fibrinopeptide-a and Acute-Disease

Topics: Acute Disease; Blood Coagulation; Coronary Disease; Death, Sudden, Cardiac; Fibrinolysis; Fibrinopeptide A; Humans; Plasminogen Inactivators

1. The concentration in plasma of fibrinogen derivatives fibrinopeptide A (FPA) and B beta 1-42 and the platelet release products beta-thromboglobulin (beta TG) and platelet factor 4 (PF4) have been determined in patients with acute and chronic liver disease. 2. In 21 patients with fulmiant hepatic failure on admission in grade III or IV coma the plasma FPA, B beta 1-42, beta TG and PF4 levels were significantly increased compared with those in normal control subjects. On heparinization before haemoperfusion the FPA levels returned to the normal range and during resin and charcoal haemoperfusion there were no significant changes in the coagulation or platelet factors, except for a small increase in FPA with charcoal haemoperfusion. 3. In ten patients with compensated chronic liver disease there was a significant increase in B beta 1-42 and beta TG levels but not FPA and PF4 as compared with normal controls. 4. Interpretation of the results is complicated by the possible reduced clearance of these proteins as a result of renal failure in some of the patients with fulminant hepatic failure and also by the damaged liver itself. However, these results have confirmed that disseminated intravascular coagulation can occur in both acute and chronic liver disease.

Topics: Acute Disease; Adolescent; Adult; Aged; beta-Thromboglobulin; Chronic Disease; Female; Fibrin Fibrinogen Degradation Products; Fibrinopeptide A; Fibrinopeptide B; Hemoperfusion; Humans; Liver Diseases; Male; Middle Aged; Peptide Fragments; Platelet Factor 4

Topics: Acute Disease; Adolescent; Adult; Child; Fibrinogen; Fibrinopeptide A; Humans; Malaria, Falciparum; Nigeria; Parasitemia; Partial Thromboplastin Time; Platelet Count; Prothrombin Time

Optimal anti-thrombotic therapy for acute coronary syndromes (ACS) should suppress pro-thrombotic activity at the site of plaque rupture. We sought to determine whether platelet reactivity is increased in blood in the immediate vicinity of a ruptured plaque and is apparent even when blood is obtained by sampling from a catheter placed proximal to the lesion.. Blood was obtained from a catheter placed in the aorta and from the same catheter after engaging the culprit coronary artery. Platelet reactivity was determined with the use of flow cytometry by surface expression of P-selectin.. In preliminary studies we demonstrated that a marker of thrombin activity, fibrinopeptide A, was similarly increased in blood taken from the coronary sinus and coronary arterial ostium of patients with ACS. Subsequently blood was obtained from the aorta and coronary arterial ostium through a coronary guide catheter for assessment of platelet reactivity in 23 subjects with ACS and 22 subjects with stable angina. The percentage of platelets expressing P-selectin in response to 0.2 microM adenosine diphosphate (ADP) was greater in coronary arterial samples from patients with ACS (aorta=6.1+/-1%, coronary artery=8.8+/-1.6%, p=0.02) compared with that in patients with stable symptoms (aorta=6.9+/-1.2, coronary artery=6.5+/-1.4, p=NS).. Coronary arterial blood obtained from the ostium through a coronary guide catheter can be used to determine whether thrombin activity and platelet reactivity are increased in the immediate vicinity of a ruptured atherosclerotic plaque. The simplicity of the approach developed should facilitate its use in future studies designed to determine the impact of optimal suppression of platelet reactivity and the pro-thrombotic state before coronary interventions on short- and long-term clinical outcomes.

