التفاصيل البيبلوغرافية
| العنوان: |
Abnormal thrombosis and neutrophil activation increase hospital-acquired sacral pressure injuries and morbidity in COVID-19 patients |
| المؤلفون: |
Narang, Jatin, Jatana, Samreen, Ponti, András K., Musich, Ryan, Gallop, Joshua, Wei, Angela H., Seck, Sokhna, Johnson, Jessica, Kokoczka, Lynne, Nowacki, Amy S., McBride, Jeffrey D., Mireles-Cabodevila, Eduardo, Gordon, Steven, Cooper, Kevin, Fernandez, Anthony P., McDonald, Christine |
| المساهمون: |
Clinical and Translational Science Collaborative of Cleveland, School of Medicine, Case Western Reserve University, U.S. Department of Defense, Crohn's and Colitis Foundation, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health |
| المصدر: |
Frontiers in Immunology ; volume 14 ; ISSN 1664-3224 |
| بيانات النشر: |
Frontiers Media SA |
| سنة النشر: |
2023 |
| المجموعة: |
Frontiers (Publisher - via CrossRef) |
| مصطلحات موضوعية: |
Immunology, Immunology and Allergy |
| الوصف: |
Hospitalized patients have an increased risk of developing hospital-acquired sacral pressure injury (HASPI). However, it is unknown whether SARS-CoV-2 infection affects HASPI development. To explore the role of SARS-CoV-2 infection in HASPI development, we conducted a single institution, multi-hospital, retrospective study of all patients hospitalized for ≥5 days from March 1, 2020 to December 31, 2020. Patient demographics, hospitalization information, ulcer characteristics, and 30-day-related morbidity were collected for all patients with HASPIs, and intact skin was collected from HASPI borders in a patient subset. We determined the incidence, disease course, and short-term morbidity of HASPIs in COVID-19(+) patients, and characterized the skin histopathology and tissue gene signatures associated with HASPIs in COVID-19 disease. COVID-19(+) patients had a 63% increased HASPI incidence rate, HASPIs of more severe ulcer stage (OR 2.0, p<0.001), and HASPIs more likely to require debridement (OR 3.1, p=0.04) compared to COVID-19(-) patients. Furthermore, COVID-19(+) patients with HASPIs had 2.2x increased odds of a more severe hospitalization course compared to COVID-19(+) patients without HASPIs. HASPI skin histology from COVID-19(+) patients predominantly showed thrombotic vasculopathy, with the number of thrombosed vessels being significantly greater than HASPIs from COVID-19(-) patients. Transcriptional signatures of a COVID-19(+) sample subset were enriched for innate immune responses, thrombosis, and neutrophil activation genes. Overall, our results suggest that immunologic dysregulation secondary to SARS-CoV-2 infection, including neutrophil dysfunction and abnormal thrombosis, may play a pathogenic role in development of HASPIs in patients with severe COVID-19. |
| نوع الوثيقة: |
article in journal/newspaper |
| اللغة: |
unknown |
| DOI: |
10.3389/fimmu.2023.1031336 |
| DOI: |
10.3389/fimmu.2023.1031336/full |
| الإتاحة: |
https://doi.org/10.3389/fimmu.2023.1031336Test |
| حقوق: |
https://creativecommons.org/licenses/by/4.0Test/ |
| رقم الانضمام: |
edsbas.C8B9C9E |
| قاعدة البيانات: |
BASE |
