Transplantation |

Posttransplant Interstitial Pneumonitis: A Risk Factor for Chronic Allograft Dysfunction Syndrome Independent of Gastroesophageal Reflux FREE TO VIEW

Benjamin Drew, BS; Andrew Mihalek, MD; Phillip Camp, MD; Anne Fuhlbrigge, MS; Hilary Goldberg, MPH
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Brigham and Women's Hospital, Boston, MA

Chest. 2013;144(4_MeetingAbstracts):1017A. doi:10.1378/chest.1704222
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SESSION TITLE: Post-Transplant Complications

SESSION TYPE: Original Investigation Slide

PRESENTED ON: Monday, October 28, 2013 at 07:30 AM - 09:00 AM

PURPOSE: We have previously shown a significant association between the presence of interstitial pneumonitis (IP) on post-lung transplant biopsy samples and the development of chronic allograft dysfunction (Chest. 2012 doi: 10.1378/chest.12-0354 [Epub ahead of print]). In this study we investigate whether interstitial pneumonitis observed on transbronchial biopsies after lung transplantation is associated with and may be a manifestation of allograft injury related to gastroesophageal reflux disease (GERD).

METHODS: We examined all recipients of primary cadaveric lung transplants at our institution between January 1st, 2006 and December 31st, 2010 (n= 128) for associations between pre-transplant GERD diagnosis/management and post-transplant IP. Patients had bronchoscopies with bronchoalveolar lavage and transbronchial biopsies performed after transplant for surveillance during post-transplant months 1, 3, 6, and 12, as well as when clinically indicated.

RESULTS: 96 transplant recipients were managed with proton pump inhibitors (PPI) prior to transplantation and 60 were formally diagnosed with GERD. Patients treated with PPI before transplantation were maintained on this medication post procedure. Neither the use of PPI (p= 0.09) nor the diagnosis of GERD (p = 0.9) predicted the presence of IP on one or more post-transplant biopsy samples. Of 42 patients with formal pre-transplant Demeester scores, 21 had scores above the 50th percentile. However, pre-transplant DeMeester score was not associated with the development of post-transplant IP (p = 1.0). Similarly, the lowest pre-transplant ph measurement in 31 recipients did not correlate with the development of IP after transplant (p= 0.17).

CONCLUSIONS: Neither clinical parameters such as the use of PPI and/or the diagnosis of GERD based on symptom management nor objective measurements using ph probe correlated with the development of IP in this cohort. Prospective studies are necessary to determine the risk factors for IP development, given its significant potential impact on allograft health.

CLINICAL IMPLICATIONS: IP may represent a new and independent marker of eventual allograft dysfunction in lung transplant recipients.

DISCLOSURE: The following authors have nothing to disclose: Benjamin Drew, Andrew Mihalek, Phillip Camp, Anne Fuhlbrigge, Hilary Goldberg

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