Topics: Acute Disease; Aged; Aorta; Case-Control Studies; Coronary Artery Disease; Coronary Circulation; Coronary Vessels; Fibrinolytic Agents; Fibrinopeptide A; Humans; Male; Middle Aged; P-Selectin; Platelet Activation; Rupture, Spontaneous; Thrombophilia

To evaluate the role of the coagulation and fibrinolysis abnormalities in the pathogenesis of ischemic stroke of undetermined etiology, we assayed plasma concentration of fibrinopeptide-A and thrombin-antithrombin III complex, both sensitive markers for thrombin activation and fibrin formation, and D-dimer, a marker of plasmin activity and fibrinolysis. Hemostatic markers were measured in 32 patients with acute stroke and 20 patients with chronic stroke, and compared with 21 normal subjects. Fibrinopeptide-A and thrombin-antithrombin III complex levels were not elevated significantly, whereas the D-dimer level was markedly raised in acute (p<0.001) and chronic (p<0.05) phases of ischemic stroke in comparison with the control group. Prolonged elevation of D-dimer concentration suggests that hemostatic abnormalities have a primary role in the pathogenesis of ischemic stroke. The measurement of D-dimer concentration may help to better decide the indications for therapy of the patients with ischemic stroke of undetermined etiology.

Topics: Acute Disease; Adult; Aged; Aged, 80 and over; Antithrombin III; Biomarkers; Brain Ischemia; Female; Fibrin Fibrinogen Degradation Products; Fibrinopeptide A; Hemostasis; Humans; Male; Middle Aged; Peptide Hydrolases; Thrombophilia

Given that the restoration of sinus rhythm after chronic atrial fibrillation is associated with embolic events, anticoagulation is prescribed before and after pharmacological and electrical cardioversion. However, the need for anticoagulation in patients with acute atrial fibrillation (lasting <48 hours) who undergo cardioversion is less clear. In addition, it is not known whether cardioversion to sinus rhythm determines a hypercoagulable state in these patients.. In 21 patients with acute nonvalvular atrial fibrillation, plasma median concentrations of thrombin-antithrombin complex, a marker of thrombin generation, significantly increased from 2.8 ng/mL (interquartile range, 2.1 to 4.0 ng/mL) on hospital admission to 3.5 ng/mL (interquartile range, 2.9 to 6.0 ng/mL) after cardioversion to sinus rhythm obtained by means of infusion of antiarrhythmic drugs and decreased to 2.5 ng/mL (interquartile range, 2.0 to 3.5 ng/mL) at the 1-month follow-up visit (P=.04). Similarly, the levels of fibrinopeptide A, a marker of thrombin activity, increased from 1.1 nmol/L (interquartile range, 0.7 to 1.5 nmol/L) at baseline to 1.8 nmol/L (interquartile range, 1.1 to 3.0 nmol/L) after cardioversion and returned to 0.8 nmol/L (interquartile range, 0.6 to 1.1 nmol/L) at the 1-month follow-up visit (P=.02).. A significant increase in plasma levels of the markers of thrombin generation and activity was observed in patients with acute atrial fibrillation early after pharmacological cardioversion to sinus rhythm. This is the first biochemical evidence that cardioversion of recent-onset atrial fibrillation determines a hypercoagulable state.

Topics: Acute Disease; Amiodarone; Anti-Arrhythmia Agents; Antithrombin III; Atrial Fibrillation; Biomarkers; Disease Susceptibility; Female; Fibrinopeptide A; Flecainide; Hemostasis; Humans; Male; Middle Aged; Peptide Hydrolases; Propafenone; Thrombin; Thromboembolism

