FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2041712024> ?p ?o ?g. }

• W2041712024 endingPage "16" @default.
• W2041712024 startingPage "14" @default.
• W2041712024 abstract "Over the last 20 years, lung transplantation has emerged as a valid treatment option for a wide range of advanced lung diseases. Surgical advances combined with newer immunosuppressant medications have improved outcomes; however, both the short-term and long-term survival after lung transplant continues to lag behind other solid-organ transplants. Survival for lung transplant recipients at 1 year, 3 years, and 5 years is approximately 76%, 58%, and 47%, respectively.1DeMeo DL Ginns LC Clinical status of lung transplantation.Transplantation. 2001; 72: 1713-1724Crossref PubMed Scopus (29) Google Scholar Early respiratory failure and death after lung transplant can result from airway complications, hyperacute rejection, acute rejection, infection, or ischemia/reperfusion lung injury (IRLI). Graft failure secondary to bronchial dehiscence is now rare with improved surgical techniques. Hyperacute rejection, infrequently described in lung transplantation, results from preformed antibodies that target antigens in the allograft vascular endothelium and cause extensive thrombosis and complement activation. Acute rejection occurs in > 60% of lung recipients despite current immunosuppressive protocols, but usually responds to augmented immunosuppression and rarely leads to early graft loss. Infectious complications, such as bacterial pneumonia or cytomegalovirus, have been described as a common etiology of respiratory failure and mortality in the early posttransplant period. IRLI or reimplantation response is characterized by the development of bilateral pulmonary infiltrates, declining lung compliance, and worsening of gas exchange in the immediate posttransplant period after exclusion of rejection, infection, and heart failure. Severe IRLI has been reported to occur in 15 to 30% of patients.2Christie JD Bavaria JE Palevsky HI et al.Primary graft failure following lung transplantation.Chest. 1998; 114: 51-60Abstract Full Text Full Text PDF PubMed Scopus (292) Google Scholar Despite the increasing experience with lung transplantation, all of these problems contribute to the development of early respiratory failure and a 1-year mortality of approximately 25%. In this issue of CHEST (see page 165), Chatila et al have attempted to determine the incidence and attributable mortality of acute respiratory failure from any cause after lung transplantation. They studied 80 consecutive patients who underwent single or bilateral lung transplantation between 1994 and 1999 at a single center. Postoperative respiratory failure was defined as the need for mechanical ventilation for > 48 h after transplant or the need for reintubation prior to hospital discharge. They found that 44 of 80 lung transplant recipients (55%) acquired acute respiratory failure. In-hospital mortality was significantly higher among patients who acquired acute respiratory failure compared to those who did not, 45% vs 3%. More than 50% of the episodes of acute respiratory failure were attributable to IRLI, and < 10% were attributed to infectious etiologies. Allograft rejection and airway complications contributed to 5% and 11% of the episodes of respiratory failure, respectively. Similar to prior studies,2Christie JD Bavaria JE Palevsky HI et al.Primary graft failure following lung transplantation.Chest. 1998; 114: 51-60Abstract Full Text Full Text PDF PubMed Scopus (292) Google Scholar they found that the development of IRLI was associated with an increased incidence of acute respiratory failure and in-hospital mortality. Based on the results of Chatila et al, it appears the main cause of early morbidity and mortality after lung transplant has shifted away from infections to IRLI. Improved antimicrobial prophylactic regimens and diagnostic testing are likely to have contributed to a decrease in the incidence of infections in the early posttransplant period. In contrast, the incidence of IRLI after lung transplant may be increasing. The exact pathophysiology of IRLI is unknown. Up-regulation of inflammatory cytokines such as interleukin-83Perrot MD Sekine Y Fischer S et al.Interleukin-8 release during early reperfusion predicts graft function in human lung transplantation.Am J Respir Crit Care Med. 2002; 165: 211-215Crossref PubMed Scopus (229) Google Scholar or matrix metalloproteinase 94Yano M Omoto Y Yamakawa Y et al.Increased matrix metalloproteinase 9 activity and mRNA expression in lung ischemia-reperfusion injury.J Heart Lung Transplant. 2001; 20: 679-686Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar may occur as a result of donor lung injury or surgical trauma. Nuclear factor-κB regulates many genes that are responsible for the development of acute inflammation in this setting, and represents a promising target for intervention. In a porcine model of lung transplantation IRLI, an inhibitor of nuclear factor-κB significantly improved lung function at 4 h compared to control subjects.5Ross SD Kron IL Gangemi JJ et al.Attenuation of lung reperfusion injury after transplantation using an inhibitor of nuclear factor-κB.Am J Physiol Lung Cell Mol Physiol. 2000; 279: L528-L536PubMed Google Scholar Preformed antibodies directed against endothelial cell human leukocyte antigens (HLAs) may also contribute to acute lung injury. An elevated level of panel reactive antibodies against HLA has been shown to increase the incidence of early graft dysfunction in lung and other solid-organ recipients.6Scornik JC Zander DS Baz MA et al.Susceptibility of lung transplants to preformed donor-specific HLA antibodies as detected by flow cytometry.Transplantation. 1999; 68: 1542-1546Crossref PubMed Scopus (50) Google Scholar The improved sensitivity of flow cytometry has resulted in an increasing number of lung transplant recipients who are recognized to have antibodies against donor HLAs.6Scornik JC Zander DS Baz MA et al.Susceptibility of lung transplants to preformed donor-specific HLA antibodies as detected by flow cytometry.Transplantation. 