Thrombin activatable fibrinolysis inhibitor and thrombin-antithrombin-III-complex levels in patients with gastric cancer

Fidan, Evren; Kavgacı, Halil; Örem, Asım; Yılmaz, Mustafa; Yıldız, Bülent; Fidan, Sami; Akcan, Buket; Özdemir, Feyyaz; Aydin, Faruk

doi:10.1007/s13277-012-0403-6

Cited by 31 publications

(25 citation statements)

References 30 publications

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“…e l s e v i e r . c o m / l o c a t e / t h r o m r e s coagulation or pregnant women [10][11][12][13][14][15][16][17]. However, little is known about the changes in these parameters after anticoagulant therapy is stopped, or about the clinical relevance of such alterations.…”

Section: Contents Lists Available At Sciencedirectmentioning

confidence: 99%

Coagulation activation after discontinuation of VTE treatment with different oral anticoagulants and impact on 12-month clinical outcomes

Beyer‐Westendorf

Gehrisch

Stange

et al. 2015

Thrombosis Research

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Section: Contents Lists Available At Sciencedirectmentioning

confidence: 99%

Coagulation activation after discontinuation of VTE treatment with different oral anticoagulants and impact on 12-month clinical outcomes

Beyer‐Westendorf

Gehrisch

Stange

et al. 2015

Thrombosis Research

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“…Others have reported that their cancer patients with localized prostate cancer had significantly lower levels of AT III activity and higher plasma D-dimer levels (Fidan et al, 2012). Furthermore, others have advocated the use of low AT and raised D-Dimer as prognostic markers for gynecological malignancy (Koh et al, 2001;.…”

Section: Iv-d Fibrinogen and Fibrinmentioning

confidence: 99%

Platelets, Coagulation and Cancer: Multifaceted Interactions

Goubran

Burnouf²

2012

American Medical Journal

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Approach: Literature review of the multifaceted interactions between platelets, coagulation and cancer. Results: Over the years, the links existing between cancer development, progression and occurrence of metastasis on one side and coagulation on the other have become obvious. Tumors seems to activate platelets whereas, platelets, on the other hand, through their capacity to activate and release soluble factors and microparticles, interact with tumor cells and influence immune regulation. They appear to be key regulators of many cancer events. Furthermore, coagulation with its different facets also interplays and significantly crosstalks with malignancy. The objectives of this article are to review the mechanisms through which cancer interacts with platelets and the coagulation, triggering thrombosis and the role played by platelets and coagulation factors in the regulation of cancer and to underline the perspectives that are now open in the development of novel diagnostic tools and new cancer treatment strategies. Conclusion/Recommendations: Challenging issues and unresolved questions still need to be addressed to understand the complexity existing between coagulation factors and platelet components and the different stages of cancer progression. Recent discoveries are leading clinicians to consider new therapeutic applications of anticoagulant therapies or new drugs targeting specific platelet functions in cancer patients' management. Furthermore, markers of coagulation and platelet activity may prove to serve as biomarkers for dormant tumors.

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“…While an increase in TAFI levels can lead to thrombosis formation, a disposition to bleeding may occur in the event of a decrease. TAFI levels have been associated with the severity of disease in several inflammatory diseases [35-37]. To the best of our knowledge, only one study has investigated TAFI levels in patients with AP.…”

Section: Discussionmentioning

confidence: 99%

Higher Thrombin-Antithrombin III Complex Levels May Indicate Severe Acute Pancreatitis

Fidan

Erkut

Coşar

et al. 2018

Dig Dis

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Aim: Coagulation disorders may develop in association with severe acute pancreatitis (AP). Plasma thrombin-antithrombin III complex (TAT) levels are one of the principal markers of coagulation disorder. The purpose of this study was to evaluate TAT and other hemostatic parameters in patients with AP and to examine whether or not these parameters indicate the severity of AP. Method: Forty-six patients with AP (14 severe, 32 non-severe) and a 30-member healthy control group were recruited. The severity of AP was determined using the revised Atlanta classification. ELISA was used to measure patients’ plasma TAT levels. Results: The TAT levels of AP patients at presentation were higher than those of the control group (p = 0.005). The plasma TAT levels of patients with severe AP were also significantly higher than those of patients with non-severe AP (p = 0.05) and of the control group (p < 0.001). The general accuracy, sensitivity and specificity of TAT levels in predicting the severity of AP were 77.4, 77.8, and 77.3% respectively. Conclusion: The coagulation cascade was activated in the AP patients in our study, and this was shown to become more pronounced as severity of the disease increased. Plasma TAT levels at the time of presentation in patients with AP can be used as a marker for predicting the severity of the disease.

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Thrombin activatable fibrinolysis inhibitor and thrombin-antithrombin-III-complex levels in patients with gastric cancer

Cited by 31 publications

References 30 publications

Coagulation activation after discontinuation of VTE treatment with different oral anticoagulants and impact on 12-month clinical outcomes

Coagulation activation after discontinuation of VTE treatment with different oral anticoagulants and impact on 12-month clinical outcomes

Platelets, Coagulation and Cancer: Multifaceted Interactions

Higher Thrombin-Antithrombin III Complex Levels May Indicate Severe Acute Pancreatitis

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