Intravenous heparin, a fundamental therapy in the treatment of patients with acute coronary syndromes, acts by inhibiting thrombin and activated factors X, IX, XI, and XII. It has also been demonstrated that heparin reduces plasma fibrinopeptide A, a marker of thrombin activity, but it is unknown whether it decreases prothrombin fragment 1+2, an indirect marker of thrombin generation. We measured the plasma levels of prothrombin fragment 1+2, fibrinopeptide A, and antithrombin III in 64 consecutive patients with unstable angina or myocardial infarction receiving intravenous heparin. Blood samples were obtained at baseline (before any treatment) and then at 90 minutes and 24 and 48 hours after the administration of an intravenous bolus of heparin (5000 IU) followed by a continuous infusion of 1000 IU per hour to maintain activated partial thromboplastin time at more than double its baseline levels. In comparison with baseline, there was a significant decrease in fibrinopeptide A at 90 minutes and at 24 and 48 hours (baseline, 2.3 nmol/L; 90 minutes, 1.15 nmol/L; 24 hours, 1.4 nmol/L; 48 hours, 1.2 nmol/L; P < .0001) but no change in prothrombin fragment 1+2 levels (baseline, 1.27 nmol/L; 90 minutes, 1.3 nmol/L; 24 hours, 1.33 nmol/L; 48 hours, 1.29 nmol/L; P = NS). Antithrombin III activity decreased at 24 and 48 hours (baseline, 108%; 24 hours, 97%; 48 hours, 95%; P < .0001). Hence, in patients with acute coronary syndromes, intravenous heparin at a dose reaching an activated partial thromboplastin time that adequately suppresses thrombin activity does not suppress increased thrombin generation.

Topics: Acute Disease; Angina, Unstable; Antithrombin III; Biomarkers; Blood Coagulation; Enzyme Activation; Female; Fibrinopeptide A; Heparin; Humans; Injections, Intravenous; Male; Myocardial Infarction; Thrombin; Time Factors

Acute thrombosis is thought to contribute to abrupt coronary occlusion during percutaneous coronary revascularization despite the administration of heparin and aspirin. This study was designed to detect the presence of heparin-resistant thrombin activity and to define its relationship to the acute ischemic complications of coronary interventions.. Plasma levels of fibrinopeptide A (FPA) and prothrombin fragment 1.2 (F1.2), markers of thrombin and factor Xa activity, respectively, were measured in the coronary sinus with heparin-bonded catheters in 58 patients undergoing coronary interventions. Activated coagulation times were maintained > 300 seconds by the Hemochron method. Mean FPA levels decreased significantly, from 7.0 +/- 0.9 nmol/L before the procedure to 5.2 +/- 0.5 nmol/L after the heparin bolus and to 2.9 +/- 0.2 nmol/L after the procedure (P = .0001). In 26 patients (45%), FPA levels remained above the threshold for suppression angioplasty of thrombin activity determined during angiography in 7 patients without coronary artery disease (> 3.0 nmol/L). FPA concentrations after coronary interventions were increased in patients with intracoronary thrombus (P = .01), abrupt coronary occlusion (P = .06), postprocedural non-Q-wave myocardial infarction (P = .04), and clinically unsuccessful procedures (P = .04). F1.2 levels were relatively low before the procedures and did not change significantly.. Heparin administration suppresses thrombin activity in most but not all patients undergoing coronary interventions. Heparin-resistant thrombin activity is associated with angiographic evidence of intracoronary thrombus and ischemic complications of coronary interventions.

Topics: Acute Disease; Aged; Angiography; Blood Specimen Collection; Cardiac Catheterization; Factor Xa Inhibitors; Female; Fibrinopeptide A; Heparin; Humans; Male; Middle Aged; Myocardial Ischemia; Peptide Fragments; Prothrombin; Reproducibility of Results; Thrombin; Thrombosis; Whole Blood Coagulation Time

Plasma Fibrinopeptide-A (FpA) concentrations were determined using Enzyme-linked Immunosorbent Assay (ELISA) in patients with acute Plasmodium falciparum malaria infection and in 30 healthy controls. The mean FpA levels of the malaria patients were significantly raised (p < 0.001). The patients' FpA level correlated positively with malaria parasitaemia, but negatively with plasma fibrinogen concentration. A week after commencement of chloroquine therapy and subsequent disappearance of malaria parasites from the thick blood films, the patients' FpA levels decreased significantly from pre-treatment values. It is suggested that the elevated FpA and reduced plasma fibrinogen levels in the patients probably indicate a more widespread existence of overt coagulation defect in acute malaria infection.