1999; 68: 1542-1546Crossref PubMed Scopus (50) Google Scholar Early identification of sensitized recipients may provide an opportunity for intervention. Inflammatory cytokines produced from leukocytes and the presence of preformed antibodies against HLAs represent two potential mechanisms of pathophysiologic injury that warrant further study in the prevention of IRLI. Prior studies have found a greater incidence of IRLI associated with pulmonary hypertension,7Mendeloff EN Meyers BF Sundt TM et al.Lung transplantation for pulmonary vascular disease.Ann Thorac Surg. 2002; 73: 209-217Abstract Full Text Full Text PDF PubMed Scopus (80) Google Scholar cardiopulmonary bypass (CPB),8Aeba R Griffith BP Kormos RL et al.Effect of cardiopulmonary bypass on early graft dysfunction in clinical lung transplantation.Ann Thorac Surg. 1994; 57: 715-722Abstract Full Text PDF PubMed Scopus (110) Google Scholar donor characteristics,9Sommers KE Griffith BP Hardesty RL et al.Early lung allograft function in twin recipients from the same donor: risk factor analysis.Ann Thorac Surg. 1996; 62: 784-790Abstract Full Text Full Text PDF PubMed Scopus (56) Google Scholar and ischemia time,10Sleiman C Mal H Fournier M et al.Pulmonary reimplantation response in single-lung transplantation.Eur Respir J. 1995; 8: 5-9Crossref PubMed Scopus (55) Google Scholar but the results have been inconsistent. This study by Chatilla et al identified right ventricular (RV) dysfunction as a preoperative variable that is independently associated with both the development of acute respiratory failure and increased in-hospital mortality. The finding that RV dysfunction was associated with a greater incidence of acute respiratory failure in this study is not surprising. Prior studies have shown that there is a higher early mortality associated with lung transplantation for pulmonary hypertension as compared to other native diseases; however, the long-term outcomes are comparable to those of other patients.7Mendeloff EN Meyers BF Sundt TM et al.Lung transplantation for pulmonary vascular disease.Ann Thorac Surg. 2002; 73: 209-217Abstract Full Text Full Text PDF PubMed Scopus (80) Google Scholar It is unclear from the data presented how many patients with primary or secondary pulmonary hypertension underwent single vs bilateral transplantation. Furthermore, the use of a subjective grading for RV dysfunction may have limited the ability to determine if there is a critical level of reduced RV function from which recovery is not possible. Chatilla et al also found that the need for CPB as well as bilateral lung transplantation were associated with the greatest risks of respiratory failure in univariate analysis. The “postperfusion lung syndrome” associated with CPB has been noted in a wide range of patient populations including lung transplant recipients.8Aeba R Griffith BP Kormos RL et al.Effect of cardiopulmonary bypass on early graft dysfunction in clinical lung transplantation.Ann Thorac Surg. 1994; 57: 715-722Abstract Full Text PDF PubMed Scopus (110) Google Scholar It is believed that CPB can lead to complement activation and increased levels of inflammatory cytokines that produce capillary leak and noncardiogenic pulmonary edema. Both IRLI and postperfusion lung syndrome have similar clinical and pathologic manifestations. Although bilateral lung transplantation was also associated with an increased risk of acute respiratory failure in univariate analysis, neither CPB nor bilateral transplant was significant in the multivariate model. A recent review of the United Network of Organ Sharing lung transplant database of 2,260 lung transplant recipients for emphysema between 1991 and 1997 compared the mortality between single lung and double lung transplants. They found no difference in the 30-day mortality between the two groups, and the long-term survival data favored bilateral lung transplants for individuals < 60 years of age.11Meyer DM Bennett LE Novick RJ et al.Single vs bilateral, sequential lung transplantation for end-stage emphysema: influence of recipient age on survival and secondary end-points.J Heart Lung Transplant. 2001; 20: 935-941Abstract Full Text Full Text PDF PubMed Scopus (131) Google Scholar Thus, the finding of increased short-term morbidity and mortality associated with bilateral lung transplant at this single center needs to be interpreted with caution. It may be a marker of other high-risk characteristics that influence the type of operation performed at the center or simply a result of random statistical chance, given the rather large number of analyses performed in the relatively small patient population. Chatilla et al have shown that short-term mortality after lung transplantation continues to be high and that the main cause of early allograft dysfunction has shifted from infections to IRLI. While this study does a good job at identifying and describing the problems of the early posttransplant time period, several limitations make it unable to identify important risk factors for the different types of complications. This study included a diverse patient population with many different underlying lung diseases, which suffered a wide range of complications that are all grouped together as acute respiratory failure. The role of RV dysfunction, pulmonary hypertension, or CPB in contributing to IRLI remains intriguing. Future multicenter or registry studies that look at more focused populations based on underlying disease and specific complications will be better suited to define the important and potentially modifiable risk factors for IRLI. Additional translational research is also needed to better define the basic mechanisms that determine why some patients acquire fatal IRLI immediately after transplant and others are extubated within 48 h. These studies will need to accurately identify both clinical and biological risk factors and also better define the different pathologic processes that cause early allograft dysfunction and are currently grouped together as IRLI. Relative to other solid-organ transplants, lung transplantation continues to be in its infancy. The short-term and long-term mortality rates are higher than kidney, liver, or heart transplants. This important study by Chatilla et al points out some of the persistent problems facing the field of lung transplantation. It raises many questions that need to be answered in order to improve on the high morbidity and mortality that we encounter today." @default.
