Decreased <i>in vitro</i> thrombin generation and clot stability in human FXII‐null blood and plasma

Pluthero, Fred G.; Ryan, Clodagh; Williams, Suzan; Brandão, Leonardo R.; Kahr, Walter H.A.

doi:10.1111/j.1365-2141.2010.08382.x

Cited by 7 publications

(8 citation statements)

References 11 publications

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“…10,11 This was also apparent for the two cats in the present report. Interestingly, case 1 had an increased MA on both the kaolin and TF-activated TEG tracings, which may be consistent with hypercoagulability.…”

Section: Discussionsupporting

confidence: 85%

“…At very low FXII concentrations (<1% activity), TEG samples that were either inactivated or activated with celite (a contact activator similar to kaolin) did not clot within 120 mins, while a kaolin-activated sample showed a prolonged time to clot onset and decreased clot strength. 10,11 However, as FXII activity was progressively increased in plasma samples in one study, the TEG variables became less hypocoagulable. 11 In the present report, the cat with the lower FXII concentration (case 2; FXII 7%) had a longer R time and κ, and a lower angle than case 1, which had a FXII concentration of 15%.…”

Section: Discussionmentioning

confidence: 97%

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Evaluation of thromboelastography in two factor XII-deficient cats

Blois¹,

Holowaychuk²,

Wood³

2015

Journal of Feline Medicine and Surgery Open Reports

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Case summaryThe current report describes thromboelastography (TEG) findings in two cats with factor XII (FXII) deficiency. The first cat was diagnosed with bilateral perinephric pseudocysts; hemostatic testing was performed prior to performing renal aspirates. The second cat was healthy; hemostatic testing was performed prior to inclusion into a research project. Both cats had markedly prolonged partial thromboplastin times and hypocoagulable TEG tracings when samples were activated with kaolin. However, when tissue factor (TF) was used to activate the sample, both cats had normal-to-hypercoagulable TEG tracings. The cats each had a subnormal FXII level.Relevance and novel informationTEG is becoming widely used to investigate hemostasis in veterinary patients, and TEG results in cats with FXII deficiency have not been previously reported. FXII deficiency is the most common hereditary hemostatic defect in cats. While FXII deficiency does not lead to in vivo hemorrhagic tendencies, it can lead to marked prolongation in activated partial thromboplastin and activated clotting times, and cannot be differentiated from true hemorrhagic diatheses without measuring individual factor activity. With the increased use of TEG to evaluate hemostasis in veterinary patients, it is important to recognize the effects of FXII deficiency on this testing modality. The finding of a hypocoagulable kaolin-activated TEG tracing and a concurrent normal TF-activated TEG tracing in samples should prompt clinicians to consider ruling out FXII deficiency.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 97%

Evaluation of thromboelastography in two factor XII-deficient cats

Blois¹,

Holowaychuk²,

Wood³

2015

Journal of Feline Medicine and Surgery Open Reports

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show abstract

“…Beside its function as an activator for PPK, FXII directly increases the fiber density within a clot and makes it more resistant to fibrinolysis 28,29 . Consequently, deficiency of FXII in mice or human impairs thrombus stability 30,31 . The present study supports these findings, as fibrinolysis -initiated in vitro by bacteria or pure streptokinase -was faster in the absence of FXII.…”

Section: Discussionmentioning

confidence: 99%

The contact system proteases play disparate roles in streptococcal sepsis

et al. 2019

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“…To confirm a potential fibrinolytic defect we performed a modified thromboelastography (TEG) assay, as previously described (Pluthero et al, 2011), to compare citrated normal pooled plasma and patient plasma ( Fig 1E,F). A dramatically increased rate of fibrinolysis (shortened clot lysis time) was observed in patient plasma with 3 concentrations of tissue plasminogen activator (tPA) ( Fig 1F) compared to normal pooled plasma ( Fig 1E), suggesting that a fibrinolytic inhibitor, such as plasminogen activator inhibitor 1 (PAI-1) or a2-antiplasmin (a2AP), was deficient in patient plasma.…”

mentioning

confidence: 99%