Topics: Acute Disease; Adolescent; Adult; Blood Coagulation Tests; Case-Control Studies; Child; Child, Preschool; Chloroquine; Female; Fibrinopeptide A; Humans; Infant; Malaria, Falciparum; Male

Topics: Acute Disease; Altitude Sickness; Fibrinopeptide A; Humans; Mountaineering; Nifedipine; Pulmonary Edema

Cytostatic therapy is known to aggravate tumor-induced coagulopathy. Therefore, we have studied the effect of different chemotherapeutic regimens on the activation of coagulation and fibrinolysis in patients with non-Hodgkin's lymphomas or acute leukemias. In non-Hodgkin's lymphoma patients treated with an aggressive protocol (COL-BLAM) and in leukemia patients (TAD-9) fibrinopeptide A, prothrombin fragment (F1 + 2) and thrombin antithrombin III complexes (TAT) increased (Tables 4 and 6), while D-dimer did not deviate significantly. The ratio D-dimer/TAT consequently showed a significant decrease, indicating increased formation of thrombin after release of procoagulant factors, which is not paralleled by an activation of fibrinolysis. Both these groups were also characterized by an increase in uric acid and in C-reactive protein and plasminogen-activator inhibitor, two acute-phase reactants. In contrast, patients with non-Hodgkin's lymphomas treated with a less aggressive protocol (COP) showed no significant changes in hemostatic variables, uric acid, or acute-phase reactants. The release of procoagulant factors relates to the cytostatic sensitivity of the tumor and to a high tumor-cell destruction. Our results further emphasize the need for large-scale studies on antithrombotic prophylaxis in patients undergoing cytostatic treatment.

Topics: Acute Disease; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Antithrombin III; Bleomycin; Blood Coagulation; Cyclophosphamide; Doxorubicin; Fibrinolysis; Fibrinopeptide A; Humans; Leukemia; Leukemia, Myeloid, Acute; Lymphoma, Non-Hodgkin; Peptide Hydrolases; Prednisone; Procarbazine; Vincristine

A study of neurohumoral and functional determinants of the advance of Ischemic heart disease in 39 patients with unstable stenocardia with positive results of loading tests (transesophageal electrocardiostimulation and veloergometry) allowed to reveal a significant reduction of the coronary reserve and regional dysfunction of the myocardium that interrelated with changes of the prostacyclin/thromboxane balance, increase of vasopressin with unchanged angiotensin II value and increased marker of the functional state of thrombocytes--beta-thromboglobulin. These changes may be one of the leading links in the pathogenesis of destabilization.

Topics: Acute Disease; Angiotensin II; beta-Thromboglobulin; Coronary Disease; Epoprostenol; Fibrinopeptide A; Humans; Physical Exertion; Radioimmunoassay; Thromboxane A2; Vasopressins

This pilot study assessed the urinary fibrinopeptide A (uFPA) levels and the combination of uFPA test plus ventilation/perfusion (V/Q) scan in the diagnostic evaluation of acute pulmonary embolism (PE). One hundred consecutive patients were studied prospectively. Twenty-nine patients fulfilled diagnostic criteria defined in this study (seven with and 22 without PE). The uFPA concentration was significantly higher in patients with than without PE (41.1 +/- 2.6 vs 4.8 +/- 2.5 ng/mg of creatinine, p less than 0.0001). In all patients with PE, the uFPA levels were higher than threshold value derived by adding 2 standard deviations to the mean uFPA concentration of patients without PE. In patients without PE, the V/Q scan was negative in 16, the uFPA test was negative in 18, and at least one of the tests was negative in 21. These preliminary data suggest that a negative uFPA test may be helpful in excluding PE and that uFPA in combination with V/Q lung scans may correctly exclude PE in more patients than either test alone. Further studies in a large unselected population are needed to confirm these results.

