Tanja Falter1, Heidi Rossmann1, Philipp Menge2, Jan Goetje2, Steffen Groenwoldt2, Arndt Weinmann2,3, Visvakanth Sivanathan2, Andreas Schulz4, Niels A W Lemmermann5, Sven Danckwardt1,4, Karl J Lackner1, Peter R Galle2, Inge Scharrer4, Bernhard Lämmle4,6,7, Martin F Sprinzl1,2,3. 1. Institute of Clinical Chemistry and Laboratory medicine, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany. 2. Medical Department I, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany. 3. Clinical Registry Unit, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany. 4. Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany. 5. Institute of Virology, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany. 6. Department of Hematology and Central Hematology Laboratory, Inselspital, Bern University Hospital, University of Bern, CH 3010 Bern, Switzerland. 7. Haemostasis Research Unit, University College London, London WC1E 6BT, UK.
Abstract
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.
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-19patients (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-19patients. ADAMTS13 activity was mildly to moderately reduced in 4/22 patients, all having strongly elevated procalcitonin levels. CONCLUSION:DIC occurred in 7/65 COVID-19patients 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.
Authors: Andrea Lassnigg; Edith R Schmid; Michael Hiesmayr; Christian Falk; Wilfred Druml; Peter Bauer; Daniel Schmidlin Journal: Crit Care Med Date: 2008-04 Impact factor: 7.598
Authors: A D Makatsariya; E V Slukhanchuk; V O Bitsadze; J K H Khizroeva; M V Tretyakova; V I Tsibizova; I Elalamy; J-C Gris; E Grandone; N A Makatsariya; T Mashkova Journal: J Matern Fetal Neonatal Med Date: 2020-07-06
Authors: Brandon Michael Henry; Stefanie W Benoit; Maria Helena Santos de Oliveira; Giuseppe Lippi; Emmanuel J Favaloro; Justin L Benoit Journal: Int J Lab Hematol Date: 2020-12-03 Impact factor: 3.450
Authors: Helen Fogarty; Liam Townsend; Cliona Ni Cheallaigh; Colm Bergin; Ignacio Martin-Loeches; Paul Browne; Christopher L Bacon; Richard Gaule; Alexander Gillett; Mary Byrne; Kevin Ryan; Niamh O'Connell; Jamie M O'Sullivan; Niall Conlon; James S O'Donnell Journal: Br J Haematol Date: 2020-05-17 Impact factor: 8.615
Authors: María Teresa Hernández-Huerta; Alma Dolores Pérez-Santiago; Laura Pérez-Campos Mayoral; Luis Manuel Sánchez Navarro; Francisco Javier Rodal Canales; Abraham Majluf-Cruz; Carlos Alberto Matias-Cervantes; Eduardo Pérez-Campos Mayoral; Carlos Romero Díaz; Gabriel Mayoral-Andrade; Margarito Martínez Cruz; Judith Luna Ángel; Eduardo Pérez-Campos Journal: Biomolecules Date: 2021-10-20