Plasma thrombin-activatable fibrinolysis inhibitor and plasminogen activator inhibitor-1 levels in inflammatory bowel disease

Koutroubakis, Ioannis E.; Sfiridaki, Aekaterini; Tsiolakidou, Georgia; Coucoutsi, Constantina; Theodoropoulou, Anǵeliki; Kouroumalis, Elias

doi:10.1097/meg.0b013e3282faa759

Cited by 34 publications

(39 citation statements)

References 18 publications

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“…Although UC patients with active and inactive states were reported to be different in the study by Saibeni et al, a unique point of our study is that we demonstrated the transition of TAFI levels from active stage to remission stage in each UC patient. Contrary to these find- ings, Koutroubakis et al (1) reported a decrease in the TAFI levels versus an increase in plasminogen activator inhibitor-1 (PAI-1) in IBD patients. The authors speculated that this was due to activation of the TAFI pathway, leading to an imbalance in fibrinolysis.…”

Section: Discussionmentioning

confidence: 81%

“…In both forms of the disease, a hypercoagulable state and a prothrombotic condition exist, whereas abnormalities in the coagulation system are partially responsible for the clinical picture. The regulation between coagulation and fibrinolysis plays an important role in preserving a balanced hemostatic process, and it is generally accepted that both have been found to be upregulated in active and inactive states of IBD (1,2).…”

Section: Introductionmentioning

confidence: 99%

“…Apart from its well-known effects on suppressing fibrinolysis, TAFIa may also be involved in inflammation by inactivating the anaphylatoxins C3a and C5a, thrombin-cleaved osteopontin and bradykinin (5). Although the correlation between UC and hypercoagulable states has been demonstrated in previous studies, the current literature regarding these factors and the role of fibrinolysis in patients with IBD is lacking and remains quite controversial (1). This study was undertaken in order to determine whether the TAFI levels are elevated in UC patients.…”

Section: Introductionmentioning

confidence: 99%

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Plasma Thrombin-activatable Fibrinolysis Inhibitor Levels Correlate with the Disease Activity of Ulcerative Colitis

et al. 2016

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Objective Patients with ulcerative colitis (UC) are at an increased risk for thromboembolic events, particularly in patients with extensive and active disease. To date, a few studies have been published on the role of thrombin-activatable fibrinolysis inhibitor (TAFI) in UC. However, there are no reports in the literature investigating the effect of UC treatment on plasma TAFI levels. Methods The plasma TAFI antigen levels were quantitatively determined using ELISA kits for 20 UC patients at activation and remission, along with 17 healthy controls. The association between the TAFI levels and inflammatory markers was assessed to determine UC activation. To predict and determine the activation of UC, the Truelove-Witts index and the endoscopic activation index (EAI) were used for each subject. Results The plasma TAFI levels were higher in UC patients at activation of the disease compared with the remission state and in healthy controls. Spearman's correlation analyses revealed that the WBC (r: 0.586, p< 0.001), hsCRP (r: 0.593, p<0.001) and EAI (r: 0.721, p<0.001) were significantly correlated with the TAFI levels. The overall accuracy of TAFI in determining UC activation was 82.5% with a sensitivity, specificity, NPV and PPV of 80%, 85%, 81% and 84.2%, respectively (cut-off value: 156.2% and AUC: 0.879). Conclusion The present study demonstrates that the TAFI levels are elevated in the active state of UC. The assessment of TAFI levels in patients with UC in conjunction with other markers of inflammation may provide additional information for estimating UC activation and severity.

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Section: Discussionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Plasma Thrombin-activatable Fibrinolysis Inhibitor Levels Correlate with the Disease Activity of Ulcerative Colitis

et al. 2016

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“…However, more studies are needed to evaluate a possible defect in kallikreinkallistatin balance in IBD. Hypofibrinolysis process that prevails in IBD is a consequence of the reduction in fibrinolysis proteases activators (see previous paragraph), and could be explained by an increase in fibrinolysis proteases inhibitors, such as SerpinE1 or PAI-1 (plasminogen activator inhibitor) [84]. In that context, the level of SerpinC1 (antithrombin or antithrombin III), which is a potent endogenous thrombin inhibitor, is significantly decreased in the plasma of IBD patients [85,86].…”

Section: Serpinsmentioning

confidence: 99%

Proteases/Antiproteases in Inflammatory Bowel Diseases

Motta¹,

Martin²,

Vergnolle³

2011

Proteases and Their Receptors in Inflammation

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Protein turnover is orchestrated by a large array of proteases, and the gastrointestinal tract is the organ the most exposed to proteases, whether they originate from the pancreas for digestive purpose, from resident cells, from infiltrated inflammatory cells, or from microorganisms present in the intestinal lumen. To maintain tissue homeostasis, the gastrointestinal tract has developed mechanisms that tightly regulate the proteolytic balance in the tissues. Those mechanisms range from physical barriers (mucus layer, tight control of intestinal epithelial cell paraand transcellular passages) to molecular control of proteolytic activity through endogenous protease inhibitors. In the setting of inflammation, gastrointestinal tissues are overflowed with massive proteolytic activity that contributes to the generation of inflammatory symptoms. The present chapter analyses the disruption of the protease-antiprotease balance in the context of inflammatory bowel disease. It proposes to review the type of proteases that are present in the gastrointestinal tract, their known effects on the generation and/or maintenance of inflammatory symptoms, and their mechanisms of action. Further, the role of endogenous protease inhibitors is discussed, as well as the potential use of protease inhibition, as new possible therapeutic approach to treat chronic inflammatory disorders of the gut.

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“…Recently discovered thrombin activatable fibrinolysis inhibitor (TAFI) provides link between coagulation and fibrinolysis (Bouma, 2004), and primarily its levels have been linked with thrombophilia in IBD. However TAFI plasma level in IBD is equivocal thus its significance is unclear (Koutroubakis et al, 2008;Saibeni et al, 2004). In addition, Italian group (Saibeni et al, 2006) has been demonstrated a prevalence of anti -t-PA antibodies in IBD patients which may reduce systemic fibrinolysis.…”

Section: Systemic Fibrinolytic Capacitymentioning

confidence: 99%

Kallikrein – Kinin System and Coagulation System in Inflammatory Bowel Diseases

Stadnicki¹

2011

Ulcerative Colitis - Epidemiology, Pathogenesis and Complications

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Plasma thrombin-activatable fibrinolysis inhibitor and plasminogen activator inhibitor-1 levels in inflammatory bowel disease

Abstract: PAI-1 plasma levels are increased whereas TAFI levels are decreased in IBD patients. These results suggest an imbalance of fibrinolysis in IBD.

Cited by 34 publications

References 18 publications

Plasma Thrombin-activatable Fibrinolysis Inhibitor Levels Correlate with the Disease Activity of Ulcerative Colitis

Plasma Thrombin-activatable Fibrinolysis Inhibitor Levels Correlate with the Disease Activity of Ulcerative Colitis

Proteases/Antiproteases in Inflammatory Bowel Diseases

Kallikrein – Kinin System and Coagulation System in Inflammatory Bowel Diseases

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