Topics: Acute Disease; Adult; Aged; Angiography; Female; Fibrinopeptide A; Humans; Male; Middle Aged; Pilot Projects; Probability; Prospective Studies; Pulmonary Embolism; Radionuclide Imaging; Sensitivity and Specificity; Technetium Tc 99m Aggregated Albumin; Ventilation-Perfusion Ratio

The mean levels of fibrinopeptide A (FPA), thrombin-antithrombin complex (TAT), and soluble fibrin (tPA method) in cancer patients (n = 32) were intermediate between those of patients with cerebral infarction and pancreatitis who had the most abnormal results and patients with myocardial infarction and pneumonia who had the least abnormal results. Patients with disseminated malignancies (n = 16) had significantly higher mean levels of FPA (10.6 vs. 5.3 nmol/l) and TAT (11.0 vs. 4.4 pmol/l) than patients with limited malignancies (n = 16). The difference in soluble fibrin (fibrin monomer, FM; 22.1 vs. 18.0 nmol/l) was not significant. The values of FPA, FM, and TAT in the patient population correlated significantly. There was a negative correlation between the level of antithrombin and test results for FPA (-0.69), FM (-0.48), and TAT (-0.38) in the cancer patients. Even cancer patients with locally limited disease may have elevated FPA, FM, and TAT test results, indicating a state of definite hypercoagulation.

Topics: Acute Disease; Adult; Aged; Aged, 80 and over; Antithrombin III; Blood Coagulation Disorders; Blood Coagulation Tests; Cerebral Infarction; Female; Fibrin; Fibrinopeptide A; Humans; Male; Middle Aged; Myocardial Infarction; Neoplasms; Pancreatitis; Peptide Hydrolases; Pneumonia; Predictive Value of Tests; Reference Values

To assess the time course of thrombosis and fibrinolysis after acute stroke, we measured concentrations of fibrinopeptide A (FpA), B-beta 1-42 peptide (B-beta 1-42), B-beta 15-42 peptide (B-beta 15-42), and crosslinked D-dimer (XDP) in 31 patients at varying times following acute ischemic stroke and in 13 neurologically stable patients with chronic strokes. FpA levels were markedly elevated during the first week after stroke and declined slowly during the first month. Mean FpA levels were not significantly elevated in chronic stroke patients. Mean XDP levels were slightly elevated during the first week and increased during the next 2 weeks after stroke. B-beta 1-42 and B-beta 15-42 levels were not elevated at any time following acute stroke. Our data suggest that fibrin formation greatly exceeds endogenous fibrinolysis during the acute phase of ischemic stroke. Endogenous fibrinolysis develops slowly following stroke. Prolonged elevation of FpA concentration suggests that thrombin activity and fibrin formation continue for up to 4 weeks in some patients with ischemic stroke.

Topics: Acute Disease; Aged; Aged, 80 and over; Cerebrovascular Disorders; Female; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinopeptide A; Fibrinopeptide B; Humans; Male; Middle Aged; Peptide Fragments; Time Factors

Topics: Acute Disease; Adolescent; Adult; Aged; Chromatography, High Pressure Liquid; Disseminated Intravascular Coagulation; Female; Fibrinogen; Fibrinopeptide A; Humans; Leukemia; Male; Middle Aged

In order to determine the role of thrombosis in the acute coronary syndromes the blood levels of fibrinopeptide A and protein C were examined with an enzyme-immune test in 48 patients treated in the cardiological clinic of the National Centre for Cardiovascular Diseases. 27 patients were with transmural myocardial infarction and 21 patients were with non-transmural myocardial infarction. The average time of the test from the onset of pain is 18.4 +/- 12.2 hours (from 3 up to 72 hours). The mean level for fibrinopeptide A for the whole group of patients is 4.95 +/- 3.1 ng/ml and that of protein C is 70.1 +/- 9.8%. For the group of patients with transmural myocardial infarction the level of fibrinopeptide A is 6.09 +/- 3.49 ng/ml and of protein C is 65.3 +/- 8.0%. For the patients with nontransmural myocardial infarction the levels are respectively 3.49 +/- 1.7 ng/ml for fibrinopeptide A and 76.3 +/- 8.3% for protein C. The difference between the two groups is statistically significant (p less than 0.005). In the patients with non-transmural myocardial infarction from whom the blood for the test was taken before the 24th hour the fibrinopeptide A level is 4.8 +/- 2.4 ng/ml and the protein C level is 69.0 +/- 7.8%. The deviations from the reference group are statistically significant (p less than 0.04). The practical importance of these results is discussed.

