scholarly journals Plasma Exchange for COVID-19 Thrombo-Inflammatory Disease

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 27-27
Author(s):  
Mari Thomas ◽  
Nishkantha Arulkumaran ◽  
David Brearley ◽  
Ferras Alwan ◽  
Deepak Singh ◽  
...  

Introduction Severe COVID-19 disease is associated with a hyperinflammatory, pro-thrombotic state and a high mortality. A thrombotic phenotype rather than a coagulopathy is suggested and we undertook plasma exchange to determine its effects on organ function and thrombo-inflammatory markers. Methods Plasma exchange was carried out in seven critically ill adults with severe COVID-19 respiratory failure (PaO2:FiO2 ratio <200 mmHg) requiring invasive or non-invasive ventilatory support and elevated thrombo-inflammatory markers (LDH>800 IU/L and D dimer>1000 µg/L (or doubling from baseline). Patients received a daily single volume 3 litre plasma exchange for a minimum of five days. No other immunomodulatory medications were initiated during this period. Effects on organ function, thrombo-inflammatory markers and complications were monitored. Seven patients matched for age and baseline biochemistry were a comparator group. Results Coagulation screening revealed no evidence of coagulopathy. However, von Willebrand Factor (VWF) activity, antigen and VWF antigen:ADAMTS13 ratio, Factor VIII and D-dimers were all elevated. Following five days of plasma exchange, plasma levels of all the above, and ferritin levels, were significantly reduced (p<0.05, Figure 1) while lymphocyte count normalized (p<0.05). The PaO2:FiO2 ratio increased from a median(IQR) of 11.6 (10.8- 19.7) kPa to 18.1 (16.0-25.9) kPa (p<0.05). Similar improvements were not observed in controls. Acute kidney injury (AKI) occurred among 5 patients in the control arm but not in patients who underwent plasma exchange. Conclusion Plasma exchange was associated with an improvement in oxygenation, decreased incidence of AKI, normalisation of lymphocytes and reduction in circulating thrombo-inflammatory markers including D-Dimer and VWF Ag:ADAMTS13 ratio. Disclosures Thomas: Ablynx: Honoraria, Other: Advisory Board; Bayer: Honoraria, Speakers Bureau; Sanofi: Honoraria, Other: Advisory Board. Scully:Takeda: Consultancy, Speakers Bureau; Alexion: Consultancy, Speakers Bureau; Sanofi: Consultancy, Speakers Bureau; Shire/Takeda: Other: Advisory Board, Research Funding, Speakers Bureau; Novartis: Other: Advisory Board, Speakers Bureau; Takeda: Speakers Bureau; Ablynx/Sanofi: Consultancy, Other: Advisory Board, Speakers Bureau.

2021 ◽  
Author(s):  
Ahmet Murt ◽  
Mevlut Tamer Dincer ◽  
Cebrail Karaca ◽  
Sinan Trabulus ◽  
Ridvan Karaali ◽  
...  

Abstract Aim Kidneys are among the affected organs in COVID-19 and there may be different etiologies resulting in acute kidney injury (AKI) in different stages of the disease. This study aimed to analyze AKI among hospitalized COVID-19 patients in relation to the time and etiologies of AKI. Methods 1056 patients who were hospitalized with COVID-19 diagnosis in our institution were retrospectively evaluated and 383 of them met the inclusion criteria. Eighty-nine patients who developed AKI were involved in the final analysis. Patients were classified into three groups, those who had AKI on admission, those who developed AKI in the first week and those who developed AKI starting from 7th day. Initial lymphocyte counts, creatinine levels, electrolytes, acid-base status and changes in the inflammatory markers were compared between the groups. A comparison between patients who survived and who died was also performed.Results AKI had 24% mortality in COVID-19 patients who had eGFRs of over 60 ml/min/1,73 m2. Patients who developed AKI later had higher peak CRP and D-dimer levels with lower nadir lymphocyte counts (p=0,000, 0,004 and 0,003 respectively). Mortality of patients who had AKI on hospital admission (13%) was similar to the overall COVID-19 mortality for inpatients, however it was 44% for those who developed AKI after 7th day. Early AKI was related to pre-renal causes and had a milder course. However, later AKIs were more related to immunologic response and had significantly higher mortality. Conclusions AKI in COVID-19 is not of one kind. When developed, AKI should be evaluated in conjunction with the disease stage and possible etiologies. AKI that develops later has a worse prognosis.


Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 5246-5246
Author(s):  
Bruna de Moraes Mazetto ◽  
Fernanda A. Orsi ◽  
Aline Barnabé ◽  
Erich V de Paula ◽  
Joyce M Annichino-Bizzacchi

Abstract Abstract 5246 BACKGROUND: The role of inflammation on the pathophysiology of arterial thrombosis has been extensively studied. However, the relationship between inflammation and deep vein thrombosis (DVT) is not completely understood. Conflicting reports have been published about the levels of proteins involved in the inflammatory response in the context of DVT. Changes in ADAMTS13 levels have been reported in other inflammatory conditions such as sepsis, and this protease could be involved in the interplay between hemostasis and inflammation. OBJECTIVE: To evaluate ADAMTS13 activity in DVT patients and its association with inflammatory markers (IL-6, IL-8, CRP, TNF-α), D-dimer and von Willebrand Factor (VWF) levels. METHODOLOGY: Thirty-eight DVT patients, from 6 months to five years after the diagnosis of DVT, followed at the outpatient unit of thrombotic diseases from University of Campinas and 38 healthy volunteers selected as controls were included in the study. ADAMTS13 activity was determined by the residual binding of VWF to collagen. VWF, IL-6, IL-8 and TNF-alpha levels were determined by ELISA, and D-dimer levels was determined by a turbidimetric method. RESULTS: In this study population DVT was triggered by transient risk factors, particularly the use of oral contraceptives. No patient presented renal, hepatic or malignant disease. Median ADAMTS13 activity was not statistically different between patients (median: 98.2%; range: 70–146) and controls (median: 96.1%; range: 66–117; p=0.35). IL-6 and TNF-alfa levels were also higher in patients (median: 1.0pg/mL and 2.3pg/mL) compared to controls (median: 0.64pg/mL and 1.7pg/mL, p=0,01 and p=0,009). In addition, VWF and D-dimer levels were also significantly higher in patients (all P<0.01). No significant difference could be demonstrated between IL-8 and CRP levels from patients and controls. No significant correlation between ADAMTS13 levels and other inflammatory markers could be demonstrated. VWF levels correlated significantly with IL-8 (r=-0.4635, p< 0.0001). CONCLUSIONS: This study reinforces the role of inflammation in the pathogenesis of DVT. The correlation of VWF and IL-8 supports the notion that IL-8 stimulates the secretion of VWF. The role of ADAMTS13 in the context of DVT is yet to be determined. Disclosures: No relevant conflicts of interest to declare.


2020 ◽  
Author(s):  
Ahmet Murt ◽  
Mevlut Tamer Dincer ◽  
Cebrail Karaca ◽  
Sinan Trabulus ◽  
Ridvan Karaali ◽  
...  

