C‐reactive protein‐induced activated partial thromboplastin time prolongation in heparinized samples is attenuated by elevated factor VIII

2020 ◽  
Author(s):  
Vadim Kostousov ◽  
Sridevi Devaraj ◽  
Karen Bruzdoski ◽  
Lisa Hensch ◽  
Shiu‐Ki Hui ◽  
...  
Keyword(s):  
Factor Viii ◽  
Partial Thromboplastin Time ◽  
Activated Partial Thromboplastin Time ◽  
C Reactive Protein ◽  
Reactive Protein

False prolongation of the activated partial thromboplastin time (aPTT) in inflammatory patients: interference of C-reactive protein

2012 ◽  
Vol 157 (3) ◽  
pp. 394-395 ◽  
Author(s):  
André P. van Rossum ◽  
L. Tom Vlasveld ◽  
Laura J. M. van den Hoven ◽  
Carla W. M. de Wit ◽  
Ad Castel
Keyword(s):  
Partial Thromboplastin Time ◽  
Activated Partial Thromboplastin Time ◽  
C Reactive Protein ◽  
Reactive Protein

scholarly journals Anti-phospholipid antibodies in COVID-19 are different from those detectable in the anti-phospholipid syndrome

2020 ◽  
Author(s):  
Maria Orietta Borghi ◽  
Asmaa Beltagy ◽  
Emirena Garrafa ◽  
Daniele Curreli ◽  
Germana Cecchini ◽  
...  
Keyword(s):  
Critically Ill Patients ◽  
Partial Thromboplastin Time ◽  
Activated Partial Thromboplastin Time ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Functional Assays ◽  
Epitope Specificity ◽  
Glycoprotein I ◽  
Low Prevalence ◽  
Anti Phospholipid Syndrome

AbstractBackgroundCritically ill patients with coronavirus disease 2019 (COVID-19) have a profound hypercoagulable state and often develop coagulopathy which leads to organ failure and death. Because of a prolonged activated partial-thromboplastin time (aPTT), a relationship with anti-phospholipid antibodies (aPL) has been proposed, but results are controversial. Functional assays for aPL (i.e., lupus anticoagulant) can be influenced by concomitant anticoagulation and/or high levels of C reactive protein. The presence of anti-cardiolipin (aCL), anti-beta2-glycoprotein I (anti-β2GPI) and anti-phosphatidylserine/prothrombin (aPS/PT) antibodies was not investigated systematically. Epitope specificity of anti-β2GPI antibodies was not reported.ObjectiveTo evaluate the prevalence and the clinical association of aPL in a large cohort of COVID-19 patients, and to characterize the epitope specificity of anti-β2GPI antibodies.MethodsELISA and chemiluminescence assays were used to test 122 sera of patients suffering from severe COVID-19. Of them, 16 displayed major thrombotic events.ResultsAnti-β2GPI IgG/IgA/IgM were the most frequent in 15.6/6.6/9.0% of patients, while aCL IgG/IgM were detected in 5.7/6.6% by ELISA. Comparable values were found by chemiluminescence. aPS/PT IgG/IgM were detectable in 2.5 and 9.8% by ELISA. No association between thrombosis and aPL was found. Reactivity against domain 1 and 4-5 of β2GPI was limited to 3/58 (5.2%) tested sera for each domain and did not correlate with aCL/anti-β2GPI nor with thrombosis.ConclusionsaPL show a low prevalence in COVID-19 patients and are not associated with major thrombotic events. aPL in COVID-19 patients are mainly directed against β2GPI but display an epitope specificity different from antibodies in antiphospholipid syndrome.

scholarly journals Inter-individual variability in phospholipid-dependent interference of C-reactive protein on activated partial thromboplastin time

2017 ◽  
Vol 183 (4) ◽  
pp. 681-683
Author(s):  
Lale Erdem-Eraslan ◽  
Jacques J. H. Hens ◽  
André P. van Rossum ◽  
Marieke A. M. Frasa ◽  
Jeffrey F. W. Keuren
Keyword(s):  
Partial Thromboplastin Time ◽  
Individual Variability ◽  
Activated Partial Thromboplastin Time ◽  
C Reactive Protein ◽  
Reactive Protein

