Soluble P-Selectin and the Risk of Primary Graft Dysfunction After Lung Transplantation

et al. 2011

Chest

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Idiopathic pulmonary fibrosis (IPF) is a fatal and chronically progressive diffuse parenchymal lung disease that is characterized by varying degrees of fi brosis of the lung parenchyma. 1 Currently, there are few proven, standardized therapies for IPF 2 ; the only viable treatment that has shown survival benefi t for patients with advanced stages of IPF is lung transplantation. [3][4][5][6][7] Nonetheless, the survival benefi t for lung transplantation in patients with IPF is still complicated by signifi cant early mortality rates, especially within the fi rst year (approximately 28%). The 10-year survival rate after lung transplantation is worse for patients with IPF when compared with other diseases, such as idiopathic pulmonary arterial hypertension (PAH), cystic fi brosis, and a 1 -antitrypsin-defi ciency emphysema. 8 Elevated mean pulmonary arterial pressure (mPAP) in patients with IPF has been associated with decreased exercise capacity and worse survival. 9 Higher mPAP was also associated with increased mortality following lung transplantation in a large registry study. 10 One possible explanation for the link between PAH and early mortality after lung transplantation

Section: Discussionmentioning

confidence: 99%

Elevated Pulmonary Artery Pressure Is a Risk Factor for Primary Graft Dysfunction Following Lung Transplantation for Idiopathic Pulmonary Fibrosis

Fang

Studer

et al. 2011

Chest

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“…LTOG is an NHLBI-funded prospective cohort study of lung transplant recipients with the primary aim of examining clinical and genetic risk factors for PGD at nine United States centers (a full list of investigators and participating centers appears before the REFERENCES section) (22)(23)(24)(25)(26)(27)(28). Based on a reported association between obesity and early mortality after lung transplantation for COPD and ILD (21), we restricted our study sample to 512 adult LTOG participants with COPD or ILD who underwent single or bilateral lung transplantation between March 2002 and July 2009 and who had complete exposure and outcome data.…”

Section: Methods Study Design and Participantsmentioning

confidence: 99%

Obesity and Primary Graft Dysfunction after Lung Transplantation

Lederer¹,

Am J Respir Crit Care Med

Wickersham

et al. 2011

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137

102

Rationale: Obesity has been linked to acute lung injury and is a risk factor for early mortality after lung transplantation. Objectives: To examine the associations of obesity and plasma adipokines with the risk of primary graft dysfunction after lung transplantation. Methods: We performed a prospective cohort study of 512 adult lung transplant recipients with chronic obstructive pulmonary disease or interstitial lung disease enrolled in the Lung Transplant Outcomes Group Study. In a nested case-control study, we measured plasma leptin, adiponectin, and resistin before lung transplantation and 6 and 24 hours after lung transplantation in 40 cases of primary graft dysfunction and 80 control subjects. Generalized linear mixed models and logistic regression were used to estimate risk ratios and odds ratios. Measurements and Main Results: Grade 3 primary graft dysfunction developed within 72 hours of transplantation in 29% participants. Obesity was associated with a twofold increased risk of primary graft dysfunction (adjusted risk ratio 2.1; 95% confidence interval, 1.7-2.6). The risk of primary graft dysfunction increased by 40% (confidence interval, 30-50%) for each 5 kg/m 2 increase in body mass index after accounting for center, diagnosis, cardiopulmonary bypass, and transplant procedure. Higher plasma leptin levels were associated with a greater risk of primary graft dysfunction (sexadjusted P ¼ 0.02). The associations of both obesity and leptin with primary graft dysfunction tended to be stronger among those who did not undergo cardiopulmonary bypass. Conclusions: Obesity is an independent risk factor for primary graft dysfunction after lung transplantation.

“…Twenty-nine patients (28%) developed grade 3 PGD within the first 72 hours. The median CC16 level 6 hours after transplant was significantly higher in patients with PGD (13.8 ng/ml (IQR 7.9, 30.4 ng/ml)) than in patients without PGD (8.2 ng/ml (IQR 4.5,19.1 ng/ml)), p = 0.02. Elevated CC16 levels were associated…”

Section: Introductionmentioning

confidence: 89%

“…Biomarker studies have suggested important mechanistic pathways in clinical PGD (12)(13)(14)(15)(16)(17)(18)(19). Injury to the distal airway epithelium is a common finding in PGD and acute lung injury (ALI).…”

Section: Introductionmentioning

confidence: 99%

Elevated Plasma Clara Cell Secretory Protein Concentration Is Associated With High-Grade Primary Graft Dysfunction

Diamond

Ahya

A13. Translational Research in Lung Transplantation: Pgd, Bos and More

et al. 2010

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Primary graft dysfunction (PGD) is the leading cause of early post-transplant morbidity and mortality after lung transplantation. Clara cell secretory protein (CC16) is produced by the nonciliated lung epithelium and may serve as a plasma marker of epithelial cell injury. We hypothesized that elevated levels of CC16 would be associated with increased odds of PGD. We performed a prospective cohort study of 104 lung transplant recipients. Median plasma CC16 levels were determined at three time points: pre-transplant and 6 and 24 hours post transplant. The primary outcome was the development of grade 3 PGD within the first 72 hours after transplantation. Multivariable logistic regression was performed to evaluate for confounding by donor and recipient demographics and surgical characteristics. Twenty-nine patients (28%) developed grade 3 PGD within the first 72 hours. The median CC16 level 6 hours after transplant was significantly higher in patients with PGD (13.8 ng/ml (IQR 7.9, 30.4 ng/ml)) than in patients without PGD (8.2 ng/ml (IQR 4.5,19.1 ng/ml)), p = 0.02. Elevated CC16 levels were associated