Topics: Acute Disease; Aged; Coronary Disease; Enzyme-Linked Immunosorbent Assay; Female; Fibrinogen; Fibrinopeptide A; Humans; Male; Middle Aged; Myocardial Infarction; Protein C

The plasma concentrations of protein C, an anticoagulant protein, and fibrinopeptide A were measured in 37 patients with acute hemispheric stroke and in age-matched controls with nonvascular neurologic diseases. In 11 stroke patients who died within 15 days after the onset (nonsurvivors) protein C antigen concentration on admission was lower than in the control group (p less than 0.005), with a mean value of 63% of the concentrations found in the 26 survivors (p less than 0.001). The difference in protein C concentrations was not associated with different prothrombin time ratios and serum albumin concentration in survivors and nonsurvivors of stroke and was independent of the size of the cerebral lesion. Increased fibrinopeptide A concentration on admission was found in all stroke patients (p less than 0.001), but it was higher in nonsurvivors than in survivors (p less than 0.01), suggesting that lower protein C concentrations in nonsurvivors might be due to increased thrombin-dependent protein C activation. In survivors, protein C concentration was slightly but significantly higher than in controls (p less than 0.05) and was unchanged 2 months after stroke, a time when fibrinopeptide A concentrations had returned to normal. These results show that protein C is involved in the hemostatic derangement caused by stroke and provide a rationale for clinical trials evaluating the therapeutic supplementation with protein C of patients with acute ischemic stroke.

Topics: Acute Disease; Aged; Cerebrovascular Disorders; Fibrin; Fibrinopeptide A; Humans; Middle Aged; Protein C

Topics: Acute Disease; Aged; Blood Coagulation; Brain Injuries; Cerebral Hemorrhage; Disseminated Intravascular Coagulation; Female; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Fibrinopeptide A; Fibrinopeptide B; Humans; Hypertension; Male; Middle Aged; Peptide Fragments

Coagulation abnormalities associated with severe pancreatitis were studied in 24 dogs. Group I consists of six control subjects who had duodenotomy alone. Group II consists of six dogs with pancreatitis induced by bile injection ( lcm3 /kg) into the pancreatic duct. The six dogs in Group III and the six in Group IV were given aprotinin (trasylol) 1.0 mg/kg and S-2441 (10mg/kg), a new synthetic protease inhibitor, respectively. These were given over 10 minutes by intravenous infusion, 20 minutes after bile induced pancreatitis. Blood was drawn for amylase, prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen, and platelets, in addition to markers for hypercoagulation, fibrinopeptide A, antithrombin III, and markers for fibrinolysis, B beta 15-42 immunoreactive peptides and alpha 2 antiplasmin at baseline, 30 minutes, 1 hour, 3 hours, 6 hours, and daily for 3 days after injection of bile or duodenotomy. There was no significant difference in PT, platelets, antithrombin III, and fibrinopeptide A among the four groups. Fibrinogen levels and PTT were minimally elevated in animals with bile induced pancreatitis, but these changes reached significance only at 24 hours and 48 hours, respectively (P less than 0.05). Immunoreactive B beta 15-42 became elevated at 30 minutes indicating fibrinolysis in animals with pancreatitis, and these changes were significant compared with Group I control subjects (P less than 0.05) throughout the study. Levels of alpha 2 antiplasmin were decreased in Group II animals with pancreatitis, which also suggests fibrinolysis. Amylase was elevated in Group II animals with pancreatitis (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Disease; alpha-2-Antiplasmin; Amylases; Animals; Antithrombin III; Aprotinin; Blood Coagulation; Disease Models, Animal; Dogs; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Fibrinopeptide A; Oligopeptides; Pancreatitis; Peptide Fragments; Platelet Count; Protease Inhibitors; Prothrombin Time

