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Results for “Factor XII Deficiency”

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PubMed1991

[Increased activated partial thrombin time: analysis of 250 cases discovered at laboratory].

This study evaluates and discusses the potential utility (clinical value) of complementary coagulation tests performed in cases with a prolonged aPTT of no obvious etiology from a total of 85,500 routine coagulation tests carried out in our general hospital. aPTT was measured using Actin F.S.L. (Dade, plant-derived and rabbit phospholipids complex with ellagic acid as activator) and Diagen (Biotrol, rabbit phospholipids with kaolin). Tests for acquired anticoagulants and endogenous pathway factors (XII, XI, IX, VIII) were assayed if the aPTT was prolonged by 7 sec or more. 250 abnormal aPTT of previously unknown etiology were found over a 14 months period. 46% of them were without any obvious cause, and were considered "spontaneous" increases: 2/3 of these spontaneous increases were 7-9 (group A), and 1/3 were 10-19 (group B). The diagnoses found in group A were mostly deficits in the contact system, while group B contained mostly cases with acquired anticoagulants and deficits in the contact system. In group C (increases over 20"), an etiology could be established in all cases, with a predominance of acquired anticoagulants and some deficits in factors VIII and XII.

Blood Coagulation Disorders↗
PubMed1985

Cold promoted activation and factor XII, prekallikrein and C1-inhibitor.

During incubation of plasma in the cold an amidolytic activity due to the kallikrein-alpha 2-macroglobulin complex appears in the plasma of about 40% of the women under hormonal contraception. The factor XII and prekallikrein activity are significantly increased 151.9% and 112.4% respectively in the cold promoted activation positive plasmas (CPA pos) whereas the activity of C1-inhibitor is decreased, 76%. The quotient of the product of the C1-inhibitor and alpha 2-macroglobulin values divided by the product of the FXII and prekallikrein values is significantly lower in the CPA pos plasma 0.49 than in CPA neg plasma 0.96 (p less than 0.05). These results alone do not explain the cold promoted activation, since a patient with a C1-inhibitor as low as 9% showed no increase of the amidolytic activity after a 24 hr incubation at 4 degrees C. However, the addition of purified C1-inhibitor to a CPA pos. plasma inhibits the cold activation. Heparin at a concentration of 0.5 IU/ml delays the appearance of the amidolytic activity.

Adolescent↗
PubMed1987

Identification of a defective factor XI cross-reacting material in a factor XI-deficient patient.

A homozygous factor XI-deficient girl, who appeared to be positive for cross-reacting material (CRM+) was studied for clarification. Factor XI antigen (F XI:Ag) was measured by radial immunodiffusion using monospecific, heterologous anti-factor XI antibodies. Factor XI coagulant activity (F XI:C) was determined in a modified activated partial thromboplastin time (APTT) test. The ratio of F XI:C to F XI:Ag was 0.04 for the proposita, as compared with 0.7 to 0.74 in the other family members. In contrast, 12 normal individuals had ratios of F XI:C to F XI:Ag of 1.04 +/- 0.15. F XI esterolytic activity was clearly higher than F XI:C in the proband, but not in her relatives. Immunoblotting studies demonstrated F XI CRM in the patient's plasma. Chromatography on diethylaminoethanol (DEAE)-Sephadex at pH 8.4 led to an almost complete removal of F XI from the plasma. The defective F XI was not bound to a negatively charged kaolin surface due to an abnormal interaction with high-mol-wt kininogen (HMWK).

Antigens↗
PubMed1979

Relationship between kallikrein release and factor XII in normal persons and carriers of the Hageman trait.

In four healthy subjects with Factor XII levels equal to or below 50% (selected at random from 100 persons) the release of Kallikrein was studied in order to establish the relationship between the above data and those found in four Hageman trait carriers showing levels of Factor XII above the lowest normal limits. It was found that for similar amounts of Hageman activity three of the carriers showed significantly less release of Kallikrein than the control subjects in whom it was normal. The conclusion was reached that the additional determination of the amount of Kallikrein released may be of value in the detection of carriers of the Hageman trait.

Factor XII↗
PubMed1989

The effect of trace amounts of tissue factor on thrombin generation in platelet rich plasma, its inhibition by heparin.

Amounts of human brain thromboplastin that do not stimulate thrombin generation in platelet poor plasma, were shown to advance by about 4 min an explosive formation of thrombin that occurs after recalcification in the presence of blood platelets. This synergistic effect is inhibited by the specific thrombin inhibitor hirudin and mimicked by adding low concentrations (less than 5 nM) of thrombin to platelet rich plasma. It is our conclusion that small amounts of thrombin, generated under the influence of thromboplastin induced procoagulant activity in the blood platelets. This activity is most likely mainly due to procoagulant phospholipids. Heparin inhibits this effect and retards the explosive thrombin formation. It does not, however, diminish the peak amount of thrombin eventually formed, because heparin neutralizing material released from the activated platelets quenches the heparin effect.

Blood Platelets↗