Reds Lung Fluid Monitoring For Assessing Lung Disease In Patients With Covid-19 Infection
HFSA ePoster Library. Curran L. 09/10/21; 343478; 244
Lisa Curran
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Abstract
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Background: Although the incidence of Post-transplant lymphoproliferative disease which is associated with Epstein-Barr virus (EBV) is relatively high and its presence is associated with severe complications, impact of EBV serostatus on post heart transplantation (HT) survival is not clear. We sought to determine the impact of donor and recipient EBV serostatus on post HT survival.
Methods: We identified adult patients who underwent HT between 2000 and 2018 in the Scientific Registry of Transplant Recipients. These patients were categorized as per recipient and donor EBV serological status. We compared survival with the Kaplan-Meier method. We constructed Cox proportional hazards regression models to determine the risk-adjusted influence of EBV serostatus on post HT survival.
Results: Out of 20, 533 HT identified, 16,222 were +/+, 1081 were +/-, 2544 were -/+ and 186 were -/- EBV serological statuses. Compared to positive donor to negative recipient EBV serostatus, other donor and recipient EBV serostatuses were associated with decreased mortality (Figure and Table).
Conclusion: A primary EBV infection in EBV-seronegative patients receiving an EBV-seropositive donor organ or a reactivation in those who are already latently infected pre-transplantation can lead to uninhibited growth of EBV-infected B cells which can impact post HT survival. In the absence of effective preventive strategies, such as vaccines and antiviral agents the role of EBV viral load monitoring and immunosuppression regimen modulation needs investigation.
Methods: We identified adult patients who underwent HT between 2000 and 2018 in the Scientific Registry of Transplant Recipients. These patients were categorized as per recipient and donor EBV serological status. We compared survival with the Kaplan-Meier method. We constructed Cox proportional hazards regression models to determine the risk-adjusted influence of EBV serostatus on post HT survival.
Results: Out of 20, 533 HT identified, 16,222 were +/+, 1081 were +/-, 2544 were -/+ and 186 were -/- EBV serological statuses. Compared to positive donor to negative recipient EBV serostatus, other donor and recipient EBV serostatuses were associated with decreased mortality (Figure and Table).
Conclusion: A primary EBV infection in EBV-seronegative patients receiving an EBV-seropositive donor organ or a reactivation in those who are already latently infected pre-transplantation can lead to uninhibited growth of EBV-infected B cells which can impact post HT survival. In the absence of effective preventive strategies, such as vaccines and antiviral agents the role of EBV viral load monitoring and immunosuppression regimen modulation needs investigation.
| Mortality | EBV Pos/Pos | EBV Pos/Neg | EBV Neg/Pos | EBV Neg/Neg |
| 30-Day | 641 (3.8) | 33 (3.1) | 119 (4.7) | 5 (2.7) |
| HR (95% CI) | 0.76 (0.63-0.93) | 0.66 (0.45-0.98) | Referent | 0.69 (0.28-1.69) |
| p-value | 0.007 | 0.038 | 0.419 | |
| 1-Year | 1525 (9.1) | 86 (8.0) | 273 (10.7) | 11 (5.9) |
| HR (95% CI) | 0.80 (0.70-0.91) | 0.75 (0.56-0.96) | Referent | 0.61 (0.33-1.11) |
| p-value | <0.001 | 0.023 | 0.103 | |
| 3-Year | 2290 (13.7 | 130 (12.0) | 416 (16.4) | 17 (9.1) |
| HR (95% CI) | 0.82 (0.74-0.92) | 0.77 (0.63-0.94) | Referent | 0.60 (0.37-0.97) |
| p-value | <0.001 | 0.009 | 0.037 | |
| 5-Year | 2755 (16.5) | 158 (14.6) | 504 (19.8) | 23 (12.4) |
| HR (95% CI) | 0.85 (0.77-0.93) | 0.78 (0.65-0.93) | Referent | 0.65 (0.43-0.99) |
| p-value | <0.001 | 0.007 | 0.045 |
Background: Although the incidence of Post-transplant lymphoproliferative disease which is associated with Epstein-Barr virus (EBV) is relatively high and its presence is associated with severe complications, impact of EBV serostatus on post heart transplantation (HT) survival is not clear. We sought to determine the impact of donor and recipient EBV serostatus on post HT survival.
