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1.
PubMed; 2021.
Preprint in English | PubMed | ID: ppcovidwho-333686

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome-related coronavirus-2 (SARS-CoV-2) has now caused over 2 million deaths worldwide and continues to expand. Currently, much is unknown about functionally neutralizing human antibody responses and durability to SARS-CoV-2. Using convalescent sera collected from 101 COVID-19 recovered individuals 21-212 days after symptom onset with forty-eight additional longitudinal samples, we measured functionality and durability of serum antibodies. We also evaluated associations between individual demographic and clinical parameters with functional neutralizing antibody responses to COVID-19. We found robust antibody durability out to six months, as well as significant positive associations with the magnitude of the neutralizing antibody response and male sex. We also show that SARS-CoV-2 convalescent neutralizing antibodies are higher in individuals with cardio-metabolic comorbidities. SIGNIFICANCE: In this study we found that neutralizing antibody responses in COVID-19 convalescent individuals vary in magnitude but are durable and correlate well with RBD Ig binding antibody levels compared to other SARS-CoV-2 antigen responses. In our cohort, higher neutralizing antibody titers are independently and significantly associated with male sex compared to female sex. We also show for the first time, that higher convalescent antibody titers in male donors are associated with increased age and symptom grade. Furthermore, cardio-metabolic co-morbidities are associated with higher antibody titers independently of sex. Here, we present an in-depth evaluation of serologic, demographic, and clinical correlates of functional antibody responses and durability to SARS-CoV-2.

2.
Research and Practice in Thrombosis and Haemostasis ; 5(SUPPL 2), 2021.
Article in English | EMBASE | ID: covidwho-1509119

ABSTRACT

Background : COVID-19 demonstrates a high mortality because of rapidly progress to severe and critical cases with respiratory distress syndrome, coagulation dysfunction, multiple organ failure, etc. Therefore, early identification of the disease expansion is very important to the clinical diagnosis and treatment of COVID-19. Aims : The aim of our study was to investigate the value of some coagulation parameters -prothrombin test (PT), activated partial thromboplastin time (APTT), fibrinogen (Fg), D-dimer (DD), factor VIII activity (FVIII), ristocetin-cofactor von Willebrand's factor activity (vWF:RCo), von Willebrand's factor antigen (vWF:Ag), antithrombin (AT) and homocysteine (HCY) -in predicting of prognosis of COVID-19. Methods : These laboratory data were collected at hospitalization in 104 patients with COVID-19. Outcomes were divided into two types: hospital discharge ( n = 81) and death ( n = 23). Statistical analysis was performed by non-parametric methods (median (Me), 95% confidence interval (95% CI) and Mann-Whitney U test, Statistica 12.0), P < 0.05 was considered statistically significant. Results : Coagulation profiles observed in both groups of patients reflect a hypercoagulability, but PT and AT were significantly lower, while DD and HCY levels -significantly higher in patients with poor prognosis, and no difference in the other parameters was observed (data shown in the table). Conclusions : The results of this study showed that hypercoagulation was present in patients with COVID-19. Severe coagulation dysfunction is more likely to occur in critically ill patients. PT, AT, DD and HCY could serve as diagnostic indicators for disease outcome.

3.
Research and Practice in Thrombosis and Haemostasis ; 5(SUPPL 2), 2021.
Article in English | EMBASE | ID: covidwho-1509068

ABSTRACT

Background : COVID-19 course is characterized of thrombosis complications, respiratory failure, and a multiple organ failure development. One of the central pathogenic mechanism of COVID-19 is endothelial dysfunction which can lead to the hypercoagulability. Studying of the endothelial dysfunction markers in patients with COVID-19 could be useful for improving of disease's outcomes. Aims : To estimate potential endothelial damage in COVID-19 patients by measuring biomarkers of endothelial disfunction. Methods : The study included 221 patients with COVID-19 and 68 healthy controls. We studied ristocetin-cofactor von Willebrand's factor activity (vWF:RCo, %), antigen von Willebrand's factor (vWF:Ag,%), and homocysteine (HCY, μmol/l) . STATISTICA 12.0 package was used. Statistical analysis was performed by non-parametric methods (median (Me), 95% confidence interval (95% CI), Mann-Whitney U test), P < 0.05 was considered statistically significant. Results : Conclusions : The increase of vWF:RCo activity, vWF:Ag and HCY may indicate endothelial damage in COVID-19 patients that can lead to hypercoagulability and predispose to thromboembolic complications. High vWF:Ag could be predictive marker of poor outcomes in COVID-19 patients.