Abstract Introduction Kidneys are among the affected organs in COVID-19 and there may be different etiologies resulting in acute kidney injury (AKI) in different stages of the disease. This study aimed to analyze AKI among hospitalized COVID-19 patients in relation to the time and etiologies of AKI.Materials & Methods 1056 patients who were hospitalized with COVID-19 diagnosis in our institution were retrospectively evaluated and 383 of them met the inclusion criteria. Eighty-nine patients who developed AKI were involved in the final analysis. As immunologic response is generally accepted to start with the second week of COVID-19 course, patients were classified into three groups, those who had AKI on admission, those who developed AKI in the first week and those who developed AKI starting from 7th day. Initial lymphocyte counts, creatinine levels and inflammatory markers as well as changes in these parameters were compared between the groups.Results AKI was seen in 23% of the patients and 23% of those who developed AKI died. Patients who developed AKI later had higher peak CRP and D-dimer levels with lower nadir lymphocyte counts (p=0,000, 0,004 and 0,003 respectively). Additionally, patients who died had higher initial inflammatory marker levels and lower lymphocyte counts than those who survived. Mortality of patients who had AKI on hospital admission (13%) was similar to the overall COVID-19 mortality for inpatients, however it was as high as 44% for those who developed AKI after 7th day.Conclusion Early AKI was more related to pre-renal causes and had a milder course. However, later AKIs were more related to immunologic response and had significantly higher mortality. Findings of this study suggest that AKI in COVID-19 is not of one kind. When developed, AKI should be evaluated in conjunction with the disease stage and possible etiologies.


2020 ◽  
Vol 19 (3) ◽  
pp. 243-249 ◽  
Author(s):  
Sevket Balta

: Vascular diseases are the main reason for morbidity and mortality worldwide. As we know, the earlier phase of vascular diseases is endothelial dysfunction in humans, the endothelial tissues play an important role in inflammation, coagulation, and angiogenesis, via organizing ligand-receptor associations and the various mediators’ secretion. We can use many inflammatory non-invasive tests (flowmediated dilatation, epicedial fat thickness, carotid-intima media thickness, arterial stiffness and anklebrachial index) for assessing the endothelial function. In addition, many biomarkers (ischemia modified albumin, pentraxin-3, E-selectin, angiopoietin, endothelial cell specific molecule 1, asymmetrical dimethylarginine, von Willebrand factor, endothelial microparticles and endothelial progenitor cells) can be used to evaluate endothelial dysfunction. We have focused on the relationship between endothelial dysfunction and inflammatory markers of vascular disease in this review.


2011 ◽  
Vol 45 (2) ◽  
pp. 179-185
Author(s):  
Hideyo Oguchi ◽  
Marohito Murakami ◽  
Takashi Araki ◽  
Mariko Meguro ◽  
Akinori Hashiguchi ◽  
...  

Vestnik ◽  
2021 ◽  
pp. 103-106
Author(s):  
А.Е. Кожашева ◽  
С.О. Белесбек ◽  
Д.Ж. Абдимитова ◽  
Б.М. Сакен ◽  
А.П. Бориходжаева ◽  
...  

Появляются доказательства того, что COVID-19 может вызывать выброс цитокинов, состояние гиперкоагуляции и повреждение эндотелия, которое может привести к острому нарушению мозгового кровообращения (ОНМК). В данной статье авторы обсуждают взаимосвязь между COVID-19 и ОНМК, и о возможных факторах, способствующих возникновению инсульта. Как свидетельствует увеличение D-димера, фибриногена, фактора VIII и фактора фон Виллебранда, инфекция SARS-CoV-2 вызывает коагулопатию, нарушает функцию эндотелия и способствует состоянию гиперкоагуляции. В совокупности это предрасполагает пациентов к цереброваскулярным нарушениям. Механизм, лежащий в основе COVID-19 и инсульта, требует дальнейшего изучения, равно как и разработка эффективных терапевтических или профилактических мер. Evidence is emerging that COVID-19 can cause cytokine release, hypercoagulable states, and endothelial damage that can lead to acute cerebrovascular accident (ACVI). In this article, the authors discuss the relationship between COVID-19 and stroke and the possible contributing factors to stroke. As evidenced by an increase in D-dimer, fibrinogen, factor VIII and von Willebrand factor, SARS-CoV-2 infection causes coagulopathy, disrupts endothelial function and hypercoagulability. Collectively, this predisposes patients to cerebrovascular disorders. The mechanism underlying COVID-19 and stroke requires further study, as does the development of effective therapeutic or preventive measures.


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