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At least 19 recordsLinked to original sources
PubMed1978

Quantitative estimation of coagulation factors in liver disease. The diagnostic and prognostic value of factor XIII, factor V and plasminogen.

20 coagulation parameters were investigated in 144 patients with different liver diseases. The groups of acute hepatitis, chronic active hepatitis and liver cirrhosis were compared and the prognostic value of the coagulation analyses investigated. It is clear that the determination of the factor V activity is a good and easy test for detection of actual liver function. Repeated controls over several weeks revealed with a statistical significance (p less than 0.0005) that all patients with a factor XIII below 35% and a plasminogen below 19% will die in liver coma, if they have not died beforehand from acute gastrointestinal haemorrhage, acute infection or cardiac arrest. Plasminogen is also lower in the group of non-survivors but the values of the two groups are overlapping and of no prognostic help in a single case. The possible causes of the diminution of factor XIII activity are discussed.

Adolescent↗
PubMed1977

Comparison of the cross-linking patterns of lamprey fibrinogen and fibrin by the action of the intrinsic lamprey factor XIII and human factor XIII during the process of blood coagulation.

Intrinsic lamprey factor XIII cross-links the gamma chain of lamprey fibrin (50,000 daltons) to the gamma-dimer (100,000 daltons). The alpha-chain (110,000 daltons) is cross-linked very slowly to alpha-dimer (210,000 daltons) and alpha-trimer (330,000 daltons). In contrast, human factor XIII, when added in combination with intrinsic lamprey factor XIII, cross-links the alpha-chain of lamprey fibrin to a high molecular weight polymer, and any remaining gamma-chain is also cross-linked to a polymer. However, the gamma-chain that has previously cross-linked to the gamma-dimer by the intrinsic lamprey factor XIII remains as a gamma-dimer. Factor XIII-free lamprey fibrin cross-links all its subunits (alpha, beta, gamma) to high molecular weight polymers when human factor XIII is added. In contrast to human and bovine fibrin where alpha-chain cross-linking in the process of blood coagulation commences when all of the gamma-chain has cross-linked, the lamprey alpha-chain will begin to cross-link when approximately half of the gamma-chain has cross-linked to the gamma-dimer.

Animals↗
PubMed1978

Studies on factor XIII antigen in congenital factor XIII deficiency. A tentative classification of the disease in two groups.

Immunological and immunofluorescent studies carried out on plasma and platelets of three cases of congenital factor XIII deficiency are reported. Two of these patients were originally thought to have normal factor XIII subunit S and no subunit A. However, repeated assays carried out using different lots of antiserum showed that in reality the patients lacked both subunit S and subunit A. The false positive finding was due to the presence of a anti-factor VIII contaminant in the antiserum originally used. The third patient had a normal subunit S and no subunit A. No factor XIII antigen was found by the indirect immunofluorescent technique in normal, factor XIII deficiency and von Willebrand's disease platelets. On the contrary, by using the non-monospecific antiserum a fluorescent pattern similar to that observed by using an anti-factor VIII antiserum, had been noted. On the basis of the data presented in this paper a tentative classification of factor XIII deficiency in two groups is proposed: Type I is characterized by the lack of both factor XIII subunit S and A. Type II is characterized by a normal subunit S and no subunit A. The need for a re-evaluation of published case of factor XIII deficiency by means of monospecific antisera is indicated.

Antigens↗
PubMed1979

Factor XIII deficiency. A family study by measurement of factor XIII subunits A and S.

A girl with congenital factor XIII deficiency and her large family have been studied by electroimmunoassay of factor XIII subunits A and S. The homozygote has absence of subunit A and a decreased level of subunit S. The heterozygotes have decreased levels of both subunits, and were more readily identified by measurement of subunit A than by the ratio subunit S/subunit A. The mother of the propositus appears to be a new heterozygote, but heterozygosity on the paternal side is traced through three generations.

Adult↗
PubMed1977

Factor XIII (fibrin stabilising factor) in Henoch-Schönlein's purpura.

