Browsing by Author "Calfee, Carolyn S."

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    The relationship between plasma lipid peroxidation products and primary graft dysfunction after lung transplantation is modified by donor smoking and reperfusion hyperoxia
    (Elsevier, 2016-04) Diamond, Joshua M.; Porteous, Mary K.; Roberts, L. Jackson; Wickersham, Nancy; Rushefski, Melanie; Kawut, Steven M.; Shah, Rupal J.; Cantu, Edward; Lederer, David J.; Chatterjee, Shampa; Lama, Vibha N.; Bhorade, Sangeeta; Crespo, Maria; McDyer, John; Wille, Keith; Orens, Jonathan; Weinacker, Ann; Arcasoy, Selim; Shah, Pali D.; Wilkes, David S.; Hage, Chadi; Palmer, Scott M.; Snyder, Laurie; Calfee, Carolyn S.; Ware, Lorraine B.; Christie, Jason D.; Medicine, School of Medicine
    BACKGROUND: Donor smoking history and higher fraction of inspired oxygen (FIO2) at reperfusion are associated with primary graft dysfunction (PGD) after lung transplantation. We hypothesized that oxidative injury biomarkers would be elevated in PGD, with higher levels associated with donor exposure to cigarette smoke and recipient hyperoxia at reperfusion. METHODS: We performed a nested case-control study of 72 lung transplant recipients from the Lung Transplant Outcomes Group cohort. Using mass spectroscopy, F2-isoprostanes and isofurans were measured in plasma collected after transplantation. Cases were defined in 2 ways: grade 3 PGD present at day 2 or day 3 after reperfusion (severe PGD) or any grade 3 PGD (any PGD). RESULTS: There were 31 severe PGD cases with 41 controls and 35 any PGD cases with 37 controls. Plasma F2-isoprostane levels were higher in severe PGD cases compared with controls (28.6 pg/ml vs 19.8 pg/ml, p = 0.03). Plasma F2-isoprostane levels were higher in severe PGD cases compared with controls (29.6 pg/ml vs 19.0 pg/ml, p = 0.03) among patients reperfused with FIO2 >40%. Among recipients of lungs from donors with smoke exposure, plasma F2-isoprostane (38.2 pg/ml vs 22.5 pg/ml, p = 0.046) and isofuran (66.9 pg/ml vs 34.6 pg/ml, p = 0.046) levels were higher in severe PGD compared with control subjects. CONCLUSIONS: Plasma levels of lipid peroxidation products are higher in patients with severe PGD, in recipients of lungs from donors with smoke exposure, and in recipients exposed to higher Fio2 at reperfusion. Oxidative injury is an important mechanism of PGD and may be magnified by donor exposure to cigarette smoke and hyperoxia at reperfusion.
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    The Impact of Donor Smoking on Primary Graft Dysfunction and Mortality after Lung Transplantation
    (American Thoracic Society, 2024) Diamond, Joshua M.; Cantu, Edward; Calfee, Carolyn S.; Anderson, Michaela R.; Clausen, Emily S.; Shashaty, Michael G. S.; Courtwright, Andrew M.; Kalman, Laurel; Oyster, Michelle; Crespo, Maria M.; Bermudez, Christian A.; Benvenuto, Luke; Palmer, Scott M.; Snyder, Laurie D.; Hartwig, Matthew G.; Todd, Jamie L.; Wille, Keith; Hage, Chadi; McDyer, John F.; Merlo, Christian A.; Shah, Pali D.; Orens, Jonathan B.; Dhillon, Gundeep S.; Weinacker, Ann B.; Lama, Vibha N.; Patel, Mrunal G.; Singer, Jonathan P.; Hsu, Jesse; Localio, A. Russell; Christie, Jason D.; Medicine, School of Medicine
    Rationale: Primary graft dysfunction (PGD) is the leading cause of early morbidity and mortality after lung transplantation. Prior studies implicated proxy-defined donor smoking as a risk factor for PGD and mortality. Objectives: We aimed to more accurately assess the impact of donor smoke exposure on PGD and mortality using quantitative smoke exposure biomarkers. Methods: We performed a multicenter prospective cohort study of lung transplant recipients enrolled in the Lung Transplant Outcomes Group cohort between 2012 and 2018. PGD was defined as grade 3 at 48 or 72 hours after lung reperfusion. Donor smoking was defined using accepted thresholds of urinary biomarkers of nicotine exposure (cotinine) and tobacco-specific nitrosamine (4-[methylnitrosamino]-1-[3-pyridyl]-1-butanol [NNAL]) in addition to clinical history. The donor smoking–PGD association was assessed using logistic regression, and survival analysis was performed using inverse probability of exposure weighting according to smoking category. Measurements and Main Results: Active donor smoking prevalence varied by definition, with 34–43% based on urinary cotinine, 28% by urinary NNAL, and 37% by clinical documentation. The standardized risk of PGD associated with active donor smoking was higher across all definitions, with an absolute risk increase of 11.5% (95% confidence interval [CI], 3.8% to 19.2%) by urinary cotinine, 5.7% (95% CI, −3.4% to 14.9%) by urinary NNAL, and 6.5% (95% CI, −2.8% to 15.8%) defined clinically. Donor smoking was not associated with differential post–lung transplant survival using any definition. Conclusions: Donor smoking associates with a modest increase in PGD risk but not with increased recipient mortality. Use of lungs from smokers is likely safe and may increase lung donor availability.