scholarly journals Long-term post-discharge coagulation abnormalities in patients with moderate to severe COVID-19

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
G Artemyeva ◽  
A Kalinskaya ◽  
O Dukhin ◽  
A Lebedeva ◽  
A Rozin ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Endothelial Function ◽  
Anticoagulation Therapy ◽  
Clot Formation ◽  
Clot Lysis ◽  
Control Group ◽  
Normal Range ◽  
Post Discharge ◽  
Coagulation Abnormalities ◽  
Impedance Aggregometry

Abstract Introduction Coagulopathy plays a significant role in COVID-19 pathogenesis. Benefit from anticoagulation is well established in hospitalized patients. But since there is a lack of data on coagulopathy resolution: there is no consensus in guidelines if extended anticoagulation is required. Purpose The purpose of our work was to analyze coagulation abnormalities at 2 to 5 months after moderate to severe COVID-19. Methods COVID-19 reconvalescents (CR), discharged from our hospital, were called for follow-up at 2–3 (CR1 group, 21 patients) or 5–6 (CR2 group, 26 patients) months after discharge. All CR were not on the anticoagulation therapy by that time. In addition to clinical examination and standard lab tests, we performed an FMD-test to analyze endothelial function, impedance aggregometry to analyze platelet aggregation, and a thrombodynamics test to assess thrombogenesis and fibrinolysis. The control group was recruited before the pandemic started. Results All CR were free from thrombotic complications after discharge from the hospital. Endothelial function was not significantly impaired in CR compared with control, and was still in the normal range (7,07, IQR (3,36; 11,56) vs. 7,87 (5,42; 13,45)). Platelet aggregation was significantly lower in CR1 than in the control group in ADP-induced mode (37, IQR (19; 47) vs. 46, IQR (41; 50), p=0,02) and didn't differ in other groups and other modes (Asa, TRAP-induced). Thrombodynamics tests revealed suppression of the clot formation process in both CR1 and CR2 compared with control. There were decreased clot growth rates (μm/min) (CR1/CR2: 27,1, IQR (26,1; 29,2)/27,6, IQR (26,4; 30,0) vs. 32,2, IQR (30,0; 35,1), both p<0,001); decreased clot size (μm) (CR1/CR2: 1099, IQR (1069; 1194)/1199, IQR (1058; 1221) vs. 1304, IQR (1164; 1380), both p<0,001), and decreased optical density (arb units) (CR1/CR2: 21'607, IQR (20'363; 24'545)/22'741, IQR (21'344; 25'961) vs. 26'556, IQR (24'672; 29'387, p<0,001 and p=0,09 respectively. Fibrinolysis was enhanced in CR groups compared with control (lysis progression was significantly higher for CR2 only, CR1/CR2: 2,9, IQR (2,5; 3,8)/3,8, IQR (2,6; 5,4) vs. 2,5, IQR (1,1; 3,4) %/min, p=0,087 and p=0,007 respectively; expected clot lysis time was shorter in both CR1 and CR2: 36,5, IQR (29,8; 44,2)/31,7, IQR (24,3; 42,7) vs. 65,9. IQR (36,3; 95,5) min, p=0,019 and p=0,016 respectively). There was no statistical difference in clot formation and in fibrinolysis between CR1 and CR2. Conclusion In the deferred period (2–5 months) of COVID-19 the fibrinolysis process remains still active whereas the process of clot formation is mostly suppressed. Endothelial function assessed via the FMD test is within the normal range in the post COVID period. FUNDunding Acknowledgement Type of funding sources: None.

scholarly journals Mid-term endothelial dysfunction post COVID-19

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
S Lampsas ◽  
E Oikonomou ◽  
G Siasos ◽  
N Souvaliotis ◽  
A Goliopoulou ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Hospital Discharge ◽  
Cardiovascular Complications ◽  
Endothelial Damage ◽  
Control Group ◽  
Post Discharge ◽  
Reference Limit ◽  
Coronary Syndrome ◽  
Control Subjects ◽  
History Of

