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      Incidence of primary graft dysfunction is higher according to the new ISHLT 2016 guidelines and correlates with clinical and molecular risk factors

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          Abstract

          Background

          Primary graft dysfunction (PGD) is the most important determinant of morbidity and mortality after lung transplantation, but its definition has evolved over the past decade. The implications of this refinement in clinical definition have not been evaluated. In this single-center study, we compared PGD incidence, risk factors, and outcomes using the 2005 and the updated-2016 International Society of Heart and Lung Transplantation guidelines for PGD grading in lung transplant patients.

          Methods

          In this retrospective study, we extracted data from the medical records of 127 patients who underwent lung transplantation between 1/1/2016–12/31/2018. PGD was defined as PGD3 present at 48 and/or 72 hours post-reperfusion. We used the 2005 and the updated 2016 guidelines to assess clinical risk factors, outcomes, and baseline biomarkers for PGD.

          Results

          On the basis of the 2016 and 2005 guidelines, we identified PGD in 37% and 26% of patients, respectively. PGD was significantly associated with extracorporeal life support, large body mass index, and restrictive lung disease using the 2016 but not the 2005 guidelines. Based on the 2016 guidelines, pretransplant levels of several biomarkers were associated with PGD; using the 2005 guidelines, only increased interleukin-2 levels were significantly associated with PGD. No preoperative biomarkers were associated with PGD using either guidelines after adjusting for clinical variables. Postoperative morbidity and 1-year mortality were similar regardless of guidelines used.

          Conclusions

          Our findings suggest that refinements in the PGD scoring system have improved the detection of graft injury and associated risk factors without changing its ability to predict postoperative morbidity and mortality.

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          Most cited references26

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          Biology and regulation of IL-2: from molecular mechanisms to human therapy

          IL-2 was first identified as a growth factor capable of driving the expansion of activated human T cell populations. In the more than 40 years since its discovery, a tremendous amount has been learned regarding the mechanisms that regulate the expression of both IL-2 and its cell surface receptor, its mechanisms of signalling and its range of biological actions. More recently, the mechanisms by which IL-2 regulates CD4+ T cell differentiation and function have been elucidated. IL-2 also regulates the effector and memory responses of CD8+ T cells, and the loss of IL-2 or responsiveness to IL-2 at least in part explains the exhausted phenotype that occurs during chronic viral infections and in tumour responses. These basic mechanistic studies have led to the therapeutic ability to manipulate the action of IL-2 on regulatory T (Treg) cells for the treatment of autoimmune disease and on CD8+ T cells for immunotherapy of cancer. IL-2 can have either positive or deleterious effects, and we discuss here recent ideas and approaches for manipulating the actions and overall net effects of IL-2 in disease settings, including cancer.
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            Report of the ISHLT Working Group on Primary Lung Graft Dysfunction, part I: Definition and grading—A 2016 Consensus Group statement of the International Society for Heart and Lung Transplantation

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              Clinical risk factors for primary graft dysfunction after lung transplantation.

              Primary graft dysfunction (PGD) is the main cause of early morbidity and mortality after lung transplantation. Previous studies have yielded conflicting results for PGD risk factors. We sought to identify donor, recipient, and perioperative risk factors for PGD. We performed a 10-center prospective cohort study enrolled between March 2002 and December 2010 (the Lung Transplant Outcomes Group). The primary outcome was International Society for Heart and Lung Transplantation grade 3 PGD at 48 or 72 hours post-transplant. The association of potential risk factors with PGD was analyzed using multivariable conditional logistic regression. A total of 1,255 patients from 10 centers were enrolled; 211 subjects (16.8%) developed grade 3 PGD. In multivariable models, independent risk factors for PGD were any history of donor smoking (odds ratio [OR], 1.8; 95% confidence interval [CI], 1.2-2.6; P = 0.002); FiO2 during allograft reperfusion (OR, 1.1 per 10% increase in FiO2; 95% CI, 1.0-1.2; P = 0.01); single lung transplant (OR, 2; 95% CI, 1.2-3.3; P = 0.008); use of cardiopulmonary bypass (OR, 3.4; 95% CI, 2.2-5.3; P < 0.001); overweight (OR, 1.8; 95% CI, 1.2-2.7; P = 0.01) and obese (OR, 2.3; 95% CI, 1.3-3.9; P = 0.004) recipient body mass index; preoperative sarcoidosis (OR, 2.5; 95% CI, 1.1-5.6; P = 0.03) or pulmonary arterial hypertension (OR, 3.5; 95% CI, 1.6-7.7; P = 0.002); and mean pulmonary artery pressure (OR, 1.3 per 10 mm Hg increase; 95% CI, 1.1-1.5; P < 0.001). PGD was significantly associated with 90-day (relative risk, 4.8; absolute risk increase, 18%; P < 0.001) and 1-year (relative risk, 3; absolute risk increase, 23%; P < 0.001) mortality. We identified grade 3 PGD risk factors, several of which are potentially modifiable and should be prioritized for future research aimed at preventative strategies. Clinical trial registered with www.clinicaltrials.gov (NCT 00552357).
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                Author and article information

                Journal
                J Thorac Dis
                J Thorac Dis
                JTD
                Journal of Thoracic Disease
                AME Publishing Company
                2072-1439
                2077-6624
                June 2021
                June 2021
                : 13
                : 6
                : 3426-3442
                Affiliations
                [1 ]deptMichael E DeBakey Department of Surgery, Division of Cardiopulmonary Transplantation and Mechanical Circulatory Support , Baylor College of Medicine , Houston, TX, USA;
                [2 ]deptDepartment of Regenerative Medicine Research , Texas Heart Institute , Houston, TX, USA;
                [3 ]deptCenter for Antimicrobial Resistance and Microbial Genomics (CARMiG), Department of Internal Medicine, Division of Infectious Diseases , University of Texas Health Science Centre at Houston , Houston, TX, USA;
                [4 ]deptDepartment of Advanced Cardiopulmonary Therapies and Transplantation , University of Texas Health Science Center at Houston , Houston, TX, USA;
                [5 ]RegenMedix Consulting LLC , Montgomery, AL, USA
                Author notes

                Contributions: (I) Conception and design: L Chacon Alberty, DA Taylor, G Loor; (II) Administrative support: C Hochman Mendez, LC Sampaio, DA Taylor, G Loor; (III) Provision of study materials or patients: P Jindra, DA Taylor, G Loor; (IV) Collection and assembly of data: D Daoud, L Chacon Alberty, MHM Virk, J Mase, M Cusick, H Choi, N Debolske; (V) Data analysis and interpretation: D Daoud, L Chacon Alberty, Q Wei, MHM Virk, J Mase, P Jindra, DA Taylor, G Loor; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

                Correspondence to: Gabriel Loor. Michael E DeBakey Department of Surgery, Division of Cardiopulmonary Transplantation and Mechanical Circulatory Support, Baylor College of Medicine, Houston, TX, USA. Email: Gabriel.loor@ 123456bcm.edu .
                Article
                jtd-13-06-3426
                10.21037/jtd-20-3564
                8264697
                34277039
                a440633b-6815-42ce-ba99-23a71fd35583
                2021 Journal of Thoracic Disease. All rights reserved.

                Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

                History
                : 05 January 2021
                : 14 April 2021
                Categories
                Original Article

                lung transplantation,risk factors,primary graft dysfunction (pgd),cytokines,lung disease

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