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Pulmonary Vascular Disease |

Relative Risk of Pulmonary Arterial Hypertension in Patients With Idiopathic Pulmonary Fibrosis Given Immune Suppressive Therapies FREE TO VIEW

Brandi Blackburn, MD; Joseph Barney, MD
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University of Alabama at Birmingham, Birmingham, AL


Chest. 2015;148(4_MeetingAbstracts):954A. doi:10.1378/chest.2274403
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Abstract

SESSION TITLE: Pulmonary Arterial Hypertension Posters II

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Wednesday, October 28, 2015 at 01:30 PM - 02:30 PM

PURPOSE: This study examined the risk of secondary pulmonary arterial hypertension (PAH) in subjects with idiopathic pulmonary fibrosis (IPF) exposed to immune suppressive therapies compared to a larger cohort.

METHODS: All data was obtained from the UAB pulmonary translational research database. IRB approval was obtained prior to data acquisition. Cases were identified by the diagnosis of IPF confirmed by lung biopsy or a clinical diagnosis meeting American Thoracic Society Standards. PAH was defined by pulmonary artery mean pressure of 25mmHg or higher on right heart catheterization measurement. The PAH interval was created from the time in months of the initial diagnosis of IPF to the time of diagnosis of PAH. The use of systemic immune suppressive therapies, including prednisone at 5mg daily or higher, azathioprine, interferon gamma, or cytoxan at any dose for at least one month were recorded. All subjects on immune suppressive therapy were receiving treatment before the diagnosis of PAH. All statistical analysis was performed with JMP 10 software and bivariate analysis of each covariate of interest was assessed by the outcome of PAH. Interval time between diagnosis of IPF and diagnosis of PAH was assessed in a bivariate analysis by exposure to immune suppressive therapies.

RESULTS: Of 463 subjects, 443 had a reliable diagnosis of IPF. Almost half of subjects were treated with immune suppressive therapy. Sixteen percent of subjects developed PAH with a mean time to diagnosis of PAH of 31.9 months. Logistic regression on the influence of immunosuppression in subjects with IPF demonstrated no difference on the development of PAH. Survival analysis on the time to development of PAH with respect to immunosuppressants failed to demonstrate an appreciable difference between subjects receiving treatment and the rest of the cohort.

CONCLUSIONS: This large cohort with IPF failed to show increased risk of development of secondary PAH among subjects treated with immune suppressive therapies or differences in rates of development of PAH from time of diagnosis of IPF with exposure to immune suppressants.

CLINICAL IMPLICATIONS: Systemic immune suppressants add no increased risk in development of PAH in patients with IPF. This study suggests that inflammation may have little pathogenic role in the development of secondary PAH in fibrotic lung diseases.

DISCLOSURE: The following authors have nothing to disclose: Brandi Blackburn, Joseph Barney

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