FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4226344311> ?p ?o ?g. }

• W4226344311 endingPage "S500" @default.
• W4226344311 startingPage "S499" @default.
• W4226344311 abstract "Purpose The role of non-HLA antibodies, such as MICA and AT1R, in pediatric heart transplant (HTx) is not well delineated. While both may contribute to worse outcomes after HTx, regular surveillance monitoring and B-cell treatment is generally reserved for recipients with HLA-DSA. Methods Case report describing the development of non-HLA DSA in a patient who is s/p second HTx with concern for CAV in both allografts. Results We introduce a 16-yo male who received a HTx for familial DCM in 2007, at age 2yo. Prior to HTx he was mechanically supported with ECMO (10 dys) and a Berlin Heart (6 wks). PRA were negative and his retrospective cross match (XM) was invalid due to auto-reactivity. Immunosuppression (ISX) was maintained with tacrolimus and sirolimus. Three years (2010) after HTx de novo HLA-DSA (DQ8, DR53) were detected following a period of medical non-compliance; HLA-DSA gradually increased in strength to 20,000 MFI. While all surveillance biopsies since transplant remained without evidence of ACR or AMR, he required treatment for clinical rejection in 2011 (pulse steroids, IVIG) and 2015 (pulse steroids, ATG) and MMF was added to his ISX. He eventually developed micro-vascular CAV, presenting as heart block and diastolic dysfunction, and received a second HTx in 2016. His retrospective XM again showed autoreactivity; he had a negative virtual XM and never developed new HLA-DSA. A recent biopsy, prompted by mild diastolic dysfunction, revealed new endothelial swelling (ACR 1R, AMR 1H, C4D neg). Additional analysis showed high levels of donor-specific MICA, and AT1R antibodies; both remained high despite initiation of B-cell therapy (rituximab, bortezomib, IVIG). Further retrospective analysis revealed that the MICA antibodies were developed de novo against his first heart (targeting a common epitope present on both donors’ MICA) alongside the HLA-DSA, while AT1R antibodies were already present before his first HTx. Thus, MICA-DSA may have contributed to accelerated CAV in his first allograft, and cause endothelial swelling and AMR in his second allograft. This may have been further exacerbated by the ongoing presence of AT1R, though their role in our patient's clinical course remains less clear. Conclusion Non-HLA DSA can be injurious to cardiac allografts, and the presence of AMR or CAV without HLA-DSA warrants further evaluation for MICA-DSA and AT1R antibodies. The role of non-HLA antibodies, such as MICA and AT1R, in pediatric heart transplant (HTx) is not well delineated. While both may contribute to worse outcomes after HTx, regular surveillance monitoring and B-cell treatment is generally reserved for recipients with HLA-DSA. Case report describing the development of non-HLA DSA in a patient who is s/p second HTx with concern for CAV in both allografts. We introduce a 16-yo male who received a HTx for familial DCM in 2007, at age 2yo. Prior to HTx he was mechanically supported with ECMO (10 dys) and a Berlin Heart (6 wks). PRA were negative and his retrospective cross match (XM) was invalid due to auto-reactivity. Immunosuppression (ISX) was maintained with tacrolimus and sirolimus. Three years (2010) after HTx de novo HLA-DSA (DQ8, DR53) were detected following a period of medical non-compliance; HLA-DSA gradually increased in strength to 20,000 MFI. While all surveillance biopsies since transplant remained without evidence of ACR or AMR, he required treatment for clinical rejection in 2011 (pulse steroids, IVIG) and 2015 (pulse steroids, ATG) and MMF was added to his ISX. He eventually developed micro-vascular CAV, presenting as heart block and diastolic dysfunction, and received a second HTx in 2016. His retrospective XM again showed autoreactivity; he had a negative virtual XM and never developed new HLA-DSA. A recent biopsy, prompted by mild diastolic dysfunction, revealed new endothelial swelling (ACR 1R, AMR 1H, C4D neg). Additional analysis showed high levels of donor-specific MICA, and AT1R antibodies; both remained high despite initiation of B-cell therapy (rituximab, bortezomib, IVIG). Further retrospective analysis revealed that the MICA antibodies were developed de novo against his first heart (targeting a common epitope present on both donors’ MICA) alongside the HLA-DSA, while AT1R antibodies were already present before his first HTx. Thus, MICA-DSA may have contributed to accelerated CAV in his first allograft, and cause endothelial swelling and AMR in his second allograft. This may have been further exacerbated by the ongoing presence of AT1R, though their role in our patient's clinical course remains less clear. Non-HLA DSA can be injurious to cardiac allografts, and the presence of AMR or CAV without HLA-DSA warrants further evaluation for MICA-DSA and AT1R antibodies." @default.
