A systems biology approach to the diagnosis of venous thrombosis risk

Marlar, Richard A.; Potts, Robyn M.; Welsh, Carolyn H.

doi:10.1097/mbc.0b013e3280116c84

Cited by 5 publications

(4 citation statements)

References 5 publications

(8 reference statements)

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“…COVID-19 patients have a hypercoagulability state, and thrombosis is a life-threatening complication of them. A process leading to thrombus formation involves a combination of imbalanced factors and is not as simple as a sole factor imbalance to the other factors [ 139 ]. It seems that COVID-19 by disturbing the balance between the procoagulant systems and the regulatory mechanisms causes this predisposition to thrombus formation.…”

Section: Discussionmentioning

confidence: 99%

Status of major hemostatic components in the setting of COVID-19: the effect on endothelium, platelets, coagulation factors, fibrinolytic system, and complement

et al. 2023

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The coagulation, fibrinolytic, anticoagulation, and complement systems are in delicate balance with the vessel wall endothelium ensuring appropriate hemostasis. Coagulopathy in coronavirus disease 2019 (COVID-19) is not a simple disorder of one hemostatic component but a complicated process affecting most of the hemostasis system. COVID-19 disturbs the balance between the procoagulant systems and the regulatory mechanisms. Here, we investigate the effect of COVID-19 on key hemostatic components, including platelets, endothelial cells, coagulation factors, fibrinolytic system, anticoagulant protein system, and complement system, to improve our understanding of the pathophysiological processes underlying COVID-19 coagulopathy based on evidence.

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Section: Discussionmentioning

confidence: 99%

Status of major hemostatic components in the setting of COVID-19: the effect on endothelium, platelets, coagulation factors, fibrinolytic system, and complement

et al. 2023

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“…Ob niedrige erworbene Protein S-Spiegel selbst thromboseausl ö send sein k ö nnen oder nur ein H ä mostasesystem mit ver ä ndertem Equilibrium zwischen thrombosef ö rdernden und -verhindernden Faktoren darstellen, ist eine interessante Fragestellung, welche von Marlar et al wiederholt diskutiert wurde [19,20] . Diesbez ü glich liefert die hier vorliegende Arbeit weitere Hinweise, in dem sie bei Kenntnis der PROS1-Genetik die Auswirkungen der Einnahme eines Vitamin K-Antagonisten auf den Laborph ä notyp untersucht.…”

Section: Mutationstypunclassified

Gerinnungsphysiologische und genetische Diagnostik bei hereditärem Protein S-Mangel/Coagulation testing and genetic diagnostics in hereditary protein S deficiency

Dübgen

Dick

Marschall

et al. 2013

Laboratoriumsmedizin

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Schl ü sselw ö rter: Aktivit ä t; freies Antigen; Genetik; MLPA; PROS1; Protein S; Thrombophilie; Vitamin K-Antagonist.Abstract : Thrombophilia is the disposition for recurrent idiopathic thromboembolism and is currently seen as a multifactorial disease caused by a disbalance of complex regulated hemostasis. Despite intensive diagnostics the exact defect remains unknown in most cases. An established cause that can be diagnosed in 1 -2 % of affected individuals is a deficiency of protein S which limits thrombin formation as a cofactor of activated protein C. However, the evaluation of pathogenetic relevance of decreased protein S levels is difficult due to the much more often occurring acquired protein S deficiency under certain physiological or pathological circumstances, for example, intake of hormonal contraceptives or systemic inflammation. By adding aggregated genetic data of 136 patients, this publication gives a new perspective on protein S diagnostics and indicates under which circumstances a real, genetic defined deficiency can be postulated with higher probability.

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“…Clotting‐based methods have been thought of as the ‘all‐encompassing assay’ to assess for deficiencies. But now, we are learning that clot‐based assay methods analyse only the more common functions of a factor and may miss some of the clinically important ‘minor’ abnormalities (Marlar, Potts & Welsh, 2007). Can the laboratory evaluate for all relevant mutations without measuring all of the functions of a molecule?…”

mentioning

confidence: 99%

“…Functional assays may use different base assays (APTT, PT or RVVT) and different ancillary components (phospholipid type and concentration, calcium ion concentration and protein cofactors); all having a significant affect on assay results. On top of all of this kit component variation, the assay system may employ nonphysiologic components in the test kit (snake venom activators, artificial phospholipid types, or different species of protein cofactors) such that a dysfunctional molecule will act differently than in vivo (Marlar, Adcock & Madden, 1990; Marlar, Potts & Welsh, 2007; Marlar & Gausman, 2011).…”

mentioning

confidence: 99%

Accurate testing for dysfunctional molecules: the potential for missing the diagnosis

Marlar

2011

Int J Lab Hematology

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A systems biology approach to the diagnosis of venous thrombosis risk

Cited by 5 publications

References 5 publications

Status of major hemostatic components in the setting of COVID-19: the effect on endothelium, platelets, coagulation factors, fibrinolytic system, and complement

Status of major hemostatic components in the setting of COVID-19: the effect on endothelium, platelets, coagulation factors, fibrinolytic system, and complement

Gerinnungsphysiologische und genetische Diagnostik bei hereditärem Protein S-Mangel/Coagulation testing and genetic diagnostics in hereditary protein S deficiency

Accurate testing for dysfunctional molecules: the potential for missing the diagnosis

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