Plasma levels of fibrinopeptide A (FPA) in 30 untreated patients with acute non-lymphocytic leukemia (ANLL) were significantly higher than in 30 healthy controls (p less than 0.001). Patients without laboratory signs of disseminated intravascular coagulation (DIC) had levels of FPA higher than controls (p less than 0.02) but markedly lower than patients with DIC (p less than 0.001). Five patients with M3 leukemia had a higher mean FPA level (p less than 0.02) and a lower peripheral blast cell count (p less than 0.05) than patients with other cytological subtypes of ANLL. When patients with M3 were excluded, a significant correlation was observed between the peripheral blast cell counts and the FPA levels (r = 0.66, p less than 0.001). FPA levels were similar with body temperature either above or below 38 degrees C. After intravenous bolus of heparin FPA dropped to normal levels in 14 out of 17 patients who had high baseline values. These findings indicate that intravascular thrombin formation, which probably result from the expression of procoagulant activities of blast cells, is the main cause of high FPA in the majority of patients with acute non-lymphocytic leukemia.

Topics: Acute Disease; Adolescent; Adult; Aged; Disseminated Intravascular Coagulation; Female; Fibrinogen; Fibrinopeptide A; Heparin; Humans; Leukemia; Male; Middle Aged

The purpose of this study was to assess the predictive values of the assays of fibrinopeptide A (FPA), beta-thromboglobulin (BTG) and their combination in patients suspected of having acute deep venous thrombosis (DVT) or pulmonary embolism (PE). In 80 controls the mean (+/- SD) plasma concentrations of FPA and BTG were 0.72 +/- 0.47 and 28.2 +/- 10.1 ng/ml, respectively. In 26 patients in whom DVT was confirmed by phlebography and Doppler ultrasound, clearly raised mean FPA (5.62 ng/ml) and BTG (70.6 ng/ml) concentrations were measured compared to those in 13 patients in whom this disorder was excluded (1.00 and 33.6 ng/ml, respectively). Also in 25 patients, in whom PE was established by perfusion lung scanning, clearly increased mean FPA (6.28 ng/ml) and BTG (82.4 ng/ml) concentrations were measured compared to those in 12 patients without this disease (1.03 and 32.5 ng/ml, respectively). Raised FPA and BTG concentrations were also found in 20 patients with inflammatory disorders and in 10 with various types of malignancy. The mean FPA and BTG concentrations did not differ between patients with renal failure or diabetes mellitus and patients without these diseases. From the predictive values of these assays and their combination it can be concluded that raised FPA and BTG concentrations are not specific for thrombosis. However, when normal FPA and BTG concentrations are present, acute DVT or PE can safely be excluded in symptomatic patients. In the group with confirmed DVT/PE, anticoagulant treatment (heparin and phenprocoumon) brought down the mean FPA concentration to levels within the normal range in less than 1 hour while the mean BTG concentration remained elevated throughout the 10-day study period.

Topics: Acute Disease; Adult; Aged; Beta-Globulins; beta-Thromboglobulin; Fibrinogen; Fibrinopeptide A; Heparin; Humans; Middle Aged; Pulmonary Embolism; Thrombophlebitis

Topics: Acute Disease; Adult; Aged; Beta-Globulins; beta-Thromboglobulin; Fibrinogen; Fibrinopeptide A; Follow-Up Studies; Humans; Middle Aged; Pulmonary Embolism; Thrombophlebitis; Time Factors

In recipients of renal transplants, the biochemical defect(s) that underlies increased deposition of platelets in the graft and their shortened survival in the circulation are poorly understood. Forty-six recipients of kidney allografts, with and without rejection signs (13 acute rejections (ARs), 15 chronic rejections (CRs), and 18 functioning transplants (FTs), had lower platelet serotonin (5HT) and higher plasma beta-thromboglobulin than normal controls (NCs). These abnormalities were more pronounced in patients with ARs than with CRs but were also present in patients with FTs. All groups of transplant recipients showed an abnormal metabolism of platelet arachidonate, as expressed by low serum levels of thromboxane B2. In AR, plasma fibrinopeptide A (FPA) was significantly high whereas FPA levels were unchanged in CR and in FT. These findings suggest that in patients with renal transplants, the platelet release reaction has occurred in vivo, resulting in the secretion of granule-bound substances and the circulation of partially empty platelets. Vasoactive, mitogenic, and proaggregatory substances released from platelets might damage the graft and aggravate the rejection process.