Abstract Introduction Cardiovascular complications of Coronavirus disease (COVID-19), resulting from the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), have been documented. Endothelium-induced “cytokine storm” in critically ill COVID-19 patients is one of the leading causes of morbidity and mortality. Vascular endothelial damage caused by COVID-19 emphasizes the crucial role of endothelium in COVID-19 clinical impact. Purpose To examine the mid-term (1-month) impact of COVID-19 in endothelial function. Methods In this case control study, 20 consecutive patients who were hospitalized for COVID-19 either on Intensive Care Unit (ICU) or non-ICU were examined one month following hospital discharge. In the control group we recruited 12 consecutive subjects from the outpatient cardiology clinic. Demographic and clinical data were collected, and endothelial function was evaluated by brachial artery flow-mediated dilation (FMD). Results There was no difference in age between COVID-19 patients and control subjects (66±12 years vs. 71±5 years, p<0.17), in male sex (63% vs. 54%, p=0.66) in history of diabetes mellitus (27% vs. 36%, p=0.64), hypertension (36% vs. 54%, p=0.39), cardiovascular disease (27% vs.18%, p=0.61). From the COVID-19 subjects 65% were overweight or obese. During their hospitalization [3 ICU (15%)/17 non-ICU (85%), mean days: 17±6.7], 4 (20%) of COVID-19 patients developed ARDS, while single cases of stress-induced cardiomyopathy, pulmonary embolism, and acute coronary syndrome were detected. One month post discharge D-dimers (0.71±0.55 μg/ml) levels were above upper reference limit. Importantly, FMD one month after hospital discharge date, was significantly impaired in the COVID-19 group (3.59±1.63% vs. 9.31±2.98%, p<0.001) compared to control group. Conclusion Post COVID-19 subjects one month post discharge have significant impaired endothelial function compared to control subjects. These findings highlight the significant interaction of COVID-19 with arterial endothelium and merit further research to conclude on the exact impact of vascular endothelium in physical history of SARS-CoV-2 infection. FUNDunding Acknowledgement Type of funding sources: None.

A Comprehensive Study on Hemostasis in CAPD Patients Treated with Erythropoietin

2002 ◽  
Vol 22 (5) ◽  
pp. 582-592 ◽  
Author(s):  
Jolanta Malyszko ◽  
Ewa Suchowierska ◽  
Jacek S. Malyszko ◽  
Michal Mysliwiec
Keyword(s):  
Platelet Aggregation ◽  
Tissue Factor ◽  
Von Willebrand Factor ◽  
Factor Vii ◽  
Clot Lysis ◽  
Control Group ◽  
Primary Role ◽  
Baseline Values ◽  
Von Willebrand ◽  
Willebrand Factor

