Fibrin-related Antigen Research Articles

Preoperative prediction of postoperative deep vein thrombosis.

A range of clinical data was obtained from 124 patients about to undergo operation and several coagulation tests were performed. No patient received prophylaxis for deep vein thrombosis, and isotopic scanning after operation showed that 20 patients had developed thrombosis. a simiple prognostic index for predicting which patients would develop postoperative deep vein thrombosis was constructed using the clinical and coagulation data obtained before operation. The five variables with the best predictive power-euglobulin lysis time, age, presence of varicose veins, fibrin related antigen, and percentage overweight-produced an equation that identfied 95% of those who developed deep vein thrombosis and misallocated only 28% of those who did not develop thrombosis. In view of the complications that low-dose heparin and dextran can cause, giving prophylaxis to under a third of the patients who will not develop deep vein thrombosis is clearly better than giving it to all.

Inhibition of Fibrinolysis in the Burned-Infected Rat: Antiplasmin Induced by Burn Wound Infection

SummaryInfection is the leading cause of death in the burned patient. To study the effects of uncomplicated and lethally-infected burn wounds on certain hematologic indices, a dorsal scald burn was administered to 250 rats. One group was then infected with Pseudomonas aeruginosa. These rats expired within 10 days. A burned, uninfected, group survived. Sequential determinations were made of fibrinogen, fibrinolysis, antiplasmins, plasminogen antiactivators, cultures, and autopsy findings.Fibrinogen concentrations were higher in the infected animals within 2 days postbum and at day 3 (p <0.05). Plasminogen levels fell precipitously 3 days postburn in the burned-infected group. Acid neutralization of antiplasmins was not entirely effective. Serum from infected animals markedly prolonged the lysis time of clots in a standard test system, lowered plasmin activity in the caseinolytic assay, and transiently prolonged the euglobulin lysis time.The cause of these findings remains unknown. The marked fall in plasminogen in the infected animals may be entirely due to unneutralized antiplasmin activity and was coincident with a decline in fibrin-related antigens. These antiplasmins may exert deleterious effects on microcirculatory dynamics and were closely linked to the animals’ demise.

Defibrination after brain-tissue destruction: A serious complication of head injury.

Abstract A prospective study was conducted to evaluate defibrination after acute head trauma. Defibrination was not observed in 13 patients In whom trauma apparently did not destroy brain tissue. In contrast, evidence of defibrination — hypofibrinogenemia, elevated levels of serum fibrinogen-related or fibrin-related antigen and low levels of factors V, VIII or platelets — was found in nine of 13 patients in whom brain-tissue destruction was established by direct inspection. All nine patients had a strongly positive protamine test, suggesting that intravascular coagulation had occurred. Since test results returned toward normal within hours, the active phase of defibrination apparently was brief. Nevertheless, hemostatic abnormalities were severe enough to have affected the neurologic consequences of intracranial bleeding. Clinical findings attributable to fibrin in the microcirculation (e.g., microangiopathic hemolytic anemia or renal failure) were not encountered. The potentially salvageable patient wit...

Fibrin lysis by thrombin elevating levels of fibrinogen and fibrin-related antigen (FR-antigen) in human serum as shown by Auto Analyzer assay.

Fibrin lysis by thrombin elevating levels of fibrinogen and fibrin-related antigen (FR-antigen) in human serum as shown by Auto Analyzer assay.

Increase in fibrinogen and fibrin-related antigen in human serum due to in vitro lysis of fibrin by thrombin.

In vitro lysis of fibrin, as indicated by increased fibrinogen-fibrin-related antigen (FR-antigen) in serum is usually seen when whole blood, or plasma, or highly purified fibrinogen prepared by several different procedures is clotted and kept at temperatures above 0 degrees C. This increase is both time and temperature dependent, occurs despite the addition of various plasmin and cathepsin inhibitors, and is probably caused by thrombin evolved during clotting and/or added in vitro. In these experiments, the FR-antigen was measured by a sensitive, reproducible hemagglutination inhibition immunoassay adapted to the AutoAnalyzer. Serum from whole blood contained more than serum from plasma, and fibrin rather than fibrinogen proved to be essential for the in vitro lysis. The phenomenon was also caused by Arvin or Reptilase, suggesting that splitting of one or more arginine or lysine bonds in fibrin may be at least partially responsible. To obtain minimal levels of FR-antigen (< 0.5 mug/ml), plasma is clotted for 4 hr at 0 degrees C with 1.0-5.0 U/ml thrombin, CaCl(2) (0.0125 mole/liter), and epsilon aminocaproic acid (0.05 mole/liter). Slightly higher levels, probably adequate for clinical diagnosis, are obtained by 10-30 min clotting at room temperature. Since endogenous and/or exogenous thrombin is essential for the collection of serum FR-antigen, all the FR-antigen found in normal serum probably results from an irreducible amount of in vitro lysis rather than from continuous intravascular clotting and fibrinolysis.