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PubMed2004

[Factor XIII].

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Biomarkers↗
PubMed1979

Fatal iron intoxication with multiple coagulation defects and degradation of factor VIII and factor XIII.

A severe iron intoxication in a 15-year-old girl resulted in profound damage to vital organs and multiple clotting defects, but no haemorrhagic diathesis. Investigation revealed not only impaired synthesis of coagulation factors but also abnormal proteolysis by plasmin as well as by other proteolytic enzymes liberated from leucocytes and damaged tissue cells affecting especially factor VIII and factor XIII.

Adolescent↗
PubMed1982

Improved coagulation factor XIII B (FXIIIB) phenotyping after neuraminidase treatment of plasma and first description of the FXIIIB 2 phenotype.

The genetically determined polymorphism of the B subunit of the human coagulation factor XIII (FXIIIB) was investigated by an improved technique of immunofixation agarose gel electrophoresis (IAGE). Employing neuraminidase (CPN) treatment of fivefold-concentrated fresh plasma and monospecific anti-human FXIIIB antiserum an excellent resolution of phenotypes was possible. Six phenotypes, FXIIIB 1,2-1,2,3-1, 3-2 and 3 were detected among 178 unrelated blood donors from Hessen, Germany, the FXIIIB 2 homozygote for the first time. Our findings confirm the 'reduced' two-allele-model of Kera et al. [10]. For the first time the allele frequencies were determined in a European population: FXIIIB*1 = 0.708, FXIIIB*2 = 0.109, FXIIIB3* = 0.183. As in family studies no unexpected phenotypes were observed in the offspring, FXIIIB might become a useful genetic marker in paternity testing, the single exclusion chance for non-fathers being 23.7%.

Factor XIII↗
PubMed1978

[Parodontal alterations caused by a deficiency of fibrin-stabilizing factor (factor XIII deficiency) (author's transl)].

This article reports the results of clinical, symptomatological, and histological examinations of the gingiva and parodontium in two patients with a hereditary deficiency of fibrinstabilizing factor (factor XIII deficiency).--In a period of observation of up to seventeen years the periodontal condition deteriorated until the teeth finally fell out.--Because of inadequate possibilities of mechanically reducing the plaque, changes of the gingiva in the form of granulomatous gingivitis accompanied by osteolysis were observed. The histological phenomena are characterized by strong nonspecific plasmacytic inflammation.

Adolescent↗
PubMed2006

Prevalence of the coagulation factor XIII polymorphism Val34Leu in women with recurrent miscarriage.

BACKGROUND: Recurrent miscarriage (RM) syndrome is not an uncommon obstetrical problem of multifactorial etiology. We investigated the role of the coagulation factor XIII (FXIII) Val34Leu polymorphism in RM. METHODS: We recruited 80 subjects (40 normal and 40 with history of RM; of each group 20 pregnant and 20 non-pregnant) and analyzed the prevalence of this polymorphism. The women recruited for the present study had similar age and did not have history of any hemostatic disorders. FXIII levels and activity and the rate of fibrin cross-linking by FXIII genotype Val34Val and Val34Leu were studied. RESULTS: Genotype analyses of patients and normal revealed that the frequencies distribution of Val/Val and Val/leu were statistically similar (P<0.05): 62.5% and 60%, and 37.5% and 40%, respectively; no Leu/leu genotype was found. The FXIII-A subunit levels and activity were also found similar between Val/Val and Val/leu genotypes in the different groups, pregnant and non-pregnant, normal or with RM. The rate of FXIII alpha and gamma-chains fibrin cross-linking was not different between the 2 genotypes. CONCLUSION: From our results we conclude that FXIII Val34Leu polymorphism does not appear to be associated to RM.

Abortion, Habitual↗
PubMed2004

Rapid detection of the factor XIII Val34Leu (163 G-->T) polymorphism by real-time PCR using fluorescence resonance energy transfer detection and melting curve analysis.

