No Evidence for Classic Thrombotic Microangiopathy in COVID-19.

Autor: Falter T; Institute of Clinical Chemistry and Laboratory medicine, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany., Rossmann H; Institute of Clinical Chemistry and Laboratory medicine, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany., Menge P; Medical Department I, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany., Goetje J; Medical Department I, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany., Groenwoldt S; Medical Department I, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany., Weinmann A; Medical Department I, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.; Clinical Registry Unit, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany., Sivanathan V; Medical Department I, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany., Schulz A; Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany., Lemmermann NAW; Institute of Virology, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany., Danckwardt S; Institute of Clinical Chemistry and Laboratory medicine, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.; Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany., Lackner KJ; Institute of Clinical Chemistry and Laboratory medicine, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany., Galle PR; Medical Department I, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany., Scharrer I; Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany., Lämmle B; Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.; Department of Hematology and Central Hematology Laboratory, Inselspital, Bern University Hospital, University of Bern, CH 3010 Bern, Switzerland.; Haemostasis Research Unit, University College London, London WC1E 6BT, UK., Sprinzl MF; Institute of Clinical Chemistry and Laboratory medicine, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.; Medical Department I, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.; Clinical Registry Unit, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany.
Jazyk: angličtina
Zdroj: Journal of clinical medicine [J Clin Med] 2021 Feb 09; Vol. 10 (4). Date of Electronic Publication: 2021 Feb 09.
DOI: 10.3390/jcm10040671
Abstrakt: Background: Coronavirus disease-2019 (COVID-19) triggers systemic infection with involvement of the respiratory tract. There are some patients developing haemostatic abnormalities during their infection with a considerably increased risk of death.
Materials and Methods: Patients ( n = 85) with SARS-CoV-2 infection attending the University Medical Center, Mainz, from 3 March to 15 May 2020 were retrospectively included in this study. Data regarding demography, clinical features, treatment and laboratory parameters were analyzed. Twenty patients were excluded for assessment of disseminated intravascular coagulation (DIC) and thrombotic microangiopathy (TMA) due to lack of laboratory data.
Results: COVID-19 patients ( n = 65) were investigated, 19 with uncomplicated, 29 with complicated, and 17 with critical course; nine (13.8%) died. Seven patients showed overt DIC according to the ISTH criteria. The fibrinogen levels dropped significantly in these patients, although not below 100 mg/dl. Hallmarks of TMA, such as thrombocytopenia and microangiopathic haemolytic anaemia, were not detected in any of our COVID-19 patients. ADAMTS13 activity was mildly to moderately reduced in 4/22 patients, all having strongly elevated procalcitonin levels.
Conclusion: DIC occurred in 7/65 COVID-19 patients but fibrinogen and platelet consumption were compensated in almost all. ADAMTS13 assays excluded TTP and hallmarks of classic TMA were absent in all investigated patients. We hypothesize that the lacking erythrocyte fragmentation and only mild platelet consumption in severe COVID-19 are due to a microangiopathy predominantly localized to the alveolar microcirculation with a low blood pressure gradient.
Databáze: MEDLINE
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