Objective Bleeding diathesis and simultaneous thrombotic complications may be seen in dialyzed patients. Erythropoietin (EPO) may shift the precarious balance of the hemostatic system toward thrombosis. Platelets and tissue factor (TF) play a major role in plug formation. Tissue factor pathway inhibitor (TFPI) appears to play a primary role in regulating TF-induced coagulation. Thrombin activatable fibrinolysis inhibitor (TAFI) is a key protein linking coagulation and fibrinolysis. The aim of the study was to assess whether 6 months of EPO therapy affects platelet function, that is, platelet aggregation and P-selectin level; moieties of the extrinsic coagulation pathway: TF, TFPI, and TFPI/Xa complexes, and factors VII and X; markers of ongoing coagulation: thrombin–antithrombin complexes (TAT) and prothrombin fragments 1+2; a marker of ongoing fibrinolysis: plasmin–antiplasmin complexes (PAP); fibrinolytic activity: euglobulin clot lysis time (ECLT); and markers of endothelial cell injury: von Willebrand factor, thrombomodulin, E-selectin, and TAFI, in continuous ambulatory peritoneal dialysis (CAPD) patients. Patients and Methods 22 patients on CAPD were given EPO 6000 U/week. 12 patients with chronic renal failure and 12 healthy volunteers served as control groups. All parameters were studied before, and after 1, 3, and 6 months of EPO therapy. Setting Department of Nephrology and Internal Medicine, Medical Academy of Bialystok, Poland. Results Platelet aggregation in whole blood did not change significantly during EPO treatment. A significant rise in arachidonic acid-induced platelet aggregation in platelet-rich plasma was observed after 3 and 6 months, and in collagen-induced platelet aggregation after 6 months of EPO therapy, compared to the baseline values. The TFPI concentration decreased significantly after 6 months of EPO therapy. The activity of factor VII increased transiently after 1 month of EPO therapy, compared to the baseline values. The TAFI concentration and activity in the CAPD group were significantly higher than in the control group. Erythropoietin therapy resulted in a significant decrease in TAFI concentration and activity after 6 months of EPO treatment. The ECLT was shortened significantly as early as after 1 month of EPO therapy. Thrombomodulin, von Willebrand factor concentration and activity, PAP, TAT, TFPI/Xa complexes, prothrombin fragments 1+2, factor X activity, P-selectin, E-selectin, and lipoprotein(a) did not change significantly during EPO treatment. Conclusion Erythropoietin treatment has a minimal effect on hemostasis in CAPD patients. A tendency toward a decline in TAFI is of unknown clinical relevance so far, and awaits further research.

Influence of Simvastatin on Aspects of Thrombogenesis in CAPD Patients

2003 ◽  
Vol 23 (3) ◽  
pp. 260-266 ◽  
Author(s):  
Jolanta Malyszko ◽  
Jacek S. Malyszko ◽  
Tomasz Hryszko ◽  
Michal Mysliwiec
Keyword(s):  
Platelet Aggregation ◽  
Adhesion Molecule ◽  
Cell Injury ◽  
Activity Index ◽  
Receptor Protein ◽  
Intercellular Adhesion Molecule ◽  
Clot Lysis ◽  
Control Group ◽  
Protein Z ◽  
Simvastatin Therapy

← Background Patients on continuous ambulatory peritoneal dialysis (CAPD) are prone to dyslipidemia and have a high risk of cardiovascular death. Statins show beneficial effects on serum lipids and thrombogenesis in various groups of patients, but prospective studies have so far not been performed on CAPD patients. ← Aim To determine the effects of 6 month's treatment with simvastatin on platelet function and some hemostatic parameters, markers of endothelial cell injury, in 14 CAPD patients with hypercholesterolemia. ← Methods Simvastatin was given in a dose of 10 mg at bedtime. Commercially available kits were used for all determinations. ← Results Cholesterol and low density lipoprotein fell significantly as early as after 1 month of the therapy ( p < 0.001). Platelet aggregation in whole blood and plateletrich plasma was transiently decreased by simvastatin therapy. The fibrinolytic activity index increased significantly after 6 months of simvastatin administration ( p < 0.05), reaching values observed in the control group, whereas euglobulin clot lysis time, which was also significantly shortened after 6 months ( p < 0.05), did not reach values obtained in healthy volunteers. Vascular cell adhesion molecule, thrombomodulin, and protein Z decreased significantly after 3 months of the therapy ( p < 0.05, p < 0.05, and p < 0.01, respectively), whereas intercellular adhesion molecule decreased after 6 months ( p < 0.05). Vascular endothelial growth factor and its receptor, protein Z, total tissue factor pathway inhibitor (TFPI), TFPI/Xa complexes, and thrombin activatable fibrinolysis inhibitor concentration and activity fell significantly after 6 months of treatment with simvastatin (all p < 0.05). Tissue plasminogen activator concentration increased after 1 month ( p < 0.01 after 1 month, p < 0.05 after 3 and 6 months), whereas total homocysteine fell after 6 months of simvastatin therapy ( p < 0.05). Truncated TFPI decreased significantly as early as after 1 month of therapy ( p < 0.05 after 1 month, p < 0.01 after 3 and 6 months). ← Conclusion Simvastatin is an effective hypolipemic agent in CAPD patients. It favorably affects platelet aggregation and the extrinsic coagulation pathway, improves fibrinolysis, and ameliorates endothelial dysfunction. Simvastatin might reduce the risk of thrombotic complications in CAPD patients.

scholarly journals Platelet Apoptosis and PAI-1 Content Are Involved in the Procoagulant Profile of Immune Thrombocytopenia Patients Responders to Agonists of Thrombopoietin Receptor.

