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Results for “Factor XI Deficiency”

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PubMed1979

Activated partial thromboplastin time and minor coagulopathies.

Five commercially available activated partial thromboplastin time (APTT) test systems were compared with the kaolin partial thromboplastin time (KPTT) method to determine sensitivity in detecting minor coagulation defects. All reagent systems detected severe factor VIII-, IX-, and XI-deficient hemophilia. Homozygous states of factor XII deficiency, Fletcher factor deficiency, and high-molecular-weight kininogen deficiency (Fitzgerald trait) also showed abnormally long APTTs by all systems. Of 19 samples from patients with deficiencies of factors XII, VIII, IX, XI, and II ranging from 2.5 to 52%, eight had deficiencies that were not detected by reagent A (ellagic acid); two, by reagent B (ellagic acid); two, by reagent C (kaolin); one, by reagent D (silica); one, by the KPTT method. All deficiencies were detected by reagent E (celite). Heparin effect on plasma was less well detected by reagent A (ellagic acid) than with the other test systems. APTT test systems can vary greatly in their abilities to detect minor coagulation abnormalities.

Adult↗
PubMed1997

Evaluation of bedside prothrombin time and activated partial thromboplastin time measurement by coagulation analyzer CoaguCheck Plus in various clinical settings.

In the present study CoaguCheck Plus (CCP), a coagulation test system using whole blood, was evaluated with respect to its comparability with widely distributed conventional routine coagulation assays. A correlation of r = 0.997 (p < 0.0001) was found between INR of CCP-prothrombin time (CCP-PT) and Thrombotest (KC-1 analyzer) in patients on oral anticoagulant therapy. A correlation of r = 0.899 (p < 0.001) between CCP-aPTT and Actin ES aPTT (STA analyzer) was found in heparinized patients. Impaired hepatic hepatic coagulation factor synthesis in liver cirrhosis patients was detected by CCP-PT with a sensitivity of 0.75 and by Normotest (STA analyzer) with a sensitivity of 0.92. Those patients with normal CCP-PT values and liver disease had, only mild reductions (> 30% of normals) in coagulation factors II, V, VII or X. CCP-aPTT was also performed in patients with a deficiency in the so called endogenous coagulation factors VIII, IX, XI and XII. CCP-aPTT showed a sensitivity similar to that of Actin FS aPTT in the detection even of mild deficiencies in factors VIII, IX and XII; factor XI deficiency was however detected only in patients with severe (< 12% of normals) disease; lupus anticoagulants were detected with a high sensitivity.

Blood Coagulation Tests↗
PubMed2004

[Factor XI].

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Biomarkers↗
PubMed1971

The first component of the kinin-forming system in human and rabbit plasma. Its relationship to clotting factor XII (Hageman Factor).

The isolation and characterization of the first component of the kinin-forming system in human and rabbit plasma are presented. Functionally, the molecule is the precursor of the activator of prekallikrein (Pre-PKA) and evidence is presented that it is identical with Hageman factor (clotting factor XII). The component from each plasma possessed similar characteristics. This molecule was found to have a mol wt of 110,000 and sedimentation rate of 4.6S. It migrated in electrophoresis as a beta-globulin, having an isoelectric point of 6.1. Upon activation with glass, kaolin, diatomaceous earth, ellagic acid, or trypsin, the activated molecule converted purified prekallikrein (prokininogenase) to the active enzyme. Clot-promoting activity was associated with the capacity to activate prekallikrein through each procedure of isolation. The clot-promoting factor was in precursor form, requiring treatment with kaolin or trypsin to gain activity. Evidence indicated that the protein was Hageman factor (factor XII): it promoted clotting of factor XII-deficient, but not Factor XI- or IX-deficient plasma, and did not convert fibrinogen to fibrin it bound to and was activated by kaolin or other negatively charged particles in the presence of chelating agents; the activation by kaolin could be prevented by pretreating the kaolin with hexadimethrine bromide (H Br); prekallikrein-activating and clot-promoting activities were identical in their physical properties; and the prekallikrein activator could not be detected in Hageman factor-deficient plasma. Activation of Hageman factor was accompanied by cleavage of the molecule into several fragments, one of which possessed prekallikrein-activating (PKA) and clot-promoting properties. The PKA fragment sedimented at 2.6S and by gel filtration was found to have a molecular weight of 32,000. The PKA possessed only 1/50 the clot-promoting capacity of the freshly activated native molecule.

Animals↗
PubMed1989

Laboratory evaluation of hemorrhagic coagulopathies in small animal practice.

Assessment of animals with a suspected hemorrhagic diathesis of unknown cause(s) should be methodical. Most acquired coagulopathies result from thrombocytopenia. A platelet estimate (from a blood smear) and/or a platelet count on a fresh blood sample therefore are useful first steps in case evaluation. If thrombocytopenia is present, the most likely causes are immune-mediated destruction of platelets, DIC, or megakaryocytic hypoplasia. These diagnoses can be pursued by further test, including antiplatelet antibody assays (for example, the platelet factor 3 tests or an ELISA test), measurement of FDP, and bone marrow biopsy, respectively. If the platelet count is normal, a buccal mucosa bleeding time test is a useful second step. If this is prolonged, most likely causes are vWD or a thrombocytopathy (functional platelet defect). von Willebrand's disease can be diagnosed by measurement of vWf concentration or activity. A normal bleeding time does not exclude a diagnosis of vWD, but suggests that the functional activity of vWf is not compromised markedly. If the bleeding time is normal, APTT and PT should be measured. A prolonged APTT with normal PT, in the clinical setting, implies a deficiency of factor XI, IX, or VIII. A prolonged PT with normal APTT indicates factor VII deficiency. Prolongation of both APTT and PT usually is caused by a deficiency of several factors and is seen most often in cases with vitamin K deficiency or antagonism. Obviously, if a particular cause is suspected from the case history or for other reasons, appropriate tests should be evaluated at the beginning. If these do not confirm the provisional diagnosis, the just-described protocol might be a useful one to follow.

Animals↗