Transplantation/ImmunologyLaparoscopic Antireflux Surgery for Gastroesophageal Reflux Disease After Lung Transplantation
Introduction
The long-term morbidity and mortality after lung transplantation is largely attributable to bronchiolitis obliterans syndrome (BOS), a form of chronic rejection that occurs after lung transplantation 1, 2. Evidence suggests that the fibrosing process responsible for BOS may be the result of a nonimmunologic chronic injury, such as that promoted by aspiration of gastroesophageal contents in patients with gastroesophageal reflux disease (GERD) [3]. The reasons why GERD has been given much attention as a risk factor for the development and progression of BOS are 2-fold. First, lung transplant patients have a high prevalence of GERD 4, 5, 6. Second, surgical control of GERD has been shown to stabilize or improve lung function in some patients with BOS 6, 7, 8, 9. GERD therefore may be a modifiable risk factor for the progression of BOS because GERD and aspiration can be stopped by laparoscopic antireflux surgery [LARS]. Collectively, these observations have led to an increased emphasis on the diagnosis and surgical treatment of GERD after lung transplantation. However, information regarding the pathophysiology of GERD and the perioperative outcomes of the surgical treatment in these patients is limited, although initial evidence suggests that LARS may be performed safely in the lung transplant population 10, 11, 12, 13. We hypothesized that lung transplant patients have distinct pathophysiologic characteristics that differentiate them from the patients with GERD, and that despite the higher surgical risk of lung transplant patients, LARS can be performed with equivalent 30-d morbidity and mortality.
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Patients and Methods
We retrospectively compared the pathophysiologic characteristics and the perioperative outcomes of 29 consecutive patients who had single lung transplantation, double lung transplantation, or re-transplantation with those of 23 consecutive patients without lung disease or lung transplantation (control group) who underwent LARS for GERD between November 2008 and May 2010. We excluded patients with open fundoplication and patients who had a fundoplication for paraesophageal hernia. All patients
Demographics
Lung transplant patients and patients in the control group were of comparable age, sex, and race. However, control patients had a larger body habitus (Table 1). The median time between lung transplant and LARS was 41 mo. The distribution of the underlying end-stage lung disease (obstructive or restrictive) in the transplant group is shown in Fig. 1. Specifically, eight patients (28%) had restrictive end-stage lung disease: six had idiopathic pulmonary fibrosis and two had scleroderma. Patients
Discussion
Recent investigation has revealed that GERD and putative microaspiration of gastroduodenal contents may be a risk factor in the pathogenesis of BOS 3, 21, 22. Indeed, GERD is highly prevalent after lung transplantation as reported by our group (51%), Young et al. (65%), Hadjiliadis et al. (70%), and Davis et al. (73%) 4, 5, 6, 23 Furthermore, surgical correction of GERD has been associated with a delay in the onset or progression of BOS, and in some cases even improvement in lung function 6, 8,
Conclusions
Our report is the first case-control study comparing the pathophysiologic characteristics of GERD in lung transplant patients with a control group, and the second largest institutional series describing LARS for GERD after lung transplantation. This study indicates that lung transplant patients differ from those without a lung transplant or pulmonary disease in that they rarely have a hiatal hernia and have more frequent and severe proximal reflux. Furthermore, we have objectively verified that
Acknowledgments
The authors acknowledge Dr. Stephen Sontag from the Department of Gastroenterology, Edward Hines Jr. Veteran Administration Medical Center, Hines IL, for his scientific supervision during the revisions of this manuscript.
This work was supported in part by the Dr. Ralph and Marian C. Falk Medical Research Trust and a grant from the National Institute on Alcohol Abuse and Alcoholism (T32 AA013257).
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