying [2]. In how many of the study subjects did the presence of delayed gastric emptying correlate with the presence of GERD? Furthermore, transplant will only exacerbate the gastric emptying problems with vagal denervation and immunosuppressive drugs. Do the authors recommend any pre-transplant or post-transplant therapeutic intervention in this subset of patients?
We were also surprised to see a prevalence of GERD of only 38%, a number substantially less than our results and those published by the group at Duke [3]. Our protocol for pH studies is to stop proton pump inhibitors (PPI) at least 10 days prior to the study to ensure there is no residual parietal cell inhibition [4, 5]. Why did the authors have patients stop their acid suppressing medications for only 5 days?
We noted with interest the limited correlation between proximal and distal pH probe measurements in patients with obstructive lung disease. This differs from the Duke experience, which has asserted that proximal acid exposure correlates closely with distal acid exposure [3]. We are uncertain how this observation should influence preoperative evaluation.
We appreciate the contributions made by D'Ovidio and colleagues' [1] and the group in Toronto, and we look forward to the evolving discussion about the cause and role of reflux and micro-aspiration in chronic lung injury.
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F. D'Ovidio, L. G. Singer, D. Hadjiliadis, A. Pierre, T. K. Waddell, M. de Perrot, M. Hutcheon, L. Miller, G. Darling, and S. Keshavjee Reply. Ann. Thorac. Surg., October 1, 2006; 82(4): 1570 - 1571. [Full Text] [PDF] |
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