Search results
Results from the WOW.Com Content Network
Increased production of prothrombin heightens the risk of blood clotting. Moreover, individuals who carry the mutation can pass it on to their offspring. [8] The mutation increases the risk of developing deep vein thrombosis, [9] which can cause pain and swelling, and sometimes post-thrombotic syndrome, ulcers, or pulmonary embolism. [10]
Anchoring of bovine prothrombin to the membrane through its Gla domain. [16] The molecular weight of prothrombin is approximately 72,000 Da. The catalytic domain is released from prothrombin fragment 1.2 to create the active enzyme thrombin, which has a molecular weight of 36,000 Da. Structurally, it is a member of the large PA clan of proteases.
Hyperprothrombinemia is a state of high of prothrombin levels in the blood [1] which leads to hypercoagulability. An example of a genetic cause includes the mutation prothrombin G20210A. [2] Hyperprothrombinemia is a risk factor for venous thromboembolism. [2]
There are two types of prothrombin deficiencies that occur depending on the mutation: [5] Type I (true deficiency), includes a missense or nonsense mutation, essentially decreasing prothrombin production. This is associated with bleeding from birth. Here, plasma levels of prothrombin are typically less than 10% of normal levels. [citation needed]
Recurrent miscarriage is an indication for thrombophilia screening, particularly antiphospholipid antibodies (anti-cardiolipin IgG and IgM, as well as lupus anticoagulant), factor V Leiden and prothrombin mutation, activated protein C resistance and a general assessment of coagulation through an investigation known as thromboelastography.
The fully assembled prothrombinase complex catalyzes the conversion of the zymogen prothrombin to the serine protease thrombin. Specifically, Factor Xa cleaves prothrombin in two locations, following Arg 271 and Arg 320 in human prothrombin. [1] Because there are two cleavage events, prothrombin activation can proceed by two pathways.
Other: TCT, bleeding time, mixing test (whether an abnormality corrects if the patient's plasma is mixed with normal plasma), coagulation factor assays, antiphospholipid antibodies, D-dimer, genetic tests (e.g. factor V Leiden, prothrombin mutation G20210A), dilute Russell's viper venom time (dRVVT), miscellaneous platelet function tests ...
[20] Important negative prognostic indicators include ascites, encephalopathy, elevated Child–Pugh scores, elevated prothrombin time, and altered serum levels of various substances (sodium, creatinine, albumin, and bilirubin). Survival is also highly dependent on the underlying cause of the Budd–Chiari syndrome.