scholarly journals Thrombose und COVID-19

hautnah ◽  
2021 ◽  
Stanislava Tzaneva

ZusammenfassungDie Prävalenz der venösen thromboembolischen (VTE) Ereignisse ist bei Coronavirus diesease 2019 (COVID-19) -Patienten hoch, insbesondere bei schwer Erkrankten. Patienten mit schwerer COVID-19 und VTE haben eine signifikant höhere Mortalität im Vergleich zu Patienten ohne VTE. Die Manifestation einer schweren Infektion mit Severe acute respiratory syndrome coronavirus-2 (SARS-CoV‑2) entspricht einem systemischen proinflammatorischen und prokoagulatorischen Phänotyp, der mit vaskulären Thrombosen nicht nur in den Venen, sondern auch in den Arterien, Kapillaren sowie mit einer Inflammation der Gefäße assoziiert ist. Ein erhöhter D‑Dimer-Spiegel kann als Indikator für VTE bei Patienten mit COVID-19 verwendet werden. Die meisten medizinischen Gesellschaften empfehlen eine VTE-Prophylaxe vorzugsweise mit niedermolekularen Heparinen (LMWH) bei allen stationären Patienten. Weitere Daten von randomisierten kontrollierten Studien (RCTs) über die optimale Antikoagulation und antithrombotische Therapie werden in der nahen Zukunft erwartet.

Axel Rosell ◽  
Sebastian Havervall ◽  
Fien von Meijenfeldt ◽  
Yohei Hisada ◽  
Katherina Aguilera ◽  

Objective: Patients with coronavirus disease 2019 (COVID-19) have a high rate of thrombosis. We hypothesized that severe acute respiratory syndrome coronavirus 2 leads to induction of TF (tissue factor) expression and increased levels of circulating TF-positive extracellular vesicles (EV) that may drive thrombosis. Approach and Results: We measured levels of plasma EV TF activity in 100 patients with COVID-19 with moderate and severe disease and 28 healthy controls. Levels of EV TF activity were significantly higher in patients with COVID-19 compared with controls. In addition, levels of EV TF activity were associated with disease severity and mortality. Finally, levels of EV TF activity correlated with several plasma markers, including D-dimer, which has been shown to be associated with thrombosis in patients with COVID-19. Conclusions: Our results indicate that severe acute respiratory syndrome coronavirus 2 infection induces the release of TF-positive EVs into the circulation that are likely to contribute to thrombosis in patients with COVID-19. EV TF activity was also associated with severity and mortality.

2021 ◽  
Vol 8 ◽  
Alessandra G. D. Lopes ◽  
Camila S. H. Celestino ◽  
Tiago T. A. Barros ◽  
Aline G. Fevereiro ◽  
Debora H. Gejer ◽  

Teenagers generally present mild to no symptoms of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In the present report, we present the case of a 14-year-old boy with Angelman syndrome (AS) who presented with severe COVID-19 symptoms. He spent 20 days in the ICU with elevated inflammatory biomarkers (C-reactive protein and D-dimer) and increased peaks of neutrophil-to-lymphocyte ratio, which is uncommon for teenagers diagnosed with COVID-19. Although he showed physiological instability, he was able to produce neutralizing antibodies, suggesting a functional immune response. The literature concerning the immune response to infections in patients with AS is still poor, and to our knowledge, this was the first report of a patient with AS diagnosed with COVID-19. As such, the present study may alert other patients with AS or other rare diseases that they lack a competent immune response and could suffer severe consequences of SARS-CoV-2 infection.

