The Textarin/Ecarin ratio is a test based on the differential dependence of snake venom on phospholipid to activate the coagulation pathway. Various snake venoms contain enzymes that specifically affect the coagulation pathway by catalyzing the conversion of prothrombin to thrombin, and/or to the active intermediate meizothrombin. Because of their direct effect on prothrombin activation without dependence on the upstream clotting factors, snake venom can be used as reagents in highly specific tests for the detection of lupus anticoagulant (LA). Three groups of snake venoms are described.¹ Venom from group I snakes, such as Bothrops or Echis species convert thrombin to meizothrombin, independent of factor V, phospholipid (PL) or calcium ions. Group II snake venom from Australian tiger snakes (Notechis) species contains activators of prothrombin which are highly stimulated by factor Va, PL and calcium. Group III venom from Pseudonaja and Oxyuranus species, contains activators of prothrombin strongly dependent on PL and calcium for activity, but minimally dependent on factor Va.

Textarin, from the Australian Eastern brown snake (Pseudonaja textilis) directly activates prothrombin in the presence of factor V, calcium and phospholipid; whereas, Ecarin, a venom from the saw-scaled viper (Echis carinatus) activates prothrombin to form meizothrombin in the absence of phospholipid.¹ Textarin time is prolonged by LA due to its phospholipid-dependence and is therefore an extremely sensitive test for LA. Ecarin time is not affected by LA, so that mixing Textarin and Ecarin in ratios of 0.8 to 1.2 proves to be a very sensitive and specific test for LA.² Factor V deficiency and specific inhibitors to factor V will cause a prolongation of the Textarin time, but these appear to be the only factor deficiencies which cause a false-positive. Specific factor inhibitors or deficiencies, (except prothrombin) do not affect the Ecarin time, because Ecarin acts directly on prothrombin independent of all other factors. However, heparinoids and heparinomimetic drugs activate heparin cofactor II (HCII) and function to inhibit thrombin, which can prolong the Ecarin clotting time (ECT). ³

Because the Textarin time is factor V-dependent, a Textarin time assay can be modified to create a sensitive assay for activated protein C (APC) resistance. APC resistance is caused by a point mutation in factor V. Textarin APC-resistance test is more sensitive and specific and correlates better with the factor V genetic mutation R506Q (factor V Leiden) than the activated partial thromboplastin time (aPPT) APC-resistance test in patients and controls.⁴ Patient population included stable orally anticoagulated, previously diagnosed factor V Leiden-positive and therapeutically heparinized samples. The Textarin/Ecarin ratio test is highly sensitive and also a specific confirmatory test for the presence of LA.⁵

The Ecarin clotting time is a sensitive assay for hirudin. Ecarin activates prothrombin by catalyzing the hydrolytic cleavage of the 323Arg-324Ile bond, without the generation of the zymogen fragment. This active form of prothrombin, termed meizothrombin is not efficiently inhibited by heparin-ATIII complex. Hirudin, an anticoagulant derived from the leech inhibits meizothrombin and is a good substitute for heparin. aPTT is an insensitive assay for following patients treated with direct thrombin inhibitors such as hirudin. The Ecarin clotting time measures the ability of hirudin to complex with meizothrombin because meizothrombin is generated as Ecarin activates prothrombin; hirudin will prolong the Ecarin time.^6,7 Hirudin levels may be overestimated if prothrombin deficiency is present.⁸