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Transplantation |

Molecular Mechanisms of Airway Stenosis After Lung Transplantation

Jason Akulian*, MD; Chunling Fan, PhD; Christopher Gilbert, DO; David Feller-Kopman, MD; Roger Johns, MD; Lonny Yarmus, DO
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Johns Hopkins University, Baltimore, MD


Chest. 2012;142(4_MeetingAbstracts):1099A. doi:10.1378/chest.1389824
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Abstract

SESSION TYPE: Lung Transplantation Posters

PRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM

PURPOSE: Complications of the lung airways remain a cause of significant morbidity and may contribute to increases in mortality after lung transplantation (LTx). The most common complication reported is anastomotic and non-anastomotic stenosis, occurring in 5-30% of patients and requiring invention in approximately 50% of cases. Many questions remain regarding the incidence of posttransplant airway stenosis, what drives it and whether there are modifiable mechanisms that remain yet elucidated. This has led to our central hypothesis that there are differences in the inflammatory milieu/immune parameters when comparing the stenotic vs. astenotic bronchial segments as well as the distal airways and blood in patients that develop airway stenosis posttransplantation.

METHODS: 3 patients identified with posttransplant airway stenosis underwent bronchoscopy (rigid or flexible) and airway intervention of the stenosis as necessary. Interventions included balloon dilation, topical therapy and/or airway stenting. Prior to intervention, subjects underwent bronchoalveolar lavage, brushing of the stenotic segment and contralateral astenotic areas and a blood draw post-procedure. Airway epithelial cells were studied for response to hypoxic inducible mitogenic factor (HIMF). Analysis was performed using RT-PCR and gel electrophoresis.

RESULTS: In the three patients studied all required intervention in the form of pneumatic airway dilation with one subsequently requiring stenting. 1 of the 3 had bilateral airway stenosis and 2 of the 3 had stenosis distal to their anastomosis. RT-PCR results showed increased levels of the molecule Resistin in all of the stenotic segments sampled but did not show elevated levels in astenotic airways. RELM-B, another molecule suspected to be involved in profibrotic ischemic response was not found to be elevated in any of the segments brushed.

CONCLUSIONS: Patient’s post-lung transplantation who develop airway stenosis appear to have an elevated and perhaps disordered profibrotic response.

CLINICAL IMPLICATIONS: Discovery of potentially targetable pathways of airway stenosis posttransplant may lead to improved therapies and outcomes in patients post-lung transplantation.

DISCLOSURE: The following authors have nothing to disclose: Jason Akulian, Chunling Fan, Christopher Gilbert, David Feller-Kopman, Roger Johns, Lonny Yarmus

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Johns Hopkins University, Baltimore, MD

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