2021 ◽  
Vol 2 (2) ◽  
pp. 63-72

Severe acute respiratory syndrome coronavirus (SARS-CoV-2) merupakan famili dari coronavirus, sudah dua kali menyababkan kejadian luar biasa  yaitu di tahun 2003 dengan SARS (Severe Acute Respiratory Syndrome) dan tahun 2012 dengan penyakit  MERS (Middle East Respiratory Syndrome). Pada tahun 2019 SARS-CoV-2 telah menyebabkan pandemi global kembali. Pertama kali diidentifikasi di Wuhan, Cina. Dan telah menyebar ke seluruh negara dengan jumlah kasus yang terus meningkat secara eksponensial diseluruh dunia. Pada Maret 2020 oleh WHO dinyatakan pandemic. (Covid-19), menyebabkan pneumonia dan beberapa kondisi dapat terjadi Acute Respiratory Distress Syndrome (ARDS) serta beberapa manifestasi ekstra paru, seperti kardiovaskular, saluran cerna, ginjal ,hematologi, sekuele akibat trombosis dan progresifitas disfungsi organ.1 Prognosis pada pasien Covid-19 salah satu tanda ,gejalanya adalah terjadinya gangguan koagulasi, yang ditandai dengan meningkatnya nilai D dimer sebagai tanda awal kondisi thrombosis dan  salah satunya dapat bermanifestasi sebagai Venous Thromboembolism (VTE). Pada pasien dengan Covid-19, kondisi koagulopati adalah salah satu kunci dan tanda persisten yang terkait dengan outcome yang buruk.1,2   

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1382.2-1382
Z. Öztürk ◽  
S. M. Türk ◽  
D. Karataş ◽  
Ü. Erkorkmaz ◽  
K. Özmen Süner ◽  

Background:TCZ is a monoclonal antibody against Interleukin-6 receptor (IL-6R) which is used for relieving inflammation and reducing mortality in COVID-19 patients. Safety and efficacy of Tocilizumab (TCZ) in Covid-19 pneumonia is uncertain yet. In this study, we aimed to determine clinical outcomes in patients treated with TCZ.Objectives:In this study we aimed to share our retrospective results which we had obtained from patients with COVID-19 diagnosis received TCZ.Methods:We performed a retrospective case control study between May and August 2020 in Turkey. We compared outcomes in patients who received TCZ with those who did not. Death in hospital and intensive care unit (ICU) requirements were evaluated as endpoints. Demographic data, comorbidities, additional treatment, treatment side effects, laboratory and clinical results were retrospectively assessed. There are no significant differences between groups according to age, gender and Charlson Comorbidity Index (CCI).Results:12 (27.3%) patients died in standard group and eight (18.6%) patients died in TCZ group (p=0.150).Days of staying in the hospital were eight days in standard treatment group and 12 days in TCZ group (p=0.03). 10 of 43 patients in TCZ group were admitted to ICU. MV support was needed in 8 of these patients. 18 of 44 patients (40.9%) within the standard group were admitted to ICU and 12 patients (27.3%) were intubated (p=0.125,p=0.480). Significant IL-6 decrease was not observed post treatment in TCZ group according to pretreatment period (p=0.60). Significant decreases were examined in CRP and ferritin values through TCZ treatment. However, D-dimer and thrombocyte values increased.Conclusion:TCZ may not be an effective treatment for reducing ICU requirement, to prevent intubation or death, for shortening period for staying in hospital. The patients should be followed up closely for possible thrombosis because of increased D-dimer and thrombocytes with TCZ treatment.References:[1]Sharma A, Tiwari S, Deb MK, Marty JL. Severe acute respiratory syndrome coronavirus-2 (SARS-Cov-2): A global pandemic and treatment strategies. IntJ Antimicrob Agents. 2020 Aug; 56(2):106054.[2]Singhal T. A rewiev of coronavirus Disease-2019(COVID-19). Indian J Pediatr. 2020 Apr;87(4):281-286.[3]Mehta P, McAuley DF, Brown M, Sanchez E, Tattersall R.S, Manson J.J. COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet. 2020;395(10229):1033-[4]Teijaro J.R. Cytokine storms in infectious diseases. SeminImmunopathol. 2017;39:501–503.[5]Zhang Y, Li J, Zhan Y, Wu L, Yu X, Zhang W et al. Analysis of Serum Cytokines in Patients with Severe Acute Respiratory Syndrome. Infect Immun 2004 Aug;72(8):4410-4415.[6]Zhang C, Wu Z, Li JW, Zhao H, Wang GQ. Cytokine release syndrome in severe COVID-19: interleukin-6 receptor antagonist tocilizumab may be the key to reduce mortality. Int J Antimicrob Agents. 2020 May; 55(5):105954.[7]Xu Z, Shi L, Wang Y, Zhang J, Huang L, Zhang C et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med. 2020;8(4):420–2[8]Fu B, Xu X, Wei H. Why tocilizumab could be an effective treatment for severe COVID-19? J Transl Med 18,164 (2020).[9]Guaraldi G, Meschiari M, Cozzi-Lepri A, Milic J, Tonelli R, Menozzi M et al. Tocilizumab in patients with severe COVID-19: a retrospective cohort study. Lancet Rheumatol. 2020 Aug;2(8):e474-e484.[10]Gupta S, Wang W, Hayek S.S, Chan L, MathewsK.S, Melamed M.L et al. Association Between Early Treatment With Tocilizumab and Mortality Among Critically Ill Patients With COVID-19. JAMA Intern Med. 2021 Jan1;181(1):41-51.[11]Campochiaro C, Della-Torre E, Cavalli G, De Luca G, Ripa M, Boffini N et al Efficacy and safety of tocilizumab in severe COVID- 19 patients: a single-centre retrospective cohort study. Eur J Intern Med. 2020 Jun;76:43-49.Disclosure of Interests:None declared

