ArticleJournal of clinical medicine2021
No Evidence for Classic Thrombotic Microangiopathy in COVID-19.
Article in Journal of clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- The impact of the COVID-19 pandemic on incidence and clinical presentation of thrombotic microangiopathies: data from a laboratory centralizing ADAMTS-13 testing in Quebec.Orphanet journal of rare diseases · 2025Article
- Thrombocytopenia Secondary to COVID-19: Outcomes Analysis in Terms of Thrombotic Microangiopathy, Acute Kidney Injury, and Mortality.International journal of hematology-oncology and stem cell research · 2024Article
- Von Willebrand factor and the thrombophilia of severe COVID-19:Research and practice in thrombosis and haemostasis · 2023Article
- Observational
- Mechanisms of Immunothrombosis by SARS-CoV-2.Biomolecules · 2021Review
- Complement inhibition for the treatment of COVID-19 triggered thrombotic microangiopathy with cardiac failure: a case report.European heart journal. Case reports · 2021Article
- Imbalance of von Willebrand factor and ADAMTS13 axis is rather a biomarker of strong inflammation and endothelial damage than a cause of thrombotic process in critically ill COVID-19 patients.Journal of thrombosis and haemostasis : JTH · 2021Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCoronavirus 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
methodsPatients (
resultsCOVID-19 patients (
conclusionDIC 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.