scholarly journals Fibrinopeptide A (FPA) Levels in Venous Thrombosis and Pulmonary Embolism Before and During Anticoagulant Therapy

1977 ◽  
Author(s):  
I. Yudelman ◽  
H. L. Nossel ◽  
K. L. Kaplan ◽  
J. Hirsh
Keyword(s):  
Venous Thrombosis ◽  
Anticoagulant Therapy ◽  
Heparin Therapy ◽  
Fibrinopeptide A ◽  
Normal Range ◽  
Monitoring Therapy ◽  
Asymptomatic Patients ◽  
Initial Symptoms ◽  
Lung Scan ◽  
Marked Drop

FPA levels were measured in 60 patients subjected to venography and to lung scan for symptoms suggestive of venous thromboembolism. In all 23 patients with negative venography and/or lung scan, FPA levels were in the normal range (<1.3 pmol/ml, mean 0.6 pmol/ml). The FPA levels were elevated in 34 of the 37 patients with a positive lung scan and/or venogram. The range was 0.4–112 pmol/ml, median 6.2 pmol/ml. The FPA levels were measured serially in patients with confirmed thromboembolism who were treated with heparin. In 14 of the 15 patients there was a marked drop in FPA levels in the first 15 minutes after the initial dose of heparin. In 1 patient the FPA levels only reached the normal range after 48 hours of heparin therapy. FPA levels were measured daily in 10 patients while on anticoagulant therapy. In 4 patients FPA levels became normal and remained so and no symptoms recurred. In the other 6 patients there were 13 episodes of FPA elevations.10 of these were preceded by a recurrence of the initial symptoms. In one patient FPA elevations occurred in the absence of symptoms while the repeat lung scan showed new lesions. Suboptimal anticoagulation and/or the transition from heparin to Coumadin preceded the recurrence of symptoms in 6 out of 10 episodes. FPA levels were frequently normal in asymptomatic patients with evidence of venous thrombosis as shown byfibrinogen uptake scan. These results suggest that FPA measurements may be useful in the diagnosis and in monitoring therapy of symptomatic thromboembolism.

scholarly journals Factors affecting fibrinopeptide-A levels in patients with venous thromboembolism during anticoagulant therapy

Blood ◽  
1982 ◽  
Vol 59 (4) ◽  
pp. 787-792 ◽  
Author(s):  
I Yudelman ◽  
J Greenberg
Keyword(s):  
Pulmonary Embolism ◽  
Disease Activity ◽  
Normal Values ◽  
Heparin Therapy ◽  
Fibrinopeptide A ◽  
Minimal Resolution ◽  
Factors Affecting ◽  
Monitoring Therapy ◽  
Lung Scan ◽  
The Mean

Abstract The prompt reduction of elevated fibrinopeptide A (FPA) levels (normal less than 1.3 pmole/ml) by heparin therapy in patients with thromboembolism suggests that measuring the FPA level may provide a good index of disease activity and be a useful method of monitoring therapy. Sepsis or malignancy may elevate FPA levels and coexist with thromboembolism. FPA levels were surveyed in 51 patients with thromboembolism (including 15 with concurrent sepsis or malignancy) during heparin treatment in an attempt to distinguish the effects of coexistent disease and the progression of thromboembolism. The anticoagulant effect of heparin was within the therapeutic range for 81% of the study period. In patients with thromboembolism alone and marked resolution of emboli on repeat lung scan, the mean daily FPA levels were lower than the values in patients with minimal resolution (p less than 0.005). In patients with marked resolution of pulmonary embolism or venous thrombosis and a concurrent disorder, the mean FPA level remained elevated compared to normal values in patients with thromboembolism alone. These results suggest that FPA levels monitored during heparin therapy of thromboembolism may be useful as an index of disease activity except in the presence of coexisting sepsis or malignancy.

scholarly journals Factors affecting fibrinopeptide-A levels in patients with venous thromboembolism during anticoagulant therapy

Blood ◽  
1982 ◽  
Vol 59 (4) ◽  
pp. 787-792
Author(s):  
I Yudelman ◽  
J Greenberg
Keyword(s):  
Pulmonary Embolism ◽  
Disease Activity ◽  
Normal Values ◽  
Heparin Therapy ◽  
Fibrinopeptide A ◽  
Minimal Resolution ◽  
Factors Affecting ◽  
Monitoring Therapy ◽  
Lung Scan ◽  
The Mean

