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'''Ecarin clotting time''' (ECT) is a laboratory test used to monitor anticoagulation during treatment with [[hirudin]], an [[anticoagulant]] [[medication]] which was originally isolated from [[leech]] saliva. Ecarin, the primary reagent in this assay, is derived from the venom of the saw-scaled viper, ''[[Echis carinatus]]''.
'''Ecarin clotting time''' (ECT) is a laboratory test used to monitor anticoagulation during treatment with [[hirudin]], an [[anticoagulant]] [[medication]] which was originally isolated from [[leech]] saliva. Ecarin, the primary reagent in this assay, is derived from the venom of the saw-scaled viper, ''[[Echis carinatus]]''.


In the clinical assay, a known quantity of [[ecarin]] is added to the plasma of a patient treated with hirudin. Ecarin activates [[prothrombin]] through a specific proteolytic cleavage, which produces meizothrombin, a prothrombin-thrombin intermediate which retains the full molecular weight of prothrombin, but possesses a low level of procoagulant enzymatic activity. Crucially, this activity is inhibited by hirudin and other direct thrombin inhibitors, but not by [[heparin]]. The ECT is also unaffected by prior treatment with [[coumadin]] or the presence of phospholipid-dependent anticoagulants, such as [[lupus anticoagulant]]. Thus, the ECT is prolonged in a specific and linear fashion with increasing concentrations of hirudin. An enhancement of the ECT is the ecarin chromogenic assay (ECA) in which diluted sample is mixed with an excess of purified prothrombin and the generated meizothrombin is measured with a specific chromogenic substrate. This assay shows no interference from prothrombin or fibrinogen in the sample and is suitable for the measurement of all direct thrombin inhibitors {{cite journal |author=Nowak G |title=The ecarin clotting time, a universal method to quantify direct thrombin inhibitors |journal=Pathophysiol. Haemost. Thromb. |volume=33 |issue=4 |pages=173–83 |year=2003 |pmid=15583446 |doi=10.1159/000081505}}<ref name="Fab01">Fabrizio MC. 2001. Use of Ecarin Clotting Time (ECT) with Lepirudin Therapy in Heparin-Induced Thrombocytopenia and Cardiopulmonary Bypass. JECT 33:117–125. [http://www.amsect.org/ce/HIT/ject_2001_v33_n2_fabrizio.pdf PDF] at [http://www.amsect.org/ Journal of The American Society of ExtraCorporeal Technology]. Accessed 5 June 2007.</ref><ref name="TET">[http://www.specialtylabs.com/books/display.asp?id=1060 Textarin/Ecarin Time] at [http://www.specialtylabs.com/ Specialty Laboratories]. Accessed 5 June 2007.</ref>
In the clinical assay, a known quantity of [[ecarin]] is added to the plasma of a patient treated with hirudin. Ecarin activates [[prothrombin]] through a specific proteolytic cleavage, which produces meizothrombin, a prothrombin-thrombin intermediate which retains the full molecular weight of prothrombin, but possesses a low level of procoagulant enzymatic activity. Crucially, this activity is inhibited by hirudin and other direct thrombin inhibitors, but not by [[heparin]]. The ECT is also unaffected by prior treatment with [[coumadin]] or the presence of phospholipid-dependent anticoagulants, such as [[lupus anticoagulant]]. Thus, the ECT is prolonged in a specific and linear fashion with increasing concentrations of hirudin. An enhancement of the ECT is the ecarin chromogenic assay (ECA) in which diluted sample is mixed with an excess of purified prothrombin and the generated meizothrombin is measured with a specific chromogenic substrate. This assay shows no interference from prothrombin or fibrinogen in the sample and is suitable for the measurement of all direct thrombin inhibitors {{cite journal |author=Nowak G |title=The ecarin clotting time, a universal method to quantify direct thrombin inhibitors |journal=Pathophysiol. Haemost. Thromb. |volume=33 |issue=4 |pages=173–83 |year=2003 |pmid=15583446 |doi=10.1159/000081505}}<ref name="Fab01">Fabrizio MC. 2001. Use of Ecarin Clotting Time (ECT) with Lepirudin Therapy in Heparin-Induced Thrombocytopenia and Cardiopulmonary Bypass. JECT 33:117–125. [http://www.amsect.org/ce/HIT/ject_2001_v33_n2_fabrizio.pdf PDF] {{webarchive|url=https://web.archive.org/web/20070927190645/http://www.amsect.org/ce/HIT/ject_2001_v33_n2_fabrizio.pdf |date=2007-09-27 }} at [http://www.amsect.org/ Journal of The American Society of ExtraCorporeal Technology]. Accessed 5 June 2007.</ref><ref name="TET">[http://www.specialtylabs.com/books/display.asp?id=1060 Textarin/Ecarin Time]{{dead link|date=September 2017 |bot=InternetArchiveBot |fix-attempted=yes }} at [http://www.specialtylabs.com/ Specialty Laboratories]. Accessed 5 June 2007.</ref>
Lange U, Nowak G, Bucha E. Ecarin chromogenic assay—a new method for quantitative determination of direct thrombin inhibitors like hirudin. Pathophysiol Haemost Thromb. 2003 Jul-2004 Aug;33(4):184-91.
Lange U, Nowak G, Bucha E. Ecarin chromogenic assay—a new method for quantitative determination of direct thrombin inhibitors like hirudin. Pathophysiol Haemost Thromb. 2003 Jul-2004 Aug;33(4):184-91.