Topics: Acute Disease; Adolescent; Adult; beta-Thromboglobulin; Blood Platelets; Cell Survival; Child; Chronic Disease; Female; Fibrinopeptide A; Graft Rejection; Humans; Kidney Transplantation; Male; Middle Aged; Platelet Count; Serotonin; Thromboxane B2

Twenty-seven young adults (mean age 46) with ischemic cerebrovascular disease (ICD) were reinvestigated about 5 years after discharge and compared to 67 healthy controls. Factor VIII related antigen was again found significantly (p less than 0.005 and p less than 0.001) increased in male as well as female patients and a significant (r = 0.66, p less than 0.001) correlation was found with earlier data. Factor VIII biological activity was again found increased, significantly (p less than 0.001) in males. In contrast to earlier results antithrombin antigen and activity were significantly (p less than 0.001) decreased in males. This finding and decreased levels of factor XII in female patients (p less than 0.001) and of prekallikrein in male patients (p less than 0.01) could reflect disturbed regulatory functions or possibly constitutional differences. As in most subjects no increase of fibrinopeptide A was found, there was no sign of continuous activation of the whole coagulation sequence. Since hemostatic abnormalities were unrelated to acute phase reacting proteins they were obviously of a different nature than unspecific response to tissue damage and acute stress. High levels of factor VIII and low levels of antithrombin imply that the coagulation system could be more easily activated when other factors coincide, e.g. intimal lesions in carotide arteries.

Topics: Acute Disease; Adult; Aged; Antigens; Antithrombins; Blood Coagulation; Blood Coagulation Factors; Brain Ischemia; Factor VIII; Factor XII; Female; Fibrinogen; Fibrinopeptide A; Follow-Up Studies; Humans; Kallikreins; Male; Middle Aged; Prekallikrein; Sex Factors; von Willebrand Factor

Topics: Acute Disease; Fibrinogen; Fibrinopeptide A; Humans; Myocardial Infarction

Plasma fibrinopeptide A (FPA) levels were determined in 20 unselected adult patients with acute nonlymphocytic and lymphocytic leukemia. The mean FPA level in patients with active disease (15.0 ng/ml) was significantly higher than during clinical remission (2.4 ng/ml, p less than 0.01). Elevated FPA levels were observed in patients with all morphological forms of acute leukemia. In the group of patients in clinical remission, 20/47 FPA values remained elevated beyond the normal range, suggesting that low-grade intravascular coagulation was present even when no leukemic cells were observed. Sequential studies revealed reduction of FPA levels to the normal range in five patients who entered clinical remission after chemotherapy and rapid elevation of the levels in eight patients who entered relapse after clinical remission. FPA levels rose significantly in five patients studied during induction chemotherapy. Thus, subclinical activation of blood coagulation, as defined by elevation of plasma FPA level, may occur commonly in acute leukemia. Plasma FPA generation may relate to leukemic disease activity.

Topics: Acute Disease; Adolescent; Adult; Aged; Blood Coagulation; Female; Fibrinogen; Fibrinopeptide A; Humans; Leukemia; Leukemia, Lymphoid; Leukemia, Myeloid, Acute; Male; Middle Aged

Topics: Acute Disease; Angina Pectoris, Variant; Coronary Disease; Fibrinogen; Fibrinopeptide A; Humans

Topics: Acute Disease; Blood Coagulation; Electrocardiography; Female; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinopeptide A; Humans; Male; Middle Aged; Myocardial Infarction; Platelet Count; Time Factors