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PubMed1980

Rapid fibrinolysis, augmented Hageman factor (factor XII) titers, and decreased C1 esterase inhibitor titers in women taking oral contraceptives.

The use of OCAs has been associated with multiple hemostatic abnormalities and an increased risk of thromboembolic disease. These changes have been attributed to increased synthesis of various clotting factors and decreased titers of antithrombin III. Paradoxically, enhanced in vitro fibrinolytic activity is also found in plasmas of women using OCAs. The present study demonstrates marked elevation of both procoagulant and antigenic HF titers in plasmas of women using OCAs, accompanied by a simultaneous decrease in plasma C-1-INH concentration. Titers of plasma prekallikrein, HMW kininogen, PTA, and alpha 2-Pl were unchanged. The rate of kaolin-assisted fibrinolysis was related directly to the titer of HF and inversely to C-1-INH concentration. Further, the addition of human HF to normal plasma enhanced fibrinolytic activity to a degree similar to that observed in plasmas of women taking OCAs. These data suggest that the increase in plasma HF concentration may participate in the phenomenon of enhanced in vitro fibrinolysis associated with OCA use, possibly augmented by diminished inhibitory control by C-1-INH. The relationship of these phenomena to the increased incidence of thrombosis is not known.

Adult↗
PubMed1999

[A patient with isolated prolongation of aPTT without hemorrhagic diathesis anamnesis: severe, hereditary factor XII deficiency].

By virtue of a severely prolonged aPTT with a normal thromboplastin time (prothrombin time) and a normal thrombin time, severe FXII deficiency has been diagnosed in a woman without a bleeding diathesis or a history of thromboembolic complications. A deficiency of a factor of the contact activation system (FXII, prekallikrein, high molecular weight kininogen) is usually diagnosed during routine coagulation tests demonstrating a prolonged aPTT. The severe and partial deficiency of FXII, of prekallikrein or high molecular weight kininogen is not associated with a bleeding tendency. In contrast, severely factor XI deficient subjects may suffer from a mild hemorrhagic diathesis, whereas FVIII deficiency (hemophilia A, autoimmune "hemophilia", von Willebrand disease) and FIX deficiency (hemophilia B) are associated with a bleeding tendency of varying severity, depending on the clotting activity of FVIII or FIX, respectively. An isolated prolongation of the aPTT due to a lupus anticoagulant, however, is frequently associated with arterial and/or venous thrombosis. Therefore, in case of a prolongation of the aPTT, its cause has to be determined.

Adult↗
PubMed1997

Potent blood pressure raising effects of activated coagulation factor XII.

A new pressor protein (NPP) in trypsin-activated human plasma was recently reported, whose blood pressure raising effects in bioassay rats are potentiated 300% after treatment with angiotensin I converting enzyme inhibitors (captopril). Pure NPP showed good N-terminal sequence homology with coagulation factor beta FXIIa, and little of it was present in FXII-deficiency plasmas (> or = 99%, n = 4). The present experiments confirm this in four additional FXII-deficiency plasmas. Further, (i) adding highly purified coagulation FXII, alpha FXIIa, or beta FXIIa fragment restores pressor activity to such plasmas, but only after activation with trypsin. (ii) Such requirement for trypsin suggests that no factor is structurally identical with NPP to begin with but that all can be activated to NPP. (iii) When injected directly by vein, only beta FXIIa is pressor, suggesting closest structural resemblance to NPP and (or) readiest endogenous conversion to NPP. (iv) NPP and beta FXIIa are cardiotonic: they both raise systolic pressure more than the diastolic, with a concomitant increase in heart rate. These observations support NPP's structural relationship with beta FXIIa and connect coagulation and blood pressure mechanisms in a new way, whose significance to the physiology and pathophysiology of blood pressure regulation remains to be established.

Adolescent↗
PubMed1998

Whale Hageman factor (factor XII): prevented production due to pseudogene conversion.

In Southern blot analysis of the Hind III-digested whale genomic DNA obtained from the livers of two individual whales, we detected a single band with a size of five kilobase pairs which hybridized to full length guinea pig Hageman factor cDNA. We amplified two successive segments of the whale Hageman factor gene by polymerase chain reaction (PCR), and sequenced the PCR products with a combined total of 1367 base pairs. Although all of the exon-intron assemblies predicted were identical to those of the human Hageman factor gene, there were two nonsense mutations making stop codons and a single nucleotide insertion causing a reading frame shift. We could not detect any message of the Hageman factor gene expression by northern blot analysis or by reverse transcription-polymerase chain reaction (RT-PCR) analysis. These results suggest that in the whale, production of the Hageman factor protein is prevented due to conversion of its gene to a pseudogene. The deduced amino acid sequence of whale Hageman factor showed the highest homology with the bovine molecule among the land mammals analyzed so far.

Amino Acid Sequence↗