4.
Research and Practice in Thrombosis and Haemostasis ; 5(SUPPL 2), 2021.
Article in English | EMBASE | ID: covidwho-1509067

ABSTRACT

Background : The concept of immunothrombosis has established as a central pathogenic factor leading to thrombosis complications, respiratory failure, and a multiple organ failure in patents with COVID-19. Studying of the hypercoagulability in patients with COVID-19 could be useful for improving of disease's outcomes. Estimation of anticoagulants efficiency can be informative for thrombotic risk assessment. The highest interest presents protein C system, because, as we know, infection and inflammation lead to disfunction of this anticoagulant system. Aims : To estimate the efficiency of protein C anticoagulant system in COVID-19 patients. Methods : The study included 60 patients with COVID-19 and 21 healthy controls . Thrombin generation was assessed by CAT according to Hemker et al. Measure was conducted in platelet poor plasma with or without presence of thrombomodulin. The following parameters were determined: endogenous thrombin potential (ETP, nM∗min), peak thrombin (Peak, nM). Sensitivity ETP and Peak for thrombomodulin were calculated as percent of decreasing of these parameters after adding thrombomodulin to the assay. Reduction of sensitivity for thrombomodulin indicates dysfunction of anticoagulant protein C system. Protein C activity and free protein S level were measured by 'ACL ELIT PRO', Instrumentation Laboratory, USA. STATISTICA 12.0 package was used. Results are presented as median with 95% confidence intervals, P < 0.05 was considered statistically significant (∗). Results : Sensitivity ETP and Peak for thrombomodulin, protein C activity and free protein S level are presented in the table. Conclusions : The efficiency of protein C anticoagulant system is depressed in COVID-19 patients. It may be associate with protein S level decreasing. The disability of anticoagulant protein C system can lead to hypercoagulability and it may be cause of thrombotic complication.

5.
American Journal of Transplantation ; 21(SUPPL 4):419-420, 2021.
Article in English | EMBASE | ID: covidwho-1494444

ABSTRACT

Purpose: Organ transplant recipients (OTR) are considered at high risk for adverse outcomes from COVID-19. However, mortality rates range from <5% to >30%. Some studies found that OTR have comparable outcomes with non-transplant patients, whereas other investigators reported higher mortality rates. To our knowledge, there are no published meta-analyses comparing outcomes between OTR and nontransplant patients with COVID-19. Methods: Two independent abstractors conducted a systematic search of PUBMED and EMBASE databases, references of articles retrieved, and major transplantation journals. We included studies published between 12/1/19 and 2/11/21, and performed a study-level random-effects meta-analysis with pooling of all-cause mortality, comparing separately OTR with non-transplant and waitlisted patients. Results: We included 26 studies with a total of 3,331 OTR. 83% were kidney, 8% liver, 6% heart and 3% lung transplant recipients. 66.3% were men. OTR had higher mortality compared to controls, however the difference did not reach statistical significance, and heterogeneity was high (Fig. 1). When analyzing studies evaluating OTR and controls that were matched for potential confounders, the difference in mortality was statistically significant, with a marked decrease in heterogeneity and risk of publication bias (Fig. 2). OTR did not have significantly higher mortality compared to waitlisted patients, but, again, heterogeneity was high (Fig. 3). Conclusions: OTR with COVID-19 seem to have higher mortality rates compared to immunocompetent individuals, but not waitlisted patients. OTR should be considered a high priority group for preventive and therapeutic interventions.