The prompt reduction of elevated fibrinopeptide A (FPA) levels (normal less than 1.3 pmole/ml) by heparin therapy in patients with thromboembolism suggests that measuring the FPA level may provide a good index of disease activity and be a useful method of monitoring therapy. Sepsis or malignancy may elevate FPA levels and coexist with thromboembolism. FPA levels were surveyed in 51 patients with thromboembolism (including 15 with concurrent sepsis or malignancy) during heparin treatment in an attempt to distinguish the effects of coexistent disease and the progression of thromboembolism. The anticoagulant effect of heparin was within the therapeutic range for 81% of the study period. In patients with thromboembolism alone and marked resolution of emboli on repeat lung scan, the mean daily FPA levels were lower than the values in patients with minimal resolution (p less than 0.005). In patients with marked resolution of pulmonary embolism or venous thrombosis and a concurrent disorder, the mean FPA level remained elevated compared to normal values in patients with thromboembolism alone. These results suggest that FPA levels monitored during heparin therapy of thromboembolism may be useful as an index of disease activity except in the presence of coexisting sepsis or malignancy.

The Influence of Acenocumarole on the Fibrinogen-turnover in Normal Subjects, Venous Thrombosis and Congestive Heart Failure

1972 ◽  
Vol 28 (03) ◽  
pp. 496-508
Author(s):  
A. P. C. van der Maas ◽  
F. A. G Teulings ◽  
W Schopman ◽  
G. J. H. den Ottolander
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Venous Thrombosis ◽  
Anticoagulant Therapy ◽  
Normal Subjects ◽  
Time Interval ◽  
Normal Range ◽  
The Mean ◽  
The Moment ◽  
Continuous Deposition

SummaryUsing 131Iodine-tagged fibrinogen the influence of acenocumarole on the biological half-life of fibrinogen was investigated in healthy patients, patients with venous thrombosis and patients with congestive heart failure.In 16 healthy patients the mean t½ was 3.8 days. In two of them after administration of acenocumarole the t½ was lengthened. This supports the opinion of a continuous deposition of fibrin on the vascular endothelium in the hemostatic balance.In 13 patients with venous thrombosis the mean t½ was 2.45 days, lengthening to the normal range after acenocumarole therapy. The time interval between the start of acenocumarole therapy and the moment of normalization of the t½ was approximately 4 days. The prothrombin time-index at this moment was 2.3 (thrombotest 5%), which argues in favour of a vigorous anticoagulant therapy.In our 10 patients with congestive heart failure probably venous thrombosis occurred in 40%. Prophylactic anticoagulant therapy as in surgical patients therefore has to be considered.

The Relevance of Blood Tests in the Management of Thromboembolism

1979 ◽  
Author(s):  
Hymie L. Nossel
Keyword(s):  
Pulmonary Embolism ◽  
Quantitative Information ◽  
Diagnostic Techniques ◽  
Fibrinopeptide A ◽  
Normal Range ◽  
New Techniques ◽  
Blood Tests ◽  
Biochemical Event ◽  
Intravenous Heparin ◽  
Lung Scan

Fibrinopeptide A (FPA) levels reflect fibrin I formed by thrombin proteolysis of fibrinogen - a single biochemical event in fibrin formation and thrombosis. Studies in symptomatic patients suspected of venous thromboembolism (TE) demonstrated a good correlation in 40/45 patients between elevated FPA levels and the presence of thrombosis and/or pulmonary embolism indicated by venogram and/or lung scan and in 50/55 patients between normal FPA levels and the absence of TE. Within 15 minutes of intravenous heparin in 30 patients with documented TE, FPA levels had reached the normal range. In 3 of 17 patients studied over 10 days of anticoagulant therapy elevated FPA levels were associated with recurrence or extension of embolism. Thus, plasma FPA measurements may be useful in the diagnosis and management of venous TE. A second biochemical event - fragment X formation by plasmin cleavage of the Aα and N-terminal Bऔ chains of fibrinogen - can be monitored as thrombinincreasable fibrinopeptide B immunoreactivity. Initial studies suggest imbalance between thrombin and plasmin action favoring thrombin during the inception of thrombosis and favoring plasmin during resolution. The use of these tests is providing specific and quantitative information concerning biochemical reactions associated with clinical TE. In correlation with 125I-fibrinogen scanning and conventional diagnostic techniques, these tests will provide basic pathophysiological understanding which will facilitate the development and use of new techniques in diagnosis, prediction and management of venous TE.