• W2041712024 created "2016-06-24" @default.
• W2041712024 creator A5006013423 @default.
• W2041712024 creator A5085761603 @default.
• W2041712024 date "2003-01-01" @default.
• W2041712024 modified "2023-09-25" @default.
• W2041712024 title "Respiratory Failure Early After Lung Transplantation" @default.
• W2041712024 cites W1918990945 @default.
• W2041712024 cites W1984438397 @default.
• W2041712024 cites W2009548520 @default.
• W2041712024 cites W2053849098 @default.
• W2041712024 cites W2059656604 @default.
• W2041712024 cites W2067837721 @default.
• W2041712024 cites W2129241145 @default.
• W2041712024 cites W2131653877 @default.
• W2041712024 cites W2141140541 @default.
• W2041712024 cites W2143838850 @default.
• W2041712024 cites W2146102937 @default.
• W2041712024 doi "https://doi.org/10.1378/chest.123.1.14" @default.
• W2041712024 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12527595" @default.
• W2041712024 hasPublicationYear "2003" @default.
• W2041712024 type Work @default.
• W2041712024 sameAs 2041712024 @default.
• W2041712024 citedByCount "11" @default.
• W2041712024 countsByYear W20417120242012 @default.
• W2041712024 countsByYear W20417120242022 @default.
• W2041712024 crossrefType "journal-article" @default.
• W2041712024 hasAuthorship W2041712024A5006013423 @default.
• W2041712024 hasAuthorship W2041712024A5085761603 @default.
• W2041712024 hasBestOaLocation W20417120241 @default.
• W2041712024 hasConcept C126322002 @default.
• W2041712024 hasConcept C177713679 @default.
• W2041712024 hasConcept C2776888751 @default.
• W2041712024 hasConcept C2777714996 @default.
• W2041712024 hasConcept C2781448352 @default.
• W2041712024 hasConcept C2911091166 @default.
• W2041712024 hasConcept C534529494 @default.
• W2041712024 hasConcept C71924100 @default.
• W2041712024 hasConceptScore W2041712024C126322002 @default.
• W2041712024 hasConceptScore W2041712024C177713679 @default.
• W2041712024 hasConceptScore W2041712024C2776888751 @default.
• W2041712024 hasConceptScore W2041712024C2777714996 @default.
• W2041712024 hasConceptScore W2041712024C2781448352 @default.
• W2041712024 hasConceptScore W2041712024C2911091166 @default.
• W2041712024 hasConceptScore W2041712024C534529494 @default.
• W2041712024 hasConceptScore W2041712024C71924100 @default.
• W2041712024 hasIssue "1" @default.
• W2041712024 hasLocation W20417120241 @default.
• W2041712024 hasLocation W20417120242 @default.
• W2041712024 hasOpenAccess W2041712024 @default.
• W2041712024 hasPrimaryLocation W20417120241 @default.
• W2041712024 hasRelatedWork W2002503247 @default.
• W2041712024 hasRelatedWork W2045626083 @default.
• W2041712024 hasRelatedWork W2054006095 @default.
• W2041712024 hasRelatedWork W2087287413 @default.
• W2041712024 hasRelatedWork W2124753996 @default.
• W2041712024 hasRelatedWork W2318299045 @default.
• W2041712024 hasRelatedWork W2417519090 @default.
• W2041712024 hasRelatedWork W2471678635 @default.
• W2041712024 hasRelatedWork W2894568182 @default.
• W2041712024 hasRelatedWork W3031286556 @default.
• W2041712024 hasVolume "123" @default.
• W2041712024 isParatext "false" @default.
• W2041712024 isRetracted "false" @default.
• W2041712024 magId "2041712024" @default.
• W2041712024 workType "article" @default.