• W4226344311 created "2022-05-05" @default.
• W4226344311 creator A5018766924 @default.
• W4226344311 creator A5028281878 @default.
• W4226344311 creator A5028635385 @default.
• W4226344311 creator A5037737471 @default.
• W4226344311 creator A5042787326 @default.
• W4226344311 creator A5055234599 @default.
• W4226344311 creator A5057486621 @default.
• W4226344311 creator A5072685522 @default.
• W4226344311 creator A5073174793 @default.
• W4226344311 creator A5089406376 @default.
• W4226344311 date "2022-04-01" @default.
• W4226344311 modified "2023-10-16" @default.
• W4226344311 title "AMR or CAV without HLA-DSA: Could MICA-DSA Be the Culprit?" @default.
• W4226344311 doi "https://doi.org/10.1016/j.healun.2022.01.1267" @default.
• W4226344311 hasPublicationYear "2022" @default.
• W4226344311 type Work @default.
• W4226344311 citedByCount "0" @default.
• W4226344311 crossrefType "journal-article" @default.
• W4226344311 hasAuthorship W4226344311A5018766924 @default.
• W4226344311 hasAuthorship W4226344311A5028281878 @default.
• W4226344311 hasAuthorship W4226344311A5028635385 @default.
• W4226344311 hasAuthorship W4226344311A5037737471 @default.
• W4226344311 hasAuthorship W4226344311A5042787326 @default.
• W4226344311 hasAuthorship W4226344311A5055234599 @default.
• W4226344311 hasAuthorship W4226344311A5057486621 @default.
• W4226344311 hasAuthorship W4226344311A5072685522 @default.
• W4226344311 hasAuthorship W4226344311A5073174793 @default.
• W4226344311 hasAuthorship W4226344311A5089406376 @default.
• W4226344311 hasBestOaLocation W42263443111 @default.
• W4226344311 hasConcept C126322002 @default.
• W4226344311 hasConcept C141071460 @default.
• W4226344311 hasConcept C147483822 @default.
• W4226344311 hasConcept C164705383 @default.
• W4226344311 hasConcept C188280979 @default.
• W4226344311 hasConcept C203014093 @default.
• W4226344311 hasConcept C2778826181 @default.
• W4226344311 hasConcept C2780252810 @default.
• W4226344311 hasConcept C2909675724 @default.
• W4226344311 hasConcept C2911091166 @default.
• W4226344311 hasConcept C500558357 @default.
• W4226344311 hasConcept C71924100 @default.
• W4226344311 hasConceptScore W4226344311C126322002 @default.
• W4226344311 hasConceptScore W4226344311C141071460 @default.
• W4226344311 hasConceptScore W4226344311C147483822 @default.
• W4226344311 hasConceptScore W4226344311C164705383 @default.
• W4226344311 hasConceptScore W4226344311C188280979 @default.
• W4226344311 hasConceptScore W4226344311C203014093 @default.
• W4226344311 hasConceptScore W4226344311C2778826181 @default.
• W4226344311 hasConceptScore W4226344311C2780252810 @default.
• W4226344311 hasConceptScore W4226344311C2909675724 @default.
• W4226344311 hasConceptScore W4226344311C2911091166 @default.
• W4226344311 hasConceptScore W4226344311C500558357 @default.
• W4226344311 hasConceptScore W4226344311C71924100 @default.
• W4226344311 hasIssue "4" @default.
• W4226344311 hasLocation W42263443111 @default.
• W4226344311 hasOpenAccess W4226344311 @default.
• W4226344311 hasPrimaryLocation W42263443111 @default.
• W4226344311 hasRelatedWork W1974361353 @default.
• W4226344311 hasRelatedWork W1987735553 @default.
• W4226344311 hasRelatedWork W2043202072 @default.
• W4226344311 hasRelatedWork W2057461145 @default.
• W4226344311 hasRelatedWork W2072374201 @default.
• W4226344311 hasRelatedWork W2086819749 @default.
• W4226344311 hasRelatedWork W2093529832 @default.
• W4226344311 hasRelatedWork W2169919872 @default.
• W4226344311 hasRelatedWork W3083160147 @default.
• W4226344311 hasRelatedWork W4294349031 @default.
• W4226344311 hasVolume "41" @default.
• W4226344311 isParatext "false" @default.
• W4226344311 isRetracted "false" @default.
• W4226344311 workType "article" @default.