scholarly journals Rapid anticoagulation using ancrod for heparin-induced thrombocytopenia [see comments]

Blood ◽  
1991 ◽  
Vol 78 (9) ◽  
pp. 2194-2197
Author(s):  
C Demers ◽  
JS Ginsberg ◽  
P Brill-Edwards ◽  
A Panju ◽  
TE Warkentin ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Anticoagulant Therapy ◽  
Bleeding Episode ◽  
Heparin Therapy ◽  
Heparin Induced Thrombocytopenia ◽  
Normal Platelet ◽  
Reasonable Approach ◽  
History Of ◽  
Recurrent Venous Thrombosis ◽  
Phlegmasia Cerulea Dolens

In order to determine the efficacy and safety of ancrod, a rapid acting defibrinogenating drug, for patients with heparin-induced thrombocytopenia, 11 consecutive patients who required anticoagulant therapy because of venous thromboembolism and who developed acute heparin-induced thrombocytopenia or had a history of heparin-induced thrombocytopenia were treated with ancrod. Heparin therapy was discontinued (in patients receiving heparin) and ancrod started at a dose of 1 to 2 U/kg every 24 hours with subsequent daily doses adjusted to maintain fibrinogen levels between 0.5 and 1.0 g/L. Ancrod was continued until warfarin had become effective. The platelet count increased to more than 150 x 10(9)/L within 2 to 10 days in all thrombocytopenic patients. Two patients with a history of heparin- induced thrombocytopenia maintained normal platelet counts while receiving ancrod. Two patients had recurrent venous thrombosis while receiving warfarin, 10 days after ancrod was discontinued: one of these patients had metastatic pancreatic carcinoma and developed phlegmasia cerulea dolens and the other patient developed a venographically proven extension of her deep venous thrombosis. One patient suffered a bleeding episode into the thigh with a 16-g/L decrease in her hemoglobin level while receiving ancrod therapy. No other side effects were noted. Our experience indicates that ancrod therapy is a reasonable approach for patients with heparin-induced thrombocytopenia who require anticoagulant therapy.

scholarly journals Rapid anticoagulation using ancrod for heparin-induced thrombocytopenia [see comments]

Blood ◽  
1991 ◽  
Vol 78 (9) ◽  
pp. 2194-2197 ◽  
Author(s):  
C Demers ◽  
JS Ginsberg ◽  
P Brill-Edwards ◽  
A Panju ◽  
TE Warkentin ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Anticoagulant Therapy ◽  
Bleeding Episode ◽  
Heparin Therapy ◽  
Heparin Induced Thrombocytopenia ◽  
Normal Platelet ◽  
Reasonable Approach ◽  
History Of ◽  
Recurrent Venous Thrombosis ◽  
Phlegmasia Cerulea Dolens

Abstract In order to determine the efficacy and safety of ancrod, a rapid acting defibrinogenating drug, for patients with heparin-induced thrombocytopenia, 11 consecutive patients who required anticoagulant therapy because of venous thromboembolism and who developed acute heparin-induced thrombocytopenia or had a history of heparin-induced thrombocytopenia were treated with ancrod. Heparin therapy was discontinued (in patients receiving heparin) and ancrod started at a dose of 1 to 2 U/kg every 24 hours with subsequent daily doses adjusted to maintain fibrinogen levels between 0.5 and 1.0 g/L. Ancrod was continued until warfarin had become effective. The platelet count increased to more than 150 x 10(9)/L within 2 to 10 days in all thrombocytopenic patients. Two patients with a history of heparin- induced thrombocytopenia maintained normal platelet counts while receiving ancrod. Two patients had recurrent venous thrombosis while receiving warfarin, 10 days after ancrod was discontinued: one of these patients had metastatic pancreatic carcinoma and developed phlegmasia cerulea dolens and the other patient developed a venographically proven extension of her deep venous thrombosis. One patient suffered a bleeding episode into the thigh with a 16-g/L decrease in her hemoglobin level while receiving ancrod therapy. No other side effects were noted. Our experience indicates that ancrod therapy is a reasonable approach for patients with heparin-induced thrombocytopenia who require anticoagulant therapy.