In 13 out of 17 consecutive children with Henoch-Schönlein's purpura the factor XIII determined with the dansyl cadaverine method was found to be decreased during the acute phase. The decrease is assumed to be due to a specific degradation by proteolytic enzymes liberated from inflammatory cells, with defective local haemostasis as a result. This assumption is strengthened by the observation that treatment with factor XIII combined with an antifibrinolytic drug controlled life-threatening gastro-intestinal bleeding in one of the patients. It would therefore appear that such treatment might offer a new possibility of controlling severe haemorrhages in Henoch-Schönlein's purpura.

Adolescent↗
PubMed1977

[Factor XIII deficiency in adults with acute leukemia: results of a substitution therapy with factor XIII (author's transl)].

A decrease in fibrin stabilizing factor (Factor XIII) is the most frequent coagulation disorder seen in adults with acute leukemia. Patients with prominent reduction of factor XIII (FSF) (less than 50%) were substituted with a factor XIII concentrate from human placenta, and factor XIII plasma concentration and bleeding tendency were followed up during the course of the disease. After substitution plasma, factor XIII activity went up to normal levels in most of the patients. As compared to the course of 12 patients with distinct factor XIII reduction without factor XIII therapy, there were less bleeding complications in 13 courses of patients with prominent reduction of factor XIII substituted with factor XIII concentrate and in 11 with normal or only slightly reduced factor XIII levels.

Acute Disease↗
PubMed1979

Factor XIII.

1. Activated factor XIII is the enzyme that covalently cross-links fibrin monomers into fibrin polymers and results in increased clot strength and resistance of the clot to fibrinolysis. 2. Small amounts (greater than 1% of normal) of factor XIII are necessary for normal in vitro and in vivo activity. 3. Factor XIII deficiency is a rare autosomal recessive illness in which a hemorrhagic diathesis is caused by the virtual absence of the active a subunit of factor XIII. Approximately 100 cases have been described. 4. The disease in homozygotes is characterized by umbilical stump bleeding, a high incidence of fetal wastage, delayed soft tissue hemorrhage, and a high incidence of intracranial bleeding. The heterozygote is asymptomatic. 5. This paper calls attention to the apparent high incidence of oligospermia and small testes seen in homozygote males. Otherwise secondary sex characterics are normal. 6. Because there is no abnormality in thrombin generation and conversion of fibrinogen to fibrin, route coagulation tests (prothrombin time, partial thromboplastin time, thrombin time, etc.) are normal. Platelet function tests are normal. 7. Clots made from recalcified plasma severely deficient in factor XIII are soluble in 5 M urea or 1% monochloroacetic acid. These screening tests are simple and nearly pathognomonic of the illness. 8. More sophisticated and quantitative tests (e.g., dansylcadaverine incorporation) are available for definitive diagnosis and heterozygote detection. 9. Replacement treatment of the illness is simple, effective, and relatively inexpensive. Due to the long half-life of infused factor XIII and the small amounts necessary for normal hemostasis, prophylaxis is feasible and encouraged.

Adult↗
PubMed1975

[Blood coagulation factor XIII and fibrin stabilization (author's transl)].

Coagulation factor XIII (fibrin stabilizing factor, FSF) is detectable in plasma, platelets, placenta and various tissues. In the activated form FSF has the enzymatic properties of a transglutaminase and is capable of stabilizing fibrin by inducing covalent bondings between fibrin monomers. In patients with congenital factor XIII deficiency or acquired immune inhibitors of fibrin stabilization a severe bleeding tendency is evident. There is not yet enough information available concerning the significance of reduced FSF-activity as cofactor in hemorrhagic diathesis and wound healing disturbances in various disease states. There are some indications from experimental studies that there might be an influence of FSF on tumor growth and metastasis as well as arteriosclerosis. The quantitation of the enzyme by radiological and immunological techniques yield reproducible results. Fibrin in its stabilized or non stabilized form can be discriminated in polyacrylamide gel electrophoresis after reduction of fibrin clots.

Adult↗
PubMed1978

An equilibrium study of metal ion binding to human plasma coagulation factor XIII.

