Plasma Fibrin Stabilizing Factor Activity in Various Diseases

Nussbaum, Murray; Morse, Bernard S.

doi:10.1182/blood.v23.5.669.669

Cited by 76 publications

(22 citation statements)

References 8 publications

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“…and stored at -220" C. until just before use. METHODS Factor-XI11 assays were performed according to Nussbaum and Morse (1964) Lysis experiments were performed in 13 x 99 mm. Lusteroid test tubes.…”

Section: Methodsmentioning

confidence: 99%

The Mechanism of Enhanced Streptokinase‐Induced Clot Lysis following In‐vitro Factor‐XIII Inactivation

Henderson

Nussbaum

1969

Br J Haematol

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Summary. Factor‐XIII (fibrin stabilizing factor, FSF) activity in human plasma may be inhibited in vitro by a variety of sulphydryl inhibitors and by several derivatives of glycine. Incorporation of small amounts (40 units) of streptokinase (SK) into a clot formed from plasma after in vitro inactivation of Factor XIII, resulted in marked shortening of clot lysis times compared to controls without Factor‐XIII inactivation. Enhancement of SK‐induced clot lysis by the sulphydryl inhibitors is in part related to Factor‐XIII inactivation. Further acceleration of lysis is noted with concentrations greater than the minimal amount necessary for complete Factor‐XIII inhibition. At higher concentrations, clotting is delayed and ultimately completely inhibited. These reagents also produce marked changes on the thromboelastogram consistent with a weakened clot structure. No evidence to suggest increased plasminogen‐plasmin conversion, enhanced plasmin activity or inhibition of anti‐plasmin by sulphydryl inhibitors could be found. Glycine ethyl ester (GEE) incorporation results in marked enhancement of SK‐induced plasma clot lysis in vitro and pronounced changes on the thromboelastogram. The enhanced clot lysis is related to Factor‐XIII inhibition. No further acceleration of clot lysis was obtained once Factor‐XIII activity was completely inhibited. GEE alone shows an additional effect of inhibiting anti‐plasmin activity. Thus enhanced SK‐induced clot lysis following in vitro inhibition of Factor‐XIII activity with sulphydryl inhibitors and derivatives of glycine is considered to be due to the greater ease with which plasmin may act on a weakened clot. GEE, in addition to promoting the formation of a weaker clot, inhibits anti‐plasmin activity, and so further increases the relative effectiveness of streptokinase.

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Section: Methodsmentioning

confidence: 99%

The Mechanism of Enhanced Streptokinase‐Induced Clot Lysis following In‐vitro Factor‐XIII Inactivation

Henderson

Nussbaum

1969

Br J Haematol

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“…FSF has also been found to be low in acute as well as in chronic renal insufficiency (Nussbaum & Morse 1964, Mandalaki et a1 1970, Melissinos et al 1971. Low levels that became normal after addition of cystein to the test system have been found in patients with cancer (Nussbaum & Morse 1964).…”

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confidence: 96%

“…The studies have been carried out with various clot dissolution tests. The FSF level has been described as low in liver diseases (Nussbaum & Morse 1964, Walls & Losowsky 1969, Cucuianu et a1 1973. Some authors (Nussbaum & Morse 1964) ascribed this lowness to defective activation of FSF and found that the level became normal after addition of cystein to the test system.…”

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confidence: 99%

“…Abnormal plasma levels of factor XI11 in various diseases have received fairly extensive attention in the literature (Nussbaum & Morse 1964, Walls & Lossowsky 1969, Melissinos et a1 1971, Cucuianu et a1 1973, but the results obtained in investigations on record vary widely, probably owing to methodological difficulties. The studies have been carried out with various clot dissolution tests.…”

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confidence: 99%

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Factor XIII in a Clinical Material

Hedner¹,

Henriksson²,

Im³

1975

Scandinavian Journal of Haematology

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In 339 patients with various diseases factor XIII (FSF) was determined with the specific amine incorporation method of Lorand et al (1969). Normal values were found in patients with renal (216 patients) or liver diseases (33 patients), in 39 patients with recurrent deep venous thrombosis and in 17 children with congenital cyanotic heart disease. Low levels were found in patients with various conditions, such as sepsis, multiple fractures and combustio complicated by an abnormal proteolytic activity (fibrinolysis and/or activation of the coagulation system with signs of disseminated coagulation). No correlation was found between the FSF and the fibrinogen values or the levels of fibrin/fibrinogen degradation products (FDP). Low FSF values were found in 4 patients with erosive gastritis, with gastrointestinal bleedings and a local fibrinolytic activity in the gastric juice. Although the FSF must be very low (<1%) if it is to cause bleedings, the low levels in these patients with many other coexisting disturbances in the coagulation system and/or an increased fibrinolytic activity most probably contribute to the increased bleeding tendency in such patients.

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“…Its activity is inhibited by SHinhibitors (Loewy & Edsell 1954), such as iodoacetamide (IAA), and transamidase inhibitors (Lorand et al 1966), such as glycinemethylester (GME). Inborn and acquired deficiencies of FSF activity are described (Duckert 1965, Nussbaum & Morse 1964.…”

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confidence: 99%

Plasmin Digestion of Stabilized and Non‐Stabilized Fibrin Illustrated by Immunoelectrophoresis and Haemagglutination Inhibiton Immuno Assays

Feddersen

Gormsen

1971

Scandinavian Journal of Haematology

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Digestion of stabilized and non‐stabilized fibrin in clots made from isolated fibrinogen, contaminated by fibrin stabilizing factor (FSF), and plasma is evaluated qualitatively by Immunoelectrophoresis and quantitatively by haemagglutination inhibition immuno assays (HIIA). Non‐stabilized systems are obtained by means of SH‐ and transamidase inhibitors and, in plasma systems, also by genuine FSF‐decient plasma. Stabilized and non‐stabilized fibrin in fibrin clots is easily degradated by plasmin (porcine) to the final D and E antigenic fragments, which are non‐reactive in HIIA. Stabilized fibrin in plasma clots is rather resistant to activator‐induced lysis, as antigenic intermediates, reactive in HIIA, remain even after sustained activator (+ plas‐minogen)‐induced lysis. These intermediates are degradated by high concentrations of plasmin to the final breakdown products, non‐reactive in HIIA.

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Plasma Fibrin Stabilizing Factor Activity in Various Diseases

Cited by 76 publications

References 8 publications

The Mechanism of Enhanced Streptokinase‐Induced Clot Lysis following In‐vitro Factor‐XIII Inactivation

The Mechanism of Enhanced Streptokinase‐Induced Clot Lysis following In‐vitro Factor‐XIII Inactivation

Factor XIII in a Clinical Material

Plasmin Digestion of Stabilized and Non‐Stabilized Fibrin Illustrated by Immunoelectrophoresis and Haemagglutination Inhibiton Immuno Assays

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