Methods: We identified adult patients who underwent HT between 2000 and 2018 in the Scientific Registry of Transplant Recipients. These patients were categorized as per recipient and donor EBV serological status. We compared survival with the Kaplan-Meier method. We constructed Cox proportional hazards regression models to determine the risk-adjusted influence of EBV serostatus on post HT survival.
Results: Out of 20, 533 HT identified, 16,222 were +/+, 1081 were +/-, 2544 were -/+ and 186 were -/- EBV serological statuses. Compared to positive donor to negative recipient EBV serostatus, other donor and recipient EBV serostatuses were associated with decreased mortality (Figure and Table).
Conclusion: A primary EBV infection in EBV-seronegative patients receiving an EBV-seropositive donor organ or a reactivation in those who are already latently infected pre-transplantation can lead to uninhibited growth of EBV-infected B cells which can impact post HT survival. In the absence of effective preventive strategies, such as vaccines and antiviral agents the role of EBV viral load monitoring and immunosuppression regimen modulation needs investigation.
Methods: We identified adult patients who underwent HT between 2000 and 2018 in the Scientific Registry of Transplant Recipients. These patients were categorized as per recipient and donor EBV serological status. We compared survival with the Kaplan-Meier method. We constructed Cox proportional hazards regression models to determine the risk-adjusted influence of EBV serostatus on post HT survival.
Results: Out of 20, 533 HT identified, 16,222 were +/+, 1081 were +/-, 2544 were -/+ and 186 were -/- EBV serological statuses. Compared to positive donor to negative recipient EBV serostatus, other donor and recipient EBV serostatuses were associated with decreased mortality (Figure and Table).
Conclusion: A primary EBV infection in EBV-seronegative patients receiving an EBV-seropositive donor organ or a reactivation in those who are already latently infected pre-transplantation can lead to uninhibited growth of EBV-infected B cells which can impact post HT survival. In the absence of effective preventive strategies, such as vaccines and antiviral agents the role of EBV viral load monitoring and immunosuppression regimen modulation needs investigation.
| Mortality | EBV Pos/Pos | EBV Pos/Neg | EBV Neg/Pos | EBV Neg/Neg |
| 30-Day | 641 (3.8) | 33 (3.1) | 119 (4.7) | 5 (2.7) |
| HR (95% CI) | 0.76 (0.63-0.93) | 0.66 (0.45-0.98) | Referent | 0.69 (0.28-1.69) |
| p-value | 0.007 | 0.038 | 0.419 | |
| 1-Year | 1525 (9.1) | 86 (8.0) | 273 (10.7) | 11 (5.9) |
| HR (95% CI) | 0.80 (0.70-0.91) | 0.75 (0.56-0.96) | Referent | 0.61 (0.33-1.11) |
| p-value | <0.001 | 0.023 | 0.103 | |
| 3-Year | 2290 (13.7 | 130 (12.0) | 416 (16.4) | 17 (9.1) |
| HR (95% CI) | 0.82 (0.74-0.92) | 0.77 (0.63-0.94) | Referent | 0.60 (0.37-0.97) |
| p-value | <0.001 | 0.009 | 0.037 | |
| 5-Year | 2755 (16.5) | 158 (14.6) | 504 (19.8) | 23 (12.4) |
| HR (95% CI) | 0.85 (0.77-0.93) | 0.78 (0.65-0.93) | Referent | 0.65 (0.43-0.99) |
| p-value | <0.001 | 0.007 | 0.045 |
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