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 3738-3738
Author(s):  
Raul Justo Sanz ◽  
Elena Monzón Manzano ◽  
Ihosvany Fernandez-Bello ◽  
Teresa Álvarez-Roman ◽  
Mónica Martín ◽  
...  
Keyword(s):  
Research Funding ◽  
Immune Thrombocytopenia ◽  
Alpha Angle ◽  
Clot Formation ◽  
Clot Lysis ◽  
Control Group ◽  
Healthy Controls ◽  
Prothrombinase Complex ◽  
Thrombopoietin Receptor ◽  
Pai 1

Abstract Background: The treatment goal for patients with immune thrombocytopenia (ITP) is to raise platelet counts to levels that minimize or stop bleeding. Thrombopoietin receptor agonists (TPO-RAs) have been successfully and extensively employed as second-line therapy for ITP. TPO-RAs, however, have a small but significant increase in the risk of thrombosis. Aim: The aim of this study was to elucidate the mechanisms involved in the procoagulant effect of TPO-RAs. Methods: This is a prospective, observational and transversal study. Eighty-two patients with chronic primary ITP, 40 without treatment for at least six months (UT-ITP) and 42 responders to TPO-RA therapy (64.3% with eltrombopag and 35.7 % with romiplostim) were recruited. One hundred and twelve healthy participants were also included. ROTEM® (naTEM test: only recalcification) was performed on platelet rich plasma adjusted to a platelet count of 25 x 109/L. Clotting time (CT, time from start of measurement until 2 mm of amplitude [in seconds], alpha angle, which reflects the rate of fibrin polymerisation (tangent to the curve at 2 mm amplitude [in degrees]), maximum clot firmness, which reflects the maximum tensile strength of the thrombus (MCF, [in mm]) and LI60, which describes the percentage of maximum clot strength present at 60 min (in %), were recorded. Surface exposure of phosphatidylserine (PS), active caspase-3, -8 or -9 and prothrombinase complex binding to platelets were assessed by flow cytometry. Plasma and platelet levels of PAI-1 were determined by ELISA (eBioscience Ltd., Hatfield, United Kingdom). The effect of TPO and romiplostim on PAI-1 content of MEG-01 cells was evaluated by Western blot. Three MEG-01 cell cultures were initiated simultaneously: control without drugs and treated with either TPO (100 ng/mL) or romiplostim (53 μg/mL). Samples were collected at the start and after 24, 48 and 72 hours to determine the PAI-1 content. The statistical analysis was performed using SPSS 9.0 software (SPSS Inc., Chicago, Illinois, USA). Results: The ROTEM® studies showed significant differences in the dynamics of clot formation when comparing the control with ITP samples. There was a delay in clot formation in the UT-ITP group, as observed by a prolonged CT [expressed as median (p25-p75): control: 516 (490- 633) s; UT-ITP: 938 (914-1348) s, p<0.001], and a diminished alpha angle (mean±SD; control: 61.7±5.6 degrees; UT-ITP: 49.2±7.3 degrees, p<0.05). Nevertheless, samples from patients with UT-ITP reached the same MCF as those from healthy controls (control: 45.3±2.4 mm; UT-ITP: 46.9±3.7 mm). On the other hand, patients with ITP undergoing TPO-RA therapy presented an initial clot formation similar to that of the control group [expressed as median (p25-p75): CT, 672 (598-928) s; alpha angle, 55.8±5.8 degrees] but achieved a higher MCF (53.1±4.5 mm, p<0.05) and a reduced clot lysis after 60 min (control: 91.8±4.0%; UT-ITP: 93.7±4.0%, TPO-RA ITP: 97.6±1.7, p<0.05). Higher values of MCF observed with platelets from ITP patients treated with TPO-RAs might be a consequence of their augmented apoptosis signs: platelets from this group exposed more PS than controls and this situation was accompanied by an increased activity of caspases-3,7, -8 and -9 (Figure 1 A and B). Moreover, platelets from ITP patients on treatment with TPO-RAs bound more prothrombinase complex than platelets from UT-ITP patients and healthy controls (Figure 1 C). Reduced clot lysis observed in ITP patients treated with TPO-RA was due, at least in part, to increased plasma and platelet levels of PAI-1 (Table 1). Increase in platelet content of PAI-1 might be the result of the effect of TPO-RAs during megakaryopoiesis since treatments of MEG-01 cells with TPO or romiplostim induced a 3-fold increase in their endogenous PAI-1 content after an incubation period of 48 hs. Conclusion: The patients with ITP undergoing TPO-RAs therapy presented a procoagulant profile due to the formation of a more fibrinolysis-resistant clot because of increased platelet and plasma PAI-1 levels. Moreover, platelets from this group of patients showed more signs of apoptosis that causes a higher exposure of PS and, consequently, a larger surface for the binding of the prothrombinase complex. Work supported by grant from FIS-FEDER PI15/01457. NB holds a Miguel Servet II (FIS-FEDER CP14/00024). Disclosures Álvarez-Roman: SOBI: Consultancy; NovoNordisk: Consultancy; Shire: Consultancy. Jimenez-Yuste:Grifols: Consultancy, Research Funding; Octapharma: Consultancy, Research Funding; CSL Behring: Consultancy; Bayer: Consultancy, Research Funding; Roche: Consultancy, Research Funding; Shire: Consultancy, Research Funding; Sobi: Consultancy, Research Funding; Pfizer: Consultancy, Research Funding; NovoNordisk: Consultancy, Research Funding. Butta:FIS-Fondos FEDER: Research Funding.