scholarly journals Fibrinopeptide a Measurements in the Study of Thrombosis

1977 ◽  
Author(s):  
H.L. Nossel
Keyword(s):  
Arterial Thrombosis ◽  
Vessel Wall ◽  
Heparin Therapy ◽  
Coagulation System ◽  
Fibrinopeptide A ◽  
Elevated Plasma ◽  
Normal Range ◽  
Diseased Vessel ◽  
Relationship Of ◽  
The Relationship

Elevated plasma fibrinopeptide A (FPA) levels have been found in all patients with acute (symptoms for 5 days or less) venous or arterial thrombosis and/or embolism studied in our institution. Heparin therapy results in a decline of fibrinopeptide A levels to the normal range. In most instances the normal level is attained within 15 minutes of the start of therapy but in some instances return to normal is delayed for up to 72 hours.FPA levels have not been tested in a formal study on the prediction of thrombosis. The results will be presented of serial FPA measurements and the relationship of FPA elevations to recurrence of symptoms and. extension of the disease in patients with thrombo-embolism. The usefulness of FPA tests in the diagnosis of prethrombotic states will depend on the pathophysiology of these states.Measurement of FPA levels may be useful in predicting thrombosis under circumstances in which activation of the coagulation system precedes thrombosis. When thrombosis results from the reaction of normal blood with diseased vessel wall FPA levels will not be useful in prediction.Since- the pathogenesis of thrombosis is likely to vary in different syndromes, the pathophysiology of these syndromes will have to be investigated separately to answer questions as to the usefulness of such tests in prediction.

Prospective Study on the Usefulness of Lung Scan in Patients with Deep Vein Thrombosis of the Lower Limbs

2001 ◽  
Vol 85 (05) ◽  
pp. 771-774 ◽  
Author(s):  
Joan Ruiz ◽  
Manuel Fraile ◽  
Montserrat Bonet ◽  
Ester Davant ◽  
Jordi Muchart ◽  
...  
Keyword(s):  
Prospective Study ◽  
Anticoagulant Therapy ◽  
Vena Cava ◽  
Blood Gases ◽  
Heparin Therapy ◽  
Clinical Suspicion ◽  
Lower Limbs ◽  
Common Finding ◽  
Arterial Blood ◽  
Lung Scan

Summary Background: Asymptomatic pulmonary embolism (PE) is a common finding in patients with deep venous thrombosis (DVT) of the lower limbs, but the usefulness of seeking for silent PE in patients with acute DVT has not been evaluated. Patients and methods: This was a prospective study involving consecutive patients with acute symptomatic proximal DVT (confirmed by objective methods) and no clinical suspicion of PE. All patients underwent chest X-ray, ventilation-perfusion lung scan and arterial blood gases on admission, and received anticoagulant therapy. Those with scintigraphic evidence of PE underwent repeated lung scan and blood gases 7 days later. The aim of the study was to assess how many patients with silent PE develop symptoms while on heparin therapy, and in how many of them such symptoms are due to recurrent PE. Results: 946 consecutive patients with acute, proximal DVT had no contraindications to full-dose anticoagulant therapy. Baseline lung scan revealed high-probability defects (silent PE) in 200 (21%). Seven of these 200 patients had symptomatic recurrences during the 7-day study period, and an inferior vena cava filter was inserted. Besides, 6 patients developed PE symptoms, but no new perfusion defects were found on repeated scan. They switched to coumarin therapy, and they did not develop any further complications. Conclusions: Lung scan in patients with symptomatic DVT and no clinical suspicion of PE may be useful, since some patients with silent PE may develop symptoms while on heparin therapy. Without a baseline scintigraphy all these patients would have been considered to have recurrent PE, and vena cava interruption could have been performed.