2021 ◽  
Vol 18 (1) ◽  
pp. 59-67
Alina Dima ◽  
Ruxandra Valentina Moroti ◽  
Daniela Nicoleta Popescu ◽  
Ioana Berza ◽  
Delia Adriana Pârvu ◽  

Abstract The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) is prone to thrombotic events with pathogenic mechanism that are still incompletely understood. Occurrence of antiphospholipid antibodies, especially anticardiolipin antibodies, was described in many viral infections and could be part of the chain in micro-thrombosis occurrence in COVID-19. We herein present three cases of COVID-19 patients without any known immune background. For two of the patients, the laboratory tests show neither inflammatory syndrome, nor elevated D-dimer. Even if pauci-symptomatic patients, pulmonary involvement in as much as 10 - 25% was identified on chest computer tomography exam. In addition, a third patient, with more important pulmonary involvement (25-50%), inflammatory response and elevated D-dimer levels is presented. None of the patients had prolonged activated partial-thromboplastin time. IgM and/ or IgG anticardiolipin antibodies were found positives in all three cases.

2021 ◽  
Vol 8 (11) ◽  
pp. 401-403
Ashwini Nagda ◽  
Vishal Sawant ◽  
Kiran Rajput ◽  
Sushma Malik ◽  
Vinaya Singh ◽  

Severe acute respiratory syndrome coronavirus 2 was declared as a pandemic in March 2020. The virus has affected more adults than children, with disease severity being lesser in children. We present a case of a neonate who tested positive for coronavirus disease 2019 infection on day of life 3, 6, and 15. The baby had fever, respiratory distress, and shock. Laboratory investigations showed raised inflammatory markers, raised D dimer suggesting coagulopathy, coronary dilatation on 2D echocardiogram, and raised N terminal pro-brain natriuretic peptide. The neonate was successfully treated with good supportive care, lung-protective ventilatory strategies, early intravenous immunoglobulin administration, corticosteroids, and remdesivir.

2020 ◽  
Vol 58 (8) ◽  
pp. 1191-1199 ◽  
Emmanuel J. Favaloro ◽  
Jecko Thachil

AbstractCoronavirus disease 2019 (COVID-19) represents a new pandemic caused by severe acute respiratory syndrome virus coronavirus 2 (SARS-CoV-2). A previous pooled analysis clearly identified elevated D-dimer levels as being associated with severity of COVID-19. Since then, several other studies have provided clearer support for this initial evidence. However, potentially under-recognized by those reporting on D-dimer is the considerable variation in reporting units for D-dimer, and thus also the potential for misreporting of D-dimer data based on poor or incomplete reporting. A PubMed search was used to identify recent papers reporting on D-dimers in COVID-19-based studies. We report that: (1) most publications did not identify either the manufacturer or D-dimer product used; (2) most did not identify whether D-dimer values were reported as D-dimer units (DDU) or fibrinogen equivalent units (FEU) (~2 ×  differences); (3) nearly half did not identify normal cut-off values; (4) some did not report numerical findings or units for D-dimer; (5) where reported, most identified units as either mg/L or μg/mL; (6) we identified at least four errors in reporting from 21 papers. It may not be possible to truly standardize D-dimer assays, but it should be feasible to harmonize D-dimer assays to a single unit of measurement.

2008 ◽  
Vol 41 (10) ◽  
pp. 12-13

2008 ◽  
Vol 1 (2) ◽  
pp. 11
D Dimer ◽  

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