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11th banff conference lung transplant pathology
1. 11 th Banff Conference on Allograft Pathology Carol F. Farver, MD Cleveland Clinic W. Dean Wallace, MD UCLA Co-Chairs, 11 th Banff Conference-Lung June 2011
15. Overall Survival (n=19 patients) 10/19 (53%) died AMR, n = 5 BOS, n = 4 Pneumonia, n = 1
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18. Immunology of AMR in Lung Transplantation 11 th Banff Conference | June 7, 2011 Medhat Askar, MD, PhD Director, Allogen Laboratories, Cleveland Clinic Associate Professor, Department of Surgery Cleveland Clinic Lerner College of Medicine at Case Western Reserve University School of Medicine
29. W. Dean Wallace, M.D. Associate Professor of Pathology David Geffen School of Medicine UCLA Medical Center Pathology of Antibody-Mediated Rejection of the Lung Allograft
57. The journey of a thousand miles begins with a single step…… Lao-tzu, Chinese philosopher 604 BC - 531 BC
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Notas del editor
Traditionally, lung rejection has been regarded as a T-cell mediated process And standard immunosuppression targeting T-cell proliferation and function has improved graft survival and made transplantation a clinical reality But a potential role for antibodies in rejection has long been suspected since HLA antibodies are detected in patients with rejection HLA antibodies are known to cause different syndromes of rejection after kidney transplantation And HLA antibodies are associated with acute cellular rejection and BOS after lung transplantation But AMR remains enigmatic after LTX
The association between the development of HLA antibodies and BOS was recognized in the late 90s The development of AB preceded the diagnosis of BOS by an average of 20 months Multiple centers corroborated these findings and AB to both class I and class II molecules were associated with BOS These findings underscore the role of humoral immunity in graft rejection after lung transplantation
The purpose of this study is to review a series of cases of AMR from our center and describe the clinicopathological findings
All patients had circulating DSA detected at the time of diagnosis The DSA was to Class I only in 2 of 19; to Class II only in 13 of 19; and to Class I and II in 4 of 19 DSA mean MFI 5841; range: 975-14232
Pneumonitis with fibrin deposition and diffuse alveolar damage Neutrophilic interstitial infiltration Alveolar hemorrhage
Neutrophils in alveolar septa
Focal capillary endothelial C4d deposition
Overall, 9 of the 12 patients with persistent DSA died compared to 1 of the 7 patients who cleared the DSA
Overall, 10 of the 19 patients have died 5 died acutely of refractory AMR 4 of BOS 1 of pneumonia
AMR may be the cause of acute graft failure But a high index of suspicion is necessary for the diagnosis Less severe cases may not result in clinical graft dysfunction similar to most cases of acute cellular rejection & may be unrecognized Yet, these cases may have an impact on BOS development