Relationship Between Fibrinopeptide A and Fibrinogen/Fibrin Fragment E in Thromboembolism, DIC and Various Non-Thromboembolic Diseases

1987 ◽  
Vol 58 (02) ◽  
pp. 758-763 ◽  
Author(s):  
G Mombelli ◽  
R Monotti ◽  
A Haeberli ◽  
P W Straub
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Liver Cirrhosis ◽  
Healthy Subjects ◽  
Vascular Diseases ◽  
Fibrinopeptide A ◽  
Normal Range ◽  
Collagen Vascular Diseases ◽  
Intravascular Coagulation ◽  
Fibrin Formation

SummaryIncreased fibrinopeptide A (FPA) levels have been reported in various non-thrombotic disorders, including cancer, acute myocardial infarction, liver cirrhosis and collagen vascular diseases. To investigate the significance of these findings, the present study combined the radioimmunoassay of FPA with that of fibrinogen/fibrin degradation fragment E (FgE) in the aforementioned disorders and compared the results with those observed in healthy subjects as well as in patients with thromboembolism and overt disseminated intravascular coagulation (DIC). Mean FPA and FgE in malignancy were 6.3 and 305 ng/ml, in myocardial infarction 5.6 and 98 ng/ml, in liver cirrhosis 2.7 and 132 ng/ml and in collagen vascular diseases 5.6 and 142 ng/ml. All these values were significantly higher than in healthy controls (mean FPA 1.6 ng/ml, mean FgE 49 ng/ml) but significantly lower than in thromboembolism (mean FPA 10.7 ng/ml, mean FgE 639 ng/ ml) and DIC (mean FPA 22.0 ng/ml, mean FgE 1041 ng/ml). The overall correlation between FPA and FgE was highly significant. Elowever, different disorders showed peculiar patterns in FPA, FgE and fibrinogen levels. In malignancy, a definite increase of FPA, FgE and plasma fibrinogen levels was observed. This finding probably indicates a compensated state of (intra- or extravascular) fibrin formation and lysis. Acute myocardial infarction was characterized by a high FPA to FgE ratio, which is interpreted to reflect acute thrombin generation and fibrin formation. FPA in cirrhosis was only marginally elevated with most single values within the normal range, indicating that intravascular coagulation was infrequent and unimportant in quantitative terms.

Hereditary Heparin Cofactor II Deficiency and the Risk of Development of Thrombosis

1987 ◽  
Vol 57 (02) ◽  
pp. 196-200 ◽  
Author(s):  
R M Bertina ◽  
I K van der Linden ◽  
L Engesser ◽  
H P Muller ◽  
E J P Brommer
Keyword(s):  
Liver Disease ◽  
Venous Thrombosis ◽  
Healthy Volunteers ◽  
Mean Value ◽  
Age Group ◽  
Normal Range ◽  
Heparin Cofactor Ii ◽  
History Of ◽  
Group 2 ◽  
Hereditary Nature

SummaryHeparin cofactor II (HC II) levels were measured by electroimmunoassay in healthy volunteers, and patients with liver disease, DIC, proteinuria or a history of venous thrombosis. Analysis of the data in 107 healthy volunteers revealed that plasma HC II increases with age (at least between 20 and 50 years). HC II was found to be decreased in most patients with liver disease (mean value: 43%) and only in some patients with DIC. Elevated levels were found in patients with proteinuria (mean value 145%). In 277 patients with a history of unexplained venous thrombosis three patients were identified with a HC II below the lower limit of the normal range (60%). Family studies demonstrated hereditary HC II deficiency in two cases. Among the 9 heterozygotes for HC II deficiency only one patient had a well documented history of unexplained thrombosis. Therefore the question was raised whether heterozygotes for HC II deficiency can also be found among healthy volunteers. When defining a group of individuals suspected of HC II deficiency as those who have a 90% probability that their plasma HC II is below the 95% tolerance limits of the normal distribution in the relevant age group, 2 suspected HC II deficiencies were identified among the healthy volunteers. In one case the hereditary nature of the defect could be established.It is concluded that hereditary HC II deficiency is as prevalent among healthy volunteers as in patients with thrombotic disease. Further it is unlikely that heterozygosity for HC II deficiency in itself is a risk factor for the development of venous thrombosis.

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