6.
Mol Biol Rep ; 48(7): 5745-5758, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-1321814

ABSTRACT

To date, the latest research results suggest that the novel severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) can enter host cells directly via the gastrointestinal tract by binding to the enterocyte-expressed ACE2 receptor, or indirectly as a result of infection of type II alveolar epithelial cells. At the same time, entry of SARS-CoV-2 through the gastrointestinal tract initiates the activation of innate and adaptive immune responses, the formation of an excessive inflammatory reaction and critical increase in the expression of proinflammatory cytokines, which, subsequently, can presumably increase inflammation and induce intestinal damage in patients suffering from inflammatory bowel disease (IBD). The aims of the present review were to reveal and analyze possible molecular pathways and consequences of the induction of an innate and adaptive immune response during infection with SARS-CoV-2 in patients with IBD. A thorough literature search was carried out by using the keywords: IBD, SARS-CoV-2, COVID-19. Based on the screening, a number of intracellular and extracellular pathways were considered and discussed, which can impact the immune response during SARS-CoV-2 infection in IBD patients. Additionally, the possible consequences of the infection for such patients were estimated. We further hypothesize that any virus, including the new SARS-CoV-2, infecting intestinal tissues and/or entering the host's body through receptors located on intestinal enterocytes may be a trigger for the onset of IBD in individuals with a genetic predisposition and/or the risk of developing IBD associated with other factors.


Subject(s)
Adaptive Immunity , COVID-19/epidemiology , Gastrointestinal Tract , Immunity, Innate , Inflammatory Bowel Diseases , COVID-19/immunology , COVID-19/virology , Gastrointestinal Tract/immunology , Gastrointestinal Tract/pathology , Gastrointestinal Tract/virology , Humans , Inflammatory Bowel Diseases/epidemiology , Inflammatory Bowel Diseases/immunology , Receptors, Virus/immunology , SARS-CoV-2/immunology , SARS-CoV-2/physiology , Virus Internalization
7.
Pediatrics ; 147(3):845-846, 2021.
Article in English | EMBASE | ID: covidwho-1177793

ABSTRACT

Background: SARS CoV-2, the virus that causes Coronavirus Disease of 2019 (COVID-19), most commonly presents as a febrile respiratory illness. Atypical symptoms are being increasingly recognized including myalgias, anosmia, vomiting, and diarrhea. Pediatric COVID-19 infections are usually mild, self-limiting, and rarely require hospitalization. We describe a case of severe upper gastrointestinal bleeding as the only initial symptom of COVID-19 infection in a child with sickle cell disease (SCD). Case: A 12-year-old male with SCD, HbSS subtype, with a history of splenectomy presented to our Emergency Department (ED) with acute onset progressively worsening hematemesis for the past 24 hours. He denied fever, cough, melena, peptic ulcer disease, family history of excessive bleeding, or regular nonsteroidal anti-inflammatory drug use. Upon arrival, the patient had tachycardia, hypotension (HR 150, BP 86/40), and cool extremities with delayed capillary refill. His temperature was 100.0F with an oxygen saturation of 100% on room air. His initial laboratory results were significant for hemoglobin of 4.1 g/dL, (baseline 7-8 g/dL), reticulocytes 13.7%, venous blood gas pH of 7.17, lactate of 7.3, white blood cell count of 21.7 K/uL, and prothrombin time (PT) of 19.9 seconds / INR of 1.7. His hepatic and renal function tests were within normal limits. In the ED, the patient received a normal saline bolus, two units of packed red blood cells, pantoprazole, famotidine, ondansetron, tranexamic acid, and ceftriaxone. His chest X-ray was unremarkable. A nasopharyngeal COVID-19 swab was sent. Pediatric gastroenterology and hematology were consulted, and he was admitted to the pediatric intensive care unit. The following day he underwent esophagogastroduodenoscopy which showed diffuse hemorrhagic gastropathy with superficial mucosal bleeding and without frank ulcers (Figure 1). An abdominal ultrasound revealed a normal gallbladder, no portal hypertension, and known absent spleen. His nasopharyngeal swab was positive for COVID-19. Helicobacter pylori testing was sent and reported negative. He received Vitamin K and two units of fresh frozen plasma for his coagulopathy resulting in normalization in his PT/INR. He did not have any further hematemesis but developed melena which improved, and he was discharged with a hemoglobin of 9.3 g/dL. Discussion: To date, we have not seen reports of either upper gastrointestinal bleeding as the only initial presenting symptom of COVID-19 or endoscopic visualization of gastric lumen during acute infection. The petechial hemorrhaging located at the body of the greater curvature and fundus of the stomach is an unusual site and indicated the underlying coagulopathy as the cause for bleeding. Our patient's mild coagulopathy is consistent with other reports of critically ill COVID-19 patients. This case highlights the importance of maintaining a high index of suspicion for COVID-19 infection in an immunocompromised pediatric patient with severe bleeding or new coagulopathy within our current medical climate.

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