| Autor: |
Yonghou Jiang, Fergal Duffy, Jennifer Hadlock, Andrew Raappana, Sheila Styrchak, Ingrid Beck, Fred D. Mast, Leslie R. Miller, William Chour, John Houck, Blair Armistead, Venkata R. Duvvuri, Winnie Yeung, Micaela Haglund, Jackson Wallner, Julie A. Wallick, Samantha Hardy, Alyssa Oldroyd, Daisy Ko, Ana Gervassi, Kim M. Murray, Henry Kaplan, John D. Aitchison, James R. Heath, D. Noah Sather, Jason D. Goldman, Lisa Frenkel, Whitney E. Harrington |
| Jazyk: |
angličtina |
| Rok vydání: |
2021 |
| Předmět: |
|
| Zdroj: |
PLoS ONE, Vol 16, Iss 11 (2021) |
| Druh dokumentu: |
article |
| ISSN: |
1932-6203 |
| Popis: |
Background Coronavirus disease 2019 (COVID-19) is associated with endothelial activation and coagulopathy, which may be related to pre-existing or infection-induced pro-thrombotic autoantibodies such as those targeting angiotensin II type I receptor (AT1R-Ab). Methods We compared prevalence and levels of AT1R-Ab in COVID-19 cases with mild or severe disease to age and sex matched negative controls utilizing multivariate logistic and quantile regression adjusted for comorbidities including hypertension, diabetes, and heart disease. Results There were trends toward increased prevalence (50% vs. 33%, p = 0.1) and level of AT1R-Ab (median 9.8 vs. 6.1 U/mL, p = 0.06) in all cases versus controls. When considered by COVID-19 disease severity, there was a trend toward increased prevalence of AT1R-Ab (55% vs. 31%, p = 0.07), as well as significantly higher AT1R-Ab levels (median 10.7 vs. 5.9 U/mL, p = 0.03) amongst individuals with mild COVID-19 versus matched controls. In contrast, the prevalence (42% vs. 37%, p = 0.9) and level (both medians 6.7 U/mL, p = 0.9) of AT1R-Ab amongst those with severe COVID-19 did not differ from matched controls. Conclusions These findings support an association between COVID-19 and AT1R-Ab, emphasizing that vascular pathology may be present in individuals with mild COVID-19 as well as those with severe disease. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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