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Predictors of vascular disease in myelodysplastic syndromes

The escalating link between somatic mutations commonly seen in myelodysplastic syndromes (MDS) and atherosclerotic vascular disease has increased the interest in management and associations of these conditions. We present a retrospective study examining clinical and molecular variables associated wi...

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Autores principales: Faber, Mark G., Lloyd, David R., Singh, Abhay, Baron, Jeffrey, Przespolewski, Amanda, Griffiths, Elizabeth A., Wang, Eunice S., Thota, Swapna
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9175714/
https://www.ncbi.nlm.nih.gov/pubmed/35845007
http://dx.doi.org/10.1002/jha2.101
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author Faber, Mark G.
Lloyd, David R.
Singh, Abhay
Baron, Jeffrey
Przespolewski, Amanda
Griffiths, Elizabeth A.
Wang, Eunice S.
Thota, Swapna
author_facet Faber, Mark G.
Lloyd, David R.
Singh, Abhay
Baron, Jeffrey
Przespolewski, Amanda
Griffiths, Elizabeth A.
Wang, Eunice S.
Thota, Swapna
author_sort Faber, Mark G.
collection PubMed
description The escalating link between somatic mutations commonly seen in myelodysplastic syndromes (MDS) and atherosclerotic vascular disease has increased the interest in management and associations of these conditions. We present a retrospective study examining clinical and molecular variables associated with vascular disease in patients with MDS. This study included a comprehensive evaluation of 236 patients with MDS. Our study has multiple findings. Mutations in ASXL1 correlated with increased risk of vascular disease for the entire cohort (P = .013). Though this has been replicated in other studies, there are no guidelines at this time for preventing vascular events in these patients. Our study also showed that lower ferritin levels may be linked to increased vascular events (P = .043), therefore the optimal use of supportive red blood cell transfusions in patients with MDS and the overall impact of inflammatory markers such as erythrocyte sedimentation rate and c‐reactive protein should be re‐addressed. Furthermore, our study showed that patients with Trisomy 8 in the low‐risk MDS cohort (based on IPSS‐R scores) were protected from vascular events (P = .036). Our findings of lower ferritin being linked with increased risk of vascular events as well as patients with Trisomy 8 being protected from vascular events may impact patient care. There do not appear to be any prior studies with these findings. In addition, given the connection between MDS and atherosclerotic vascular disease, we believe guideline‐based management of cardiac risk factors among MDS patients may improve overall outcomes. Further studies with larger patient cohorts are needed to further investigate these findings.
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spelling pubmed-91757142022-07-14 Predictors of vascular disease in myelodysplastic syndromes Faber, Mark G. Lloyd, David R. Singh, Abhay Baron, Jeffrey Przespolewski, Amanda Griffiths, Elizabeth A. Wang, Eunice S. Thota, Swapna EJHaem Haematologic Malignancy ‐ Myeloid The escalating link between somatic mutations commonly seen in myelodysplastic syndromes (MDS) and atherosclerotic vascular disease has increased the interest in management and associations of these conditions. We present a retrospective study examining clinical and molecular variables associated with vascular disease in patients with MDS. This study included a comprehensive evaluation of 236 patients with MDS. Our study has multiple findings. Mutations in ASXL1 correlated with increased risk of vascular disease for the entire cohort (P = .013). Though this has been replicated in other studies, there are no guidelines at this time for preventing vascular events in these patients. Our study also showed that lower ferritin levels may be linked to increased vascular events (P = .043), therefore the optimal use of supportive red blood cell transfusions in patients with MDS and the overall impact of inflammatory markers such as erythrocyte sedimentation rate and c‐reactive protein should be re‐addressed. Furthermore, our study showed that patients with Trisomy 8 in the low‐risk MDS cohort (based on IPSS‐R scores) were protected from vascular events (P = .036). Our findings of lower ferritin being linked with increased risk of vascular events as well as patients with Trisomy 8 being protected from vascular events may impact patient care. There do not appear to be any prior studies with these findings. In addition, given the connection between MDS and atherosclerotic vascular disease, we believe guideline‐based management of cardiac risk factors among MDS patients may improve overall outcomes. Further studies with larger patient cohorts are needed to further investigate these findings. John Wiley and Sons Inc. 2020-09-28 /pmc/articles/PMC9175714/ /pubmed/35845007 http://dx.doi.org/10.1002/jha2.101 Text en © 2020 The Authors. eJHaem published by British Society for Haematology and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Haematologic Malignancy ‐ Myeloid
Faber, Mark G.
Lloyd, David R.
Singh, Abhay
Baron, Jeffrey
Przespolewski, Amanda
Griffiths, Elizabeth A.
Wang, Eunice S.
Thota, Swapna
Predictors of vascular disease in myelodysplastic syndromes
title Predictors of vascular disease in myelodysplastic syndromes
title_full Predictors of vascular disease in myelodysplastic syndromes
title_fullStr Predictors of vascular disease in myelodysplastic syndromes
title_full_unstemmed Predictors of vascular disease in myelodysplastic syndromes
title_short Predictors of vascular disease in myelodysplastic syndromes
title_sort predictors of vascular disease in myelodysplastic syndromes
topic Haematologic Malignancy ‐ Myeloid
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9175714/
https://www.ncbi.nlm.nih.gov/pubmed/35845007
http://dx.doi.org/10.1002/jha2.101
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