The Val34Leu polymorphism in the A subunit of blood coagulation factor XIII (FXIII-A) is located in the activation peptide, just three amino acids upstream of the thrombin cleavage site. The Val-->Leu replacement accelerates the rate of the proteolytic activation of FXIII and it seems to provide protection against myocardial infarction. Methods available for the assessment of the FXIII-A Val34Leu polymorphism are rather time-consuming, laborious and not easily applicable for large-scale studies. In this study a new method based on real-time PCR with fluorescence resonance energy transfer (FRET) detection and melting curve analysis was developed. The rapid, simple method was adapted to the widely used real-time PCR instrument, LightCycler (Roche Diagnostics). The results showed 100% coincidence with those obtained by the traditional PCR-restriction fragment length polymorphism (RFLP) assay and fluorescent DNA sequencing. Using this method, an allele frequency of 24.2% was obtained (n=113), which well agrees with the allele frequency obtained by PCR-RFLP on a different group of the same ethnic Hungarian population (25.9%).

Alleles↗
PubMed1989

The influence of factor XIII on the fibrosing of a nerve anastomosis in the rat.

Although the fibrin adhesion enjoys increasing success in many areas of surgery, it has not become fully established in nerve anastomosis. It was in this area particularly that significant advantages were expected. As the fibrin clot dissolved prematurely, however, and dehiscences ensued, antifibrinolytic substances had to be added to the adhesive. Fibroses occurred frequently as a result, which to date encumber nerve adhesive. We examined Faktor XIII for his fibrosis-inducing effect because both presently available fibrin adhesives contain unphysiologically high concentrations of it. We were able to establish that Factor XIII possesses a fibrosis-promoting effect.

Anastomosis, Surgical↗
PubMedDate not supplied

Turkish population data on the factor XIII Val34Leu,glycoprotein (GP)Ibalpha Kozak and P-selectin glycoprotein ligand 1 (PSGL-1) loci.

We determined the allele and genotype frequencies of three PCR-based gene polymorphisms factor XIII (FXIII) Val34Leu, glycoprotein (GP) Ibalpha Kozak and P-selectin glycoprotein ligand 1 (PSGL-1) in the Turkish population (n = 126 for FXIII Val34Leu, n = 110 for GPIbalpha Kozak and n = 203 for PSGL-1). To detect these polymorphisms, DNA was extracted from venous blood. Genomic DNA samples were replicated and analysed by a polymerase chain reaction (PCR) method. PCR products were digested by restriction endonuclease enzymes for FXIII Val34Leu and GPIbalpha Kozak. PSGL-1 was analysed by variable number of tandem repeats (VNTR). Allele frequencies of V (Val) and L (Leu) were found to be 0.805 and 0.195 respectively for the FXIII Val34Leu polymorphism. No significant difference was observed between French and Turkish populations for FXIII Val34Leu. Allele frequencies of T and C were calculated to be 0.873 and 0.127 for the GPIbalpha Kozak polymorphism and no significant difference was found between Turkish and French populations. In contrast, the difference between Turkish and Japanese populations was statistically significant (p<0.0001). In the PSGL-1 group, allele frequencies of A, B and C were calculated as 0.818, 0.160, 0.022 respectively. For the PSGL-1, although the difference between Turkish and French populations was not significant, the difference between the Turkish and Japanese was extremely significant (p<0.0001). In conclusion, a Turkish population database has been established for three gene polymorphisms.

Adolescent↗
PubMed2004

Factor XIII Val34Leu polymorphism modulates the prothrombotic and inflammatory state associated with atrial fibrillation.

