Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.108 (TAT)
 2,389 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical relevance of determination of plasma antithrombin III(ATIII) and alpha 2-plasmin inhibitor (alpha 2 PI) activities in patients with disseminated intravascular coagulation (DIC) was analyzed. Although the plasma ATIII activity was decreased in patients with DIC, no significant correlation was observed between plasma level of ATIII and that of thrombin-antithrombin III complex or prothrombin fragment 1+2. The extent of the decrease of ATIII in DIC was the most marked in cases associated with septicemia. The plasma level of ATIII in septicemia without DIC was significantly lower than that in DIC cases without septicemia, suggesting that the decrease of ATIII level could not be related to the pathophysiology of DIC, but to that of septicemia. The plasma half-life of ATIII in septicemia without DIC was significantly shortened in the absence of the increase of TAT level, suggesting that the extravasation of ATIII might be induced probably due to the endothelial damage in septicemia. The alpha 2-Plasmin inhibitor level was decreased in DIC patients. The decrease was the most marked (lower than 60% of normal) in patients with excessive fibrinolysis in which fibrinogen degradation was induced. The plasma level of alpha 2PI was significantly higher in the DIC cases with septicemia than in those without septicemia. The ATIII/alpha 2PI ratio was significantly lower in DIC cases with septicemia than in those with solid tumor or acute leukemia. Moreover, the ATIII/alpha 2PI ratio was significantly lower in MOF cases than in non-MOF cases in septicemia. The mortality of the MOF cases did not correlate with the ATIII/alpha 2PI ratio, but with the plasma level of PAI-1, suggesting that the decrease of ATIII/alpha 2PI ratio might not reflect the irreversible endothelial cell damage. Based on these observations, the calculation of ATIII/alpha 2PI in DIC patients would provide the following information; (1) a low ATIII/alpha 2PI ratio (less than 0.6) was frequently observed in septicemia, which could be related to the occurrence of organ dysfunction; (2) a high ATIII/alpha 2PI ratio (higher than 1.0) with the marked decrease of alpha 2PI level (lower than 60% of normal) suggests the occurrence of excessive fibrinolysis in which anti-fibrinolytic therapy should be considered when clinical bleeding was present; (3) The ATIII/alpha 2PI ratio near 1.0 was observed in DIC associated with the pathological conditions other than described above, such as solid tumors, in which the coagulation and fibrinolysis was almost equally activated.
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PMID:[Clinical relevance of determination of plasma ATIII and alpha 2 PI activities in patients with DIC--application of the molecular markers for the analysis of pathophysiology of DIC]. 810 83

PT, APTT, and coagulation factor activity are measured with clotting time-based methods. When coagula- tion and fibrinolysis are enhanced, TAT and PIC are detected, but evaluations of their hypofunctional state are difficult. We devised a new method that can be used to comprehensively and continuously evaluate coagula- tion and fibrinolysis in real time. We elucidated the clinical phenotype of congenital and acquired coagulation disorders using the following methods; (1) Clot waveform analysis (CWA) to evaluate fibrin formation; (2) Thrombin generation test (TGT) to monitor one-step before fibrin formation. (3) Thrombin/Plasmin generation assay (T/P-G) to evaluate fibrinolysis simultaneously with TGT. The results revealed that (1) CWA enabled the measurement of a very low FVIII activity level (FVIII:C 0.2-1.0 IU/dL) and detected a markedly severe type with FVIII:C <0.2 IU/dL. (2) For TGT, acquired hemophilia A showed a much lower value than that of congenital severe hemophilia A, being consistent with its severe bleeding. (3) CWA parameters for acquired factor V inhibitors in patients with bleeding symptoms were more impaired than with non-bleeding. Taken together these comprehensive assays can reflect the clinical phenotype and make it possible to analyze unidentified coagulation/fibrinolysis abnormality.
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PMID:[Development of Comprehensive Coagulation Assays Reflecting the Clinical Phenotype]. 3076 81