scholarly journals Dynamics of coagulopathy in patients with different COVID-19 severity

2020 ◽  
Author(s):  
Anna Kalinskaya ◽  
Oleg Dukhin ◽  
Ivan Molodtsov ◽  
Alexandra Maltseva ◽  
Denis Sokorev ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Endothelial Function ◽  
Healthy Volunteers ◽  
Formation Process ◽  
Control Group ◽  
Plasma Coagulation ◽  
Beneficial Role ◽  
Thrombotic Complications ◽  
Severity Of The Disease ◽  
Endogenous Fibrinolysis

AbstractWith the progress of COVID-19 studies, it became evident that SARS-CoV-2 infection is often associated with thrombotic complications. The goal of our present study was to evaluate which component of clot formation process including endothelial function, platelets aggregation and plasma coagulation, as well as endogenous fibrinolysis in patients with COVID-19 correlates with the severity of the disease. We prospectively included 58 patients with COVID-19 and 47 healthy volunteers as a control group that we recruited before the pandemic started. It turns out that plasma coagulation with subsequent platelet aggregation, but not endothelial function, correlates with the severity of the COVID-19. IL-6 blockade may play a beneficial role in COVID-19 induced coagulopathy.

Abstract 34: Impact of Thrombomodulin and Thrombin-activatable Fibrinolysis Inhibitor on the Anti-coagulant and Pro-fibrinolytic Effects of Rivaroxaban

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Justin J Garabon ◽  
Michael B Boffa
Keyword(s):  
Formation Rate ◽  
Anticoagulation Therapy ◽  
Clot Formation ◽  
Clot Lysis ◽  
Anatomical Location ◽  
Wild Type ◽  
Thrombin Activatable Fibrinolysis Inhibitor ◽  
Plasma Clot ◽  
Fibrinolysis Inhibitor