UNLABELLED: Atrial fibrillation (AF) has been shown to confer a prothrombotic or hypercoagulable state, which could be related to inflammation. Factor XIII (FXIII) catalyses the cross-linking of fibrin monomers, increasing clot resistance; specifically, a common polymorphism, Val34Leu, in the FXIII-A subunit gene has been associated with more rapid FXIII activation. We hypothesised a role for this polymorphism in the prothrombotic state and inflammation in AF, and tested this hypothesis by measurement of indices of coagulation (tissue factor (TF) and fibrinogen), inflammation (interleukin-6 (IL6)) and platelet activation (soluble P selectin (sPsel)). METHODS: We studied 90 stable outpatients (73 +/- 8 years) with persistent AF. The FXIII Val34Leu polymorphism was determined by polymerase chain reaction-allelic specific restriction assay (PCR-ASRA). Prevalence of Val34Leu polymorphism of patients was compared to 585 unrelated subjects from the same geographical area. Plasma fibrinogen (Clauss), TF, IL6 and sPsel (all ELISA) were quantified in patient group. Research indices were compared to 74 controls in sinus rhythm with similar clinical characteristics. RESULTS: There were no statistical differences in FXIII polymorphism prevalence between AF patients and controls. Patients carrying the Leu34 allele had higher plasma levels of TF, IL6 and sPsel (all P < 0.05) compared to controls. Plasma IL6 and TF levels were significantly correlated (Spearman coefficient, r = 0.33, P < 0.01). On multivariate analysis, the Leu34 allele was independently associated with IL6 levels (P < 0.01), whereas TF levels were only associated with IL6 concentrations. However, sPsel and fibrinogen levels were not related to Leu34 allele. CONCLUSION: FXIII Val34Leu polymorphism was independently associated with IL6 levels in AF. The Leu34 allele may potentially influence the prothrombotic state in these patients by modulating the inflammatory state.

Aged↗
PubMed2004

Mass spectrometric phenotyping of Val34Leu polymorphism of blood coagulation factor XIII by differential peptide display.

BACKGROUND: The Val34Leu mutation in the activation peptide of factor XIII (FXIIIA) correlates with a lower incidence of myocardial infarction and ischemic stroke but an increased risk for hemorrhagic stroke. We describe mass spectrometric detection of the activation peptide variants in human serum. METHODS: We used differential peptide display (DPD) to compare comprehensive peptide maps from pairs of serum samples from healthy volunteers. Peptides were separated by liquid chromatography, and fractions were subjected to mass spectrometry. Mass spectra of all fractions were combined, giving a peptide map representing a two-dimensional display of peptide masses. After comparison of peptide mass maps, peptides that differentiated FXIIIA phenotypes were identified by mass spectrometry. RESULTS: Val34Leu polymorphisms of the activation peptide of FXIIIA were identified in 20 serum samples from 10 volunteers by DPD, and their sequences were confirmed by nanoelectrospray-ionization quadrupole time-of-flight mass spectrometry. Analysis of three (V34V, V34L, and L34L) phenotypes was confirmed by allele-specific genotypic analysis in all (n = 10) volunteers. CONCLUSION: DPD provides a simple and easy-to-use phenotype assay with advantages over PCR-based assays in being faster and directly analyzing the compound of interest.

Adult↗
PubMed1986

Release of alpha 2-plasmin inhibitor from plasma fibrin clots by activated coagulation factor XIII. Its effect on fibrinolysis.

When blood coagulation takes place in the presence of calcium ions, alpha 2-plasmin inhibitor (alpha 2PI) is cross-linked to fibrin by activated coagulation Factor XIII (XIIIa) and thereby contributes to the resistance of fibrin to fibrinolysis. It was previously shown that the cross-linking reaction is a reversible one, since the alpha 2PI-fibrinogen cross-linked complex could be dissociated. In the present study we have shown that the alpha 2PI-fibrin cross-linking reaction is also a reversible reaction and alpha 2PI which had been cross-linked to fibrin can be released from fibrin by disrupting the equilibrium, resulting in a decrease of its resistance to fibrinolysis. When the fibrin clot formed from normal plasma in the presence of calcium ions was suspended in alpha 2PI-deficient plasma of buffered saline, alpha 2PI was gradually released from fibrin on incubation. When alpha 2PI was present in the suspending milieu, the release was decreased inversely to the concentrations of alpha 2PI in the suspending milieu. The release was accelerated by supplementing XIIIa or the presence of a high concentration of the NH2-terminal 12-residue peptide of alpha 2PI (N-peptide) which is cross-linked to fibrin in exchange for the release of alpha 2PI. When the release of alpha 2PI from fibrin was accelerated by XIIIa or N-peptide, the fibrin became less resistant to the fibrinolytic process, resulting in an acceleration of fibrinolysis which was proportional to the degree of the release of alpha 2PI. These results suggest the possibility that alpha 2PI could be released from fibrin in vivo by disrupting the equilibrium of the alpha 2PI-fibrin cross-linking reaction, and that the release would result in accelerated thrombolysis.

Electrophoresis, Polyacrylamide Gel↗