In Vitro Thrombogenicity Tests of Factor IX Concentrates

1979 ◽  
Vol 42 (05) ◽  
pp. 1355-1367 ◽  
Author(s):  
C V Prowse ◽  
A Chirnside ◽  
R A Elton
Keyword(s):  
Factor Viii ◽  
Partial Thromboplastin Time ◽  
Generation Time ◽  
Activated Partial Thromboplastin Time ◽  
Factor Ix ◽  
In Vitro Tests ◽  
Factor Viii Inhibitor ◽  
Factor Ixa ◽  
Viii Inhibitor

SummaryVarious factor IX concentrates have been examined in a number of in vitro tests of thrombogenicity. The results suggest that some tests are superfluous as in concentrates with activity in any of these tests activation is revealed by a combination of the non-activated partial thromboplastin time, the thrombin (or Xa) generation time and factor VIII inhibitor bypassing activity tests. Assay of individual coagulant enzymes revealed that most concentrates contained more factor IXa than Xa. However only a small number of concentrates, chiefly those that had been purposefully activated, contained appreciable amounts of either enzyme.

Development of Prothrombotic Repertoire with Progressive HIV Disease: Data from the Women’s Interagency HIV Study (WIHS).

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1057-1057
Author(s):  
Alexandra M. Levine ◽  
Cheryl Vigen ◽  
Jay Gravink ◽  
Howard A. Liebman
Keyword(s):  
Factor Viii ◽  
Lupus Anticoagulant ◽  
Protein S ◽  
Hiv Disease ◽  
C Reactive Protein ◽  
Factor Viii Activity ◽  
Functional Protein ◽  
Reactive Protein ◽  
History Of ◽  
Hiv Negative

Abstract HIV infected patients may be at increased risk for VTE, as shown by case reports, and a recent retrospective, longitudinal medical record review of approximately 42,000 HIV-infected individuals (Sullivan, 2000). There is a well documented association between acute and chronic inflammation and activation of the hemostatic system. Inflammatory cytokines such as TNF alpha, IL-1 and IL-6 have been shown to activate coagulation via the Tissue Factor pathway. Inflammation can also result in a decrease in functional Protein S, and in an increase in Factor VIII coagulant protein. We hypothesized that the inflammatory state associated with more advanced HIV disease would be associated with hemostatic activation, and clinical development of VTE over time. Methods: We assayed plasma for factor VIII activity levels, functional protein S activity, presence of lupus anticoagulant, and C reactive protein levels in a group of 96 HIV infected women and 50 HIV negative women from the Women’s Interagency HIV Study (WIHS). All assays were performed blinded to subjects HIV status. This cross sectional sample of WIHS participants from the Los Angeles site were studied at their second study visit (1994-5). The sample was selected to represent the following groups: (1) History of clinical AIDS, CD 4< 200; (2) CD4 < 200, no clinical AIDS; (3) HIV positive, CD4 > 200; HIV-negative. Pts were excluded if they were taking any hormones or contraceptives; had been pregnant within 6 weeks of study; had any acute, active infection at the time of study visit. Hemostatic data were correlated with HIV viral load, CD4 cell count, history of clinical AIDS, history of anti-retroviral and other medication use, and levels of serum and plasma C reactive protein (CRP). Results are depicted below for median (inter-quartile range) values, adjusted for age: Group Protein S Factor VIII Serum CRP# 1. Clinical AIDS, CD4 < 200 46* (40,65) 212* (174,253) 2.0 (0.5,4.8) 2. No Clinical AIDS, CD4 < 200 62^ (55,67) 196+ (150, 234) 0.8 (0.7,2.7) 3. HIV+, No Clinical AIDS, CD4 > 200 67.5 (59,83) 154^ (111,202) 0.9 (0.4, 3.3) 4. HIV Negative 75.5 (66,85) 116.5 (97,154) 1.85 (0.8, 5.1) Models were adjusted for age. Groups are significantly different from HIV negative participants (group 4) at the indicated p-values, determined using Scheffe adjustment * p<0.0001 ^p<.05 + p<.001 # CRP Medians are not significantly different for the different groups. No patient or control was found to have a positive assay for the Lupus anticoagulant. We conclude: (1) Increasing progression of HIV disease, from asymptomatic, to immunologic (CD 4< 200) and then clinical AIDS, is associated with progressive increase in factor VIII activity, and decrease in functional protein S; (2) This progressive hemostatic changes were not associated with elevated CRP levels, suggesting that IL-6 is not involved in this process; (3) An increase in VTE is biologically plausible in the setting of HIV infection; (4) Further prospective study is warranted to determine the full range of hemostatic abnormalities associated with HIV, and to determine any correlation between these abnormalities and development of VTE in time.

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