Rivaroxaban is a novel oral anticoagulant that directly inhibits factor Xa and has recently been implemented as a favorable alternative to warfarin in anticoagulation therapy. Rivaroxaban effectively reduces the generation of thrombin, which plays a major role in the activation of thrombin activatable fibrinolysis inhibitor (TAFI) to TAFIa. Activated TAFI functions by downregulating fibrinolysis, and this effect is highly dependent on the availability of thrombomodulin (TM), as the thrombin-TM complex activates TAFI with a 1250-fold greater efficiency than thrombin alone. Additionally, a naturally occurring SNP in the gene encoding TAFI gives rise to a Thr325Ile polymorphism that increases the stability and antifibrinolytic potential of TAFIa. Since inhibition of thrombin generation could lead to decreased TAFIa formation, we hypothesized that these parameters could influence the pharmacodynamics and pharmacogenomics of rivaroxaban. To assess this, effects on coagulation and fibrinolysis were measured using an in vitro plasma clot lysis assay. Rivaroxaban and TM were titrated into TAFI-deficient plasma in the presence or absence of 10 nM wild-type or T325I recombinant TAFI. With increasing concentrations of rivaroxaban, clot formation latency was accordingly increased. TM further delayed clot formation, and this effect was equal in the absence or presence of either TAFI variant. Rivaroxaban was also shown to decrease the rate of coagulation, which was decreased further at higher concentrations of TM. The presence of either TAFI variant also seemed to decrease clot formation rate at higher levels of rivaroxaban and TM. At all concentrations of TM, TAFI-dependent resistance to fibrinolysis was attenuated by rivaroxaban. The effect of rivaroxaban was, however, greater for wild-type TAFI than for the T325I variant. In conclusion, rivaroxaban exhibits TAFI-dependent profibrinolytic effects that are influenced by the levels of TM and the by intrinsic stability of TAFIa. TM also affected the dynamics of coagulation. These findings suggest a role for the anatomical location of a procoagulant stimulus and plasma TM-altering disease phenotypes in the pharmacodynamics and a role for the T325I polymorphism in the pharmacogenomics of rivaroxaban.

Properties of Fibrinogen Cleaved by Jararhagin, a Metalloproteinase from the Venom of Bothrops jararaca

1994 ◽  
Vol 72 (02) ◽  
pp. 244-249 ◽  
Author(s):  
Aura S Kamiguti ◽  
Joseph R Slupsky ◽  
Mirko Zuzel ◽  
Charles R M Hay
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Fibrin Clot ◽  
Clot Formation ◽  
Human Fibrinogen ◽  
Activated Platelets ◽  
Bothrops Jararaca ◽  
Platelet Binding ◽  
Fibrin Monomers ◽  
Fibrinogen Molecule

SummaryHaemorrhagic metalloproteinases from Bothrops jararaca and other venoms degrade vessel-wall and plasma proteins involved in platelet plug and fibrin clot formation. These enzymes also cause proteolytic digestion of fibrinogen which has been suggested to cause defective platelet function. Fibrinogen degradation by jararhagin, a metalloproteinase from B. jararaca, and the effect of jararhagin fibrinogenolysis on both platelet aggregation and fibrin clot formation were investigated. Jararhagin was found to cleave human fibrinogen in the C-terminal region of the Aα-chain giving rise to a 285-290 kDa fibrinogen molecule lacking the Aα-chain RGD 572-574 platelet-binding site. Platelet binding and aggregation of ADP-activated platelets is unaffected by this modification. This indicates that the lost site is not essential for platelet aggregation, and that the remaining platelet binding sites located in the N-terminal portion of Aα chains (RGD 95-97) and the C-terminal of γ chains (dodecapeptide 400-411) are unaffected by jararhagin-digestion of fibrinogen. Fibrin clot formation with thrombin of this remnant fibrinogen molecule was defective, with poor polymerization of fibrin monomers but normal release of FPA. The abnormal polymerization could be explained by the loss of one of the two complementary polymerization sites required for side-by-side association of fibrin protofibrils. Jararhagin-induced inhibition of platelet function, an important cause of haemorrhage in envenomed patients, is not caused by proteolysis of fibrinogen, as had been thought, and the mechanism remains to be elucidated.

