ABSTRACT
The effect of SARS-CoV-2 vaccination on de novo donor specific antibodies (dn DSA) in lung transplant recipients (LTRs) is unknown. We reviewed dn DSA results following SARS-CoV-2 vaccination in LTRs based on SARS-CoV-2 IgG response. LTRs were tested for SARS-COV-2 Multi-target IgG at 3 and 6 months post-vaccination. LTRs who received at least 1 dose of SARS-CoV-2 vaccine between 12/01/2020 to 07/01/2021 were included in this retrospective review. We compared patients based on anti-spike (S-IgG) results. We reviewed 55 LTR charts with S-IgG results. Only 24 (44%) developed S-IgG by 6 months after vaccination. Differences between S-IgG positive and negative groups are shown in the table. Those with positive S-IgG were further from transplant, had lower mycophenolate doses, more likely to have had COVID infection pre-vaccination, and had lower rates of hypogammaglobulinemia. Only 3 patients (5.5%) developed dn DSA after vaccination;all were S-IgG positive. One had history of antibody mediated rejection (AMR), while another was initially negative for dn DSA at 6 weeks post-vaccination, but turned positive at 7 months (low level Class II DSA). One patient who had prior DSA developed clinical rejection (AMR) with Class II dn DSA (DR7) and significant rise in prior DSA (DR53, DQ2) to >20,000 MFI at 6 months (negative at 3 months) post-vaccine in the setting of new viral infection. Another patient was excluded from this study as he died of AMR and dn Class II DSA (DQ8 > 10,000 MFI, DQ6, DR4 within 5 days of dose) 2 months after his first Pfizer/BioNTech dose, but before 3 month S-IgG testing. In our cohort, dn DSA after SARS-CoV-2 vaccination was uncommon but observed in patients who developed S-IgG response. The single AMR case occurred late and may be related to infection. In the excluded patient with acute AMR early after vaccine, correlation to S-IgG is unknown as the patient did not survive to 3 months. Further studies are needed to determine the impact of additional vaccine doses and long-term outcomes and immune responses. [ FROM AUTHOR] Copyright of Journal of Heart & Lung Transplantation is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)
ABSTRACT
Background: Thrombocytopenia (<150 x109/L) is often encountered during mechanical circulatory support. Coagulopathy in SARS-COV-2 illness (COVID-19) is increasingly recognized as a risk factor for more severe illness and higher mortality. Thrombocytopenia in COVID-19 patients requiring venovenous (VV) extracorporeal membrane oxygenation (ECMO) is challenging, and therefore identification of contributing factors may aid in management of these complex patients. Methods: A retrospective review was performed for consecutive adult patients on VV ECMO for COVID-19 respiratory failure at a single institution from March to July 2020. Patient data was obtained from our internal registry with IRB approval. Group comparisons of means were made using unadjusted t-tests and proportions were evaluated with a simple chi-square test. Results: The majority (85%) of COVID-19 patients on VV ECMO developed thrombocytopenia. Twelve of 27 patients (44%) exhibited larger drops in platelet counts following ECMO initiation (73% vs 52% fall to nadir) raising concern for heparin-induced thrombocytopenia (HIT). Nine of the 12 (75%) patients tested positive for anti-PF4 antibodies;however, none tested positive via serotonin release assay. Characteristics that affected the degree of platelet decline included the need for simultaneous continuous renal replacement therapy (CRRT) and treatment with an immunomodulating agent, convalescent plasma, or azithromycin. Discussion: Thrombocytopenia in COVID-19 patients on VV ECMO is likely multifactorial, but a more severe thrombocytopenia exists in a subset of patients. CRRT therapy and certain COVID-directed pharmacotherapy agents appear to be influential factors. Anti-PF4 antibody testing may be falsely positive and should be interpreted cautiously.