Revision as of 15:03, 16 September 2017

Saw-scaled viper, Echis carinatus.

Ecarin clotting time (ECT) is a laboratory test used to monitor anticoagulation during treatment with hirudin, an anticoagulant medication which was originally isolated from leech saliva. Ecarin, the primary reagent in this assay, is derived from the venom of the saw-scaled viper, Echis carinatus.

In the clinical assay, a known quantity of ecarin is added to the plasma of a patient treated with hirudin. Ecarin activates prothrombin through a specific proteolytic cleavage, which produces meizothrombin, a prothrombin-thrombin intermediate which retains the full molecular weight of prothrombin, but possesses a low level of procoagulant enzymatic activity. Crucially, this activity is inhibited by hirudin and other direct thrombin inhibitors, but not by heparin. The ECT is also unaffected by prior treatment with coumadin or the presence of phospholipid-dependent anticoagulants, such as lupus anticoagulant. Thus, the ECT is prolonged in a specific and linear fashion with increasing concentrations of hirudin. An enhancement of the ECT is the ecarin chromogenic assay (ECA) in which diluted sample is mixed with an excess of purified prothrombin and the generated meizothrombin is measured with a specific chromogenic substrate. This assay shows no interference from prothrombin or fibrinogen in the sample and is suitable for the measurement of all direct thrombin inhibitors Nowak G (2003). "The ecarin clotting time, a universal method to quantify direct thrombin inhibitors". Pathophysiol. Haemost. Thromb. 33 (4): 173–83. doi:10.1159/000081505. PMID 15583446.[1][2] Lange U, Nowak G, Bucha E. Ecarin chromogenic assay—a new method for quantitative determination of direct thrombin inhibitors like hirudin. Pathophysiol Haemost Thromb. 2003 Jul-2004 Aug;33(4):184-91.

References

  1. ^ Fabrizio MC. 2001. Use of Ecarin Clotting Time (ECT) with Lepirudin Therapy in Heparin-Induced Thrombocytopenia and Cardiopulmonary Bypass. JECT 33:117–125. PDF Archived 2007-09-27 at the Wayback Machine at Journal of The American Society of ExtraCorporeal Technology. Accessed 5 June 2007.
  2. ^ Textarin/Ecarin Time[permanent dead link] at Specialty Laboratories. Accessed 5 June 2007.