Platelet Aggregation in Diabetes Mellitus and the Effect of Insulin in Vivo on Aggregation

1972 ◽  
Vol 27 (01) ◽  
pp. 114-120 ◽  
Author(s):  
A. A Hassanein ◽  
Th. A El-Garf ◽  
Z El-Baz
Keyword(s):  
Platelet Aggregation ◽  
Rapid Onset ◽  
Control Group ◽  
Diabetic Patients ◽  
Fasting State ◽  
Clotting Time ◽  
Cholesterol Levels ◽  
Platelet Disaggregation ◽  
Aggregation And Disaggregation

SummaryADP-induced platelet aggregation and calcium-induced platelet aggregation tests were studied in 14 diabetic patients in the fasting state and half an hour after an intravenous injection of 0.1 unit insulin/kg body weight. Platelet disaggregation was significantly diminished as compared to a normal control group, and their results were negatively correlated with the corresponding serum cholesterol levels. Insulin caused significant diminution in the ADP-induced platelet aggregation as a result of rapid onset of aggregation and disaggregation. There was also a significant increase in platelet disaggregation. In the calcium-induced platelet aggregation test, there was a significant shortening of the aggregation time, its duration, and the clotting time. The optical density fall due to platelet aggregation showed a significant increase. Insulin may have a role in correcting platelet disaggregation possibly through improvement in the intracellular enzymatic activity.

POSSIBILITY TO REDUCE THROMBOCYTOPENIA AFTER CHEMORADIOTHERAPY IN ONCOLOGICAL PATIENTS

2017 ◽  
Vol 63 (3) ◽  
pp. 466-469
Author(s):  
Luiza Korytova ◽  
Aleksey Meshechkin ◽  
Oleg Korytov ◽  
V. Krasnikova
Keyword(s):  
Combined Treatment ◽  
Treated Group ◽  
Median Number ◽  
Blood Analysis ◽  
Control Group ◽  
Level Control ◽  
Normal Range ◽  
Oncological Patients ◽  
Level Increase ◽  
And Control

Objective was to establish efficiency of sodium nucleospermat in correcting thrombocytopenia after chemoradiotherapy in oncological patients. Methods and materials. The study included data on 32 patients that had undergone combined treatment from January till May 2016. After detecting thrombocytopenia patients were randomized into two groups (16 patients in each): treated group, where patients received sodium nucleospermat, and control group, where sodium nucleospermat was not used. Thrombocyte level control was done on 5th, 10th and 15th day after treatment was over. Results and discussion. All 16 patients showed positive dynamics in increasing thrombocyte level after Sodium nucleospermat injection course was finished. This was proven by first (5th day) blood analysis. On average thrombocyte level after sodium nucleospermat treatment has risen to normal, at 161х109/1. Only 3 patients from this group had to pause radiotherapy for 5 days. Control group patients, which did not receive sodium nucleospermat, showed evidence of thrombocyte level recovery by 10th day only. On average thrombocyte level increase was insignificant, and median number was 111*109/l. Low thrombocyte level was main reason to pause radiotherapy for 11 (69%) patients in control group. Conclusion. Sodium nucleospermat allowed raising thrombocyte level to the lower normal range, which surpassed by 40%-50% in control group patients. Use of sodium nucleospermat did not show any cases of allergic reactions, toxicity or complications in oncological patients.

Feasibility of Recording Clot Lysis with the Thermometric Clot Detector

1974 ◽  
Vol 20 (11) ◽  
pp. 1435-1437 ◽  
Author(s):  
William D Bostick ◽  
Peter W Carr
Keyword(s):  
Detection System ◽  
Clot Formation ◽  
Clot Lysis ◽  
Coagulation Process

Abstract We investigated the possibility of continuously recording the process of clot lysis with a thermometric clot detector. Experiments in which fibrinolytic activators and inhibitors were used demonstrate that the detection system, without any mechanical modifications, is suitable for monitoring the complete coagulation process from clot formation to the ultimate lysis of the clot itself.

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