Relationship between fibrinopeptide A and fibrinogen/fibrin fragment E in thromboembolism, DIC and various non-thromboembolic diseases. 1987

G Mombelli, and R Monotti, and A Haeberli, and P W Straub
Ospedale La Carità, Locarno, Switzerland.

Increased 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. However, 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.

UI MeSH Term Description Entries
D008103 Liver Cirrhosis Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules. Cirrhosis, Liver,Fibrosis, Liver,Hepatic Cirrhosis,Liver Fibrosis,Cirrhosis, Hepatic
D009203 Myocardial Infarction NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION). Cardiovascular Stroke,Heart Attack,Myocardial Infarct,Cardiovascular Strokes,Heart Attacks,Infarct, Myocardial,Infarction, Myocardial,Infarctions, Myocardial,Infarcts, Myocardial,Myocardial Infarctions,Myocardial Infarcts,Stroke, Cardiovascular,Strokes, Cardiovascular
D009369 Neoplasms New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms. Benign Neoplasm,Cancer,Malignant Neoplasm,Tumor,Tumors,Benign Neoplasms,Malignancy,Malignant Neoplasms,Neoplasia,Neoplasm,Neoplasms, Benign,Cancers,Malignancies,Neoplasias,Neoplasm, Benign,Neoplasm, Malignant,Neoplasms, Malignant
D003095 Collagen Diseases Historically, a heterogeneous group of acute and chronic diseases, including rheumatoid arthritis, systemic lupus erythematosus, progressive systemic sclerosis, dermatomyositis, etc. This classification was based on the notion that "collagen" was equivalent to "connective tissue", but with the present recognition of the different types of collagen and the aggregates derived from them as distinct entities, the term "collagen diseases" now pertains exclusively to those inherited conditions in which the primary defect is at the gene level and affects collagen biosynthesis, post-translational modification, or extracellular processing directly. (From Cecil Textbook of Medicine, 19th ed, p1494) Collagen Disease,Disease, Collagen,Diseases, Collagen
D004211 Disseminated Intravascular Coagulation A disorder characterized by procoagulant substances entering the general circulation causing a systemic thrombotic process. The activation of the clotting mechanism may arise from any of a number of disorders. A majority of the patients manifest skin lesions, sometimes leading to PURPURA FULMINANS. Consumption Coagulopathy,Coagulation, Disseminated Intravascular,Disseminated Coagulation, Intravascular,Intravascular Coagulation, Disseminated,Intravascular Disseminated Coagulation,Coagulation, Intravascular Disseminated,Coagulations, Disseminated Intravascular,Coagulations, Intravascular Disseminated,Coagulopathies, Consumption,Coagulopathy, Consumption,Consumption Coagulopathies,Disseminated Coagulations, Intravascular,Disseminated Intravascular Coagulations,Intravascular Coagulations, Disseminated,Intravascular Disseminated Coagulations
D005338 Fibrin Fibrinogen Degradation Products Soluble protein fragments formed by the proteolytic action of plasmin on fibrin or fibrinogen. FDP and their complexes profoundly impair the hemostatic process and are a major cause of hemorrhage in intravascular coagulation and fibrinolysis. Antithrombin VI,Fibrin Degradation Product,Fibrin Degradation Products,Fibrin Fibrinogen Split Products,Degradation Product, Fibrin,Degradation Products, Fibrin,Product, Fibrin Degradation
D005340 Fibrinogen Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. Coagulation Factor I,Factor I,Blood Coagulation Factor I,gamma-Fibrinogen,Factor I, Coagulation,gamma Fibrinogen
D005344 Fibrinopeptide A Two small peptide chains removed from the N-terminal segment of the alpha chains of fibrinogen by the action of thrombin during the blood coagulation process. Each peptide chain contains 18 amino acid residues. In vivo, fibrinopeptide A is used as a marker to determine the rate of conversion of fibrinogen to fibrin by thrombin. Fibrinopeptides A
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D013923 Thromboembolism Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream. Thromboembolisms

Related Publications

G Mombelli, and R Monotti, and A Haeberli, and P W Straub
January 1977, Acta clinica Belgica,
G Mombelli, and R Monotti, and A Haeberli, and P W Straub
April 2002, Thrombosis and haemostasis,
G Mombelli, and R Monotti, and A Haeberli, and P W Straub
February 1981, Thrombosis research,
G Mombelli, and R Monotti, and A Haeberli, and P W Straub
April 1974, The British journal of surgery,
G Mombelli, and R Monotti, and A Haeberli, and P W Straub
January 1976, VASA. Zeitschrift fur Gefasskrankheiten,
G Mombelli, and R Monotti, and A Haeberli, and P W Straub
March 1976, The Journal of biological chemistry,
G Mombelli, and R Monotti, and A Haeberli, and P W Straub
February 1993, Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis,
G Mombelli, and R Monotti, and A Haeberli, and P W Straub
August 1980, Thrombosis research,
G Mombelli, and R Monotti, and A Haeberli, and P W Straub
January 1983, Bibliotheca haematologica,
G Mombelli, and R Monotti, and A Haeberli, and P W Straub
August 1978, Scandinavian journal of respiratory diseases,
Copied contents to your clipboard!