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At least 199 records · Page 11Linked to original sources
PubMed1992

Factor IXi-antithrombin (IXiAT) and thrombin-antithrombin (TAT) complexes in lung cancer patients.

Coagulation activation frequently occurs in cancer patients, resulting in thromboembolic complications and/or intravascular coagulation activation. The mechanisms leading to these alterations still are poorly understood. One explanation for the coagulation activation in malignant diseases is the presence of a direct factor X-activating cancer procoagulant. Coagulation activation in lung cancer patients develops at earlier stages than factor X activation; we demonstrated increased factor IXiAT complexes in addition to elevated TAT complexes. The increases of factor IXiAT complexes were not dependent upon the stage of the disease. In contrast, TAT complexes were higher in patients suffering from advanced pulmonary non-small cell carcinoma than in patients with limited disease. In conclusion, coagulation activation in pulmonary cancer patients occurs at earlier steps in the coagulation cascade than factor X activation. While this activation is not dependent upon the stage of the disease, the observation that TAT complexes showed higher elevations in patients with advanced than in those with limited pulmonary non-small cell carcinoma could be an indication of a cancer procoagulant that directly activates factor X.

Aged↗
PubMed1998

Thrombin binds to soluble fibrin degradation products where it is protected from inhibition by heparin-antithrombin but susceptible to inactivation by antithrombin-independent inhibitors.

BACKGROUND: Thrombolytic therapy induces a procoagulant state characterized by elevated plasma levels of fibrinopeptide A (FPA), but the responsible mechanism is uncertain. METHODS AND RESULTS: Washed plasma clots were incubated in citrated plasma in the presence or absence of tissue plasminogen activator (t-PA), and FPA generation was monitored as an index of unopposed thrombin activity. FPA levels are almost twofold higher in the presence of t-PA than in its absence. This primarily reflects the action of thrombin bound to soluble fibrin degradation products because (a) there is progressive FPA generation even after clots are removed from t-PA-containing plasma, and (b) clot lysates produce concentration-dependent FPA generation when incubated in citrated plasma. Using thrombin-agarose affinity chromatography, (DD)E and fragment E but not D-dimer were identified as the thrombin-binding fibrin fragments, indicating that the thrombin-binding site is located within the E domain. Heparin inhibits thrombin bound to fibrin degradation products less effectively than free thrombin. In contrast, D-Phe-Pro-ArgCH2Cl, hirudin and hirugen inhibit free thrombin and thrombin bound to fibrin degradation products equally well. CONCLUSIONS: Thrombin bound to soluble fibrin degradation products is primarily responsible for the increase in FPA levels that occurs when a clot undergoes t-PA-induced lysis. Like clot-bound thrombin, thrombin bound to fibrin derivatives is protected from inhibition by heparin but susceptible to inactivation by direct thrombin inhibitors. These findings help to explain the superiority of direct thrombin inhibitors over heparin as adjuncts to thrombolytic therapy.

Analysis of Variance↗
PubMed1991

[Effects of different administration of Salvia miltiorrhiza and heparin on antithrombin IIIAg, antithrombin III: A and alpha 2-macroglobulin in patients with cor pulmonale].

The effects of different administration of Salvia miltiorrhiza (SM) and heparin on ATIII and alpha 2-M in 102 patients with cor pulmonale were studied. The results showed that (1) the level of ATIII in patients was significantly lower than that in the controls (P less than 0.01). Heparin intravenous drip induced ATIII decreased; (2) the level of ATIII:A in patients with heparin vapour inhalation treatment was significantly higher than that with regular treatment and with heparin intravenous drip (P less than 0.05) and (P less than 0.005); (3) SM presents ATIII-like activity, after treatment with SM, the level of ATIII:A was significantly higher than that with heparin vapour inhalation, heparin intravenous drip and regular treatment (P less than 0.05-0.005), heparin may enhance the ATIII-like activity of SM; (4) the treatment combining SM intravenous drip with heparin vapour inhalation is an efficient therapy of anticoagulation on the patients with cor pulmonale. The level of alpha 2-M in each group did not reveal significant change.

Adult↗