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Genetic heterogeneity in hereditary thrombophilia.

Venous thromboembolism is a multifactorial disease that depends on variable combinations of acquired and genetic risk factors. The genetic risk factors include loss-of-function mutations in the genes that encode proteins with clot-restraining function, and gain-of-function mutations in procoagulant factors. The loss-of-function mutations are heterogeneous and comprise any mutation that impairs gene function. On the whole, these mutations are rare, with fewer than 1/200--500 individuals affected. This low prevalence in the population is probably caused by the loss of mutant alleles from the gene pool through critically ill homozygous subjects. The gain-of-function mutations in procoagulant proteins differ from the loss-of-function mutations in at least three important respects: these are more homogeneous (factor V Leiden and PT 20210), homozygous individuals are relatively mildly affected, and these are relatively prevalent (3--15%) in Caucasian populations.

3' Untranslated Regions↗

Role of coagulation factor XIII (FXIII) in angiogenesis and tissue repair.

Factor FXIII (FXIII) is a plasma transglutaminase that catalyzes the cross link formation between fibrin chains to stabilize the clot. Beside it s function in hemostasis FXIII has a role in wound healing and embryo implantation--processes that involve angiogenesis. In this review we discuss the role of FXIII in angiogenesis and the molecular mechanisms underlying its pro-angiogenic effect. In addition, FXIII role in wound repair is discussed.

Factor XIII↗

Substitution of factor XIII: a therapeutic approach to ulcerative colitis.

Three patients with ulcerative colitis in the active stage demonstrated reduced levels of F XIII activity and F XIII subunit A (61 and 80.3%, respectively). Because of the lack of clinical improvement during conservative therapy, the patients were treated additionally with F XIII concentrate (Fibrogammin HS, Behring, FRG) for 10 days. The substitution resulted in an increase in F XIII activity (144.3%) and F XIII subunit A (238%) as well as in a marked improvement in symptoms.

Adrenal Cortex Hormones↗

Fibrin elasticity and coagulation.

Sudden increase of viscosity in former times indicated the start of coagulation. Yet its measurement destroyed the structure of coagulum. By the precursor method of thrombelastography the author 1944 found elasticity to be the essential physiological property of coagulum. In the production of elastic fibrin structure its early phase is the most efficient in this respect. The speed of prime structure formation is extremely fast in presence of enough phospholipid as well as of plasma factor XIII. Even high amounts of thrombin cannot replace one or both of these substances indispensable to grow rapidly a perfect fibrin web. This phase yet does not become effective if it is not accompanied by the orbital micro-flow of the new orbitometry method. Its shear is comparable to that in a coronary artery. The special resonance effect of the method in combination with the early phase of fibrin production is generating some kind of a physiological feed back: increasing fibrin will strengthen shear stress as long as less platelets are entangled which will reduce the elastic flexibility of fibrin web. Some kind of a "coagulation spin effect" in optimal combination of shear stress, phospholipid and factorXIII, will extremely fast originate a firm fibrin structure, a mechanism which may be of significance for a fast occlusion of arterial stenoses.

Blood Coagulation↗

A simple, quick one-step ELISA assay for the determination of complex plasma factor XIII (A2B2).

A new highly sensitive sandwich ELISA assay was developed for the determination of plasma factor XIII (FXIII). Plasma FXIII is a tetrameric complex of two types of subunits (A2B2). A biotinylated monoclonal capture-antibody against the B-subunit and a peroxidase-labelled monoclonal tag-antibody against the A-subunit were added to the plasma dilution and the amount of the complex attached to streptavidin-coated microplate was quantitated by measuring peroxidase activity. Only the tetrameric plasma FXIII reacted in the assay, non-complexed A or B subunits showed no reaction. The assay is linear up-to 40 microg/L of FXIII in the assay mixture. It is a quick one-step assay which can be performed within two hours. At normal and low FXIII concentration within batch reproducibility was 2.0% and 3.3%, day to day variation was 5.5% and 8.7%, respectively. Its high sensitivity allows reliable measurement at FXIII concentrations below 1% of normal average. Plasma samples can be stored for the assay at -20 degrees C for at least one month. Plasma levels of healthy individuals were normally distributed and no gender difference was observed. A reference interval of 14-28 mg/L (67-133%) was established.

Antibodies, Monoclonal↗

[Experiences with the Port-A-Cath system in children].

In a retrospective study (1987-1997) the complications of a totally implantable venous access device (Port-A-Cath, Fa. Pharmacia, Germany) were analysed in 91 children with 99 implants. All but 2 of these children had malignant diseases. Their age ranged from 0.1 to 18.1 (median 6) years. Overall implant time was 171.2 years (62,488 days), averaging 1.63 years (595 days) per device. 11 complications were registered, i.e. infections (6), occlusions (4) and disconnection (1), resulting in an overall infection rate of 0.06 and a total occlusion rate of 0.04. The overall complication rate was thus 0.11, which compares favourably with other studies. With careful handling, the Port-a-Cath device is very reliable and involves few complications.

Adolescent↗

Depletion of plasma factor XIII prevents disseminated intravascular coagulation-induced organ damage.

The impact of clot stability affecting the vasculopathy and tissue necrosis in Shwartzman reaction was investigated using plasma Factor XIII A2-depleted rabbit (FXIII-DR). Plasma Factor XIIIA2 (FXIIIA2) was depleted by infusion of the mono-specific goat anti-rabbit FXIIIA2 IgG. Generalized Shwartzman reaction (GSR) was induced by priming and challenged by i.v. injection of LPS and local Shwartzman reaction (LSR) was primed by intradermal injection of LPS and challenged by i.v. injection of LPS. Histological examination of the GSR animals showed, extensive thrombi accumulation in renal tubules and bilateral cortical necrosis of kidney in 8 out of 10 rabbits but none in the FXIII-DR. Fibrinogen levels were elevated to 3 approximately 4 fold at 24 h and lowered at 48 h whereas a steady rise was seen in the FXIII-DR. FDP levels in GSR animals were significantly elevated at 24 h and further increased at 48 h but only slightly elevated in the FXIII-DR. Examination of the LSR tissues after 48 h showed an acute onset of progressive cutaneous vascular thrombosis, purpura, and secondary hemorrhagic necrosis whereas neither fibrin deposit nor necrosis of tissue were detected in FXIII-DR despite of an early edema formation. Fibrinogen levels were also increased two fold at 24 h but returned to basal levels at 48 h in control LSR animals but not affected at all in FXIII-DR. These results suggest that during the severe inflammatory conditions such as sepsis, the fibrinolytic system is functionally sufficient to dissipate the pathogenic accumulation of disseminated intravascular clots and exudated fibrin clots if those clots were prevented from getting crosslinked in plasma.

Animals↗

[Factor XIII].

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Biomarkers↗