1. The binding of Ca2+ to plasma coagulation Factor XIII from man and from cow caused a small decrease in the intrinsic fluorescence of the protein with a dissociation constant of 0.1 mM. A similar decrease was observed with the thrombin-activated Factors (Factors XIIa). The decrease in protein fluorescence was also caused by both Ni2+ and Mn2+ but not by Mg2+. 2. 45Ca2+ binding was directly demonstrated by equilibrium dialysis. Ca2+ at 0.2 mM bound to Factor XIII (a2b2) and Factor XIIIa (a'2b2) but not to isolated b2-protein. A tight-binding site for Ca2+ is associated with the a-subunits. 3. The Ca2+ essential for the enzyme activity of Factor XIII from man, pig and cow can be replaced by Ni2+, Cu2+, La3+, Mn2+, Fe3+, Y3+, Co2+, Sr2+ or Tb3+, but not by Mg2+.

Animals↗
PubMed1978

Factor XIII, fibrin and collagen.

It has been demonstrated that activated factor XIII may catalyze the formation of covalent cross-links between fibrin and collagen. This is shown by the disappearance of the gamma-gamma dimer band in PAA-SDS gel electrophoresis when fibrinogen is clotted in presence of collagen, factor XIII and Ca ions, and by the binding of labeled fibrinogen. This reaction may explain the outstanding physiological importance of factor XIII.

Collagen↗
PubMed1979

An acquired inhibitor to factor XIII A case report.

An elderly woman presented with a postoperative bleeding problem, and a presumptive diagnosis of factor XIII (fibrin-stablilizing factor) deficiency was made. However, on further testing, an inhibitor to factor XIII was detected. She was on isoniazid (INH) therapy at the time. INH has been implicated in other patients who have developed inhibitors to factor XIII, and it was felt that this was the reason for this patient developing the inhibitor. The patient subsequently died from a cerebral haemorrhage, a well-described complication of factor XIII deficiency.

Aged↗
PubMed1979

[Rat thrombocyte factor XIII and its role in platelet aggregation].

Factor XIII was isolated from rat platelets; it activity was 1430 units per 1 mg of protein. It was shown in experiments in vitro that addition of this factor (160--200 units/ml) to the suspension of washed platelets or those purified by passage through the column with sepharose 4B increased their aggregation capacity. Addition of inactive platelet factor XIII failed to influence the platelet aggregation induced by ADP.

Adenosine Diphosphate↗
PubMed1977

Reduction of coagulation factor XIII concentration in patients with myocardial infarction, cerebral infarction, and other thromboembolic disorders.

Coagulation factor XIII and plasma fibrinogen chromatographic assays have been performed serially in patients suffering from acute myocardial and cerebral infarction, and in others with disseminated intravascular coagulation. The findings were compared with 2 groups of "controls"; normal clinically-well subjects and hospitalized patients with cerebral infarction who exhibited minimal, stable, or improving neurological deficits. Substantial depression of factor XIII concentrations developed in the 3 patient groups, together with concomitant significant increases in the proportion and concentration of plasma high molecular weight fibrin(ogen) complexes (HMWFC). An inverse correlation (p less than 0.05) between coagulation factor XIII concentration and percentage of HMWFC was demonstrated in the early stages of the illness. These findings suggest that depression of coagulation factor XIII concentration in these states, is secondary to extravascular or intravascular coagulation and may reflect its degree.

Adult↗
PubMed1979

[Factor XIII and the risk of postoperative impaired wound healing and bleeding (author's transl)].

Factor XIII concentration was investigated pre- and postoperatively in the plasma of 139 patients undergoing major abdominal surgery. Postoperative complications (impairment of wound healing and haemorrhage) were significantly more frequently seen in patients with a low concentration of factor XIII. A low preoperative concentration of factor XIII can be interpreted as a high risk factor.

Factor XIII↗
PubMed1977

Clotting factors and platelets. Immunofluorescence evidence that fibrinogen and factor VIII are present in human washed platelets, whereas prothrombin complex factors and factor XIII are lacking.

Factor I (fibrinogen) and factor VIII were shown, by an indirect immunofluorescence technique, to be present in human washed platelets. In the case of fibrinogen, the immunofluorescent pattern had a 'clod distribution' up to a 1:128 dilution of the antiserum. Factor VIII showed a 'speckled' pattern up to the 1:64 dilution. Cross-absorption studies confirmed the presence of such factors. Factor II, VII, IX, X and XIII, however, were not found in washed platelets. A diffuse fluorescence was noted using normal rabbit sera, but this was due to a cross-reaction, since it disappeared using a 1:32 diluted sera.

Animals↗