Fibrinopeptide A (FPA) Level and Fibrinogen Kinetics in Patients with Malignant Disease

1981 ◽  
Vol 46 (04) ◽  
pp. 706-709 ◽  
Author(s):  
Yasuhiro Yoda ◽  
Tsukasa Abe

SummaryFPA level, fibrinogen turnover rate, and fibrinolytic activity were studied on 18 patients with malignant disease. It was found that the FPA levels were significantly elevated and were correlated with fibrinogen turnover rate (r=0.74, p<0.001) and FDP (r = 0.58, p<0.02). Estimated FPA turnover rate was also correlated with fibrinogen turnover rate (r = 0.70, p<0.001). These results suggest that fibrinogen catabolism in patients with malignant disease is related with thrombin proteolysis. However, ratios of 1/2 FPA turnover rate to fibrinogen turnover rate suggest that intravascular thrombin proteolysis is not the major determinant of fibrinogen catabolism. It is suspected that extravascular thrombin proteolysis is responsible for the elevation of plasma FPA level which is correlated with acceleration of fibrinogen catabolism.

Author(s):  
M Fisher ◽  
R Francis

We investigated coagulation changes in a group of patients with cerebral ischemia, ranging from transient ischemic attacks to cerebral infarction. Patients were studied acutely (within 72 hours of onset of ischemia) and again approximately 2 months following the initial examination. We evaluated platelet activation, fibrin generation, and fibrinolysis by measuring plasma beta-thromboglobulin (BTG), fibrinopeptide A (FPA), and fibrinopeptide B-beta 1-42 (FPB), respectively. We compared measurements in cerebral ischemia patients with a group of age -and sex-matched neurological inpatients without vascular disease ("patient controls") and a similarly matched group of normal volunteers ("normal controls"). BTG levels for 90 patients studied acutely were not significantly different compared to 58 of the same patients studied 2 months later, 16.4 ± 11.3 ng/ml (mean ± SD) versus 17.5 ± 10.2 ng/ml. Both values were significantly increased (p< .05) compared to normal controls (12.2 ± 6.5 ng/ml, n = 44); patient controls (13.2 ± 7.6 ng/ml, n = 18) were not significantly different from normals. In contrast, FPA measurements were significantly increased in acute patients compared to normals (3.3 ± 5.8 versus 1.0 ± 1.7 ng/ml, p< .05) while FPA levels 2 months post-ischemia (0.6 ± 0.9 ng/ml) were no different than normals. FPB measurements were not significantly different among either acute patients (6.5 ± 2.4 pmol/ml) or patients 2 months post-ischemia (4.8 ± 1.5 pmol/ml) compared to normals (6.5 ± 1.8 pmol/ml).In summary, we have found, among cerebral ischemia patients, sustained increases in BTG, acute increases in FPA, and normal FPB. These findings are compatible with a model of cerebral ischemia consisting of acutely increased fibrin generation without concomitant increased fibrinolytic activity, superimposed on a background of increased platelet activation.


1979 ◽  
Author(s):  
F.W. Peuscher ◽  
W.G. van Aken ◽  
A.L. Armstrong ◽  
E. A. Stoepman-van Dalen ◽  
J.A. van Mourik

Hypercoagulability, known to complicate malignant disease, can be detected by the measurement of fibrinopeptide A (FPA). The aim of the present study was to establish the significance of FPA production in. patients (n = 113) with various types of malignancy, without clinical signs of DIC, venous thromboembolism, not receiving cytostatic, anticoagulant or radiotherapy or bedrest. 8 patients presented laboratory abnormalities compatible with DIC; In this group mean FPA was 9.8 ng/ml (normal 1.4±0.9.2SD) and FPA generation In vitro (ΔFPA) was 15 ng/ml/10 min (normal 0.4±0.8, 230). In the remaining 105 patients, mean FPA was 5.2 ng/ml andFPA was 1.8 ng/ml/10 min. Of the 20 patients with both normal FPA and ΔFPA, 13 were clinically in remission, 5 had malignancies without detectable metastases and only 2 showed metastases. In 2 patients FPA was normal but ΔFPA was slIghtLy accelerated. 50 patients had elevated ΔFPA but normal FPA and in 33 cases both FPA and ΔFPA were increased; in these groups the majority of patients had a metastatic malignancy In 22 patients mean FPA before (4.9 ng/ml) and 20 mln after(4.2 ng/ml) receiving heparin (7500 U, i.v.) was not significantly different. These results suggest that apart from DIC tumor cells or the adjacent inflammatory area of tumors may trigger FPA generation, not being affected by heparin. It Is postulated that “heparin resistant” FPA generation Is potentially a sensitive marker of tumor activity.


1987 ◽  
Author(s):  
B J Woodhams ◽  
G Candotti ◽  
P B A Kernoff

Blood samples were collected from 17 volunteers between 8-14, 26-28 and 32-34 weeks of pregnancy. Control samples were collected from 12 non-pregnant female volunteers not using oral contraceptives. All samples were assayed for fibrinopeptide A (FPA), B beta 15-42 and for cross linked D-dimer fragments. A sample was collected for measurement of the in vitro rate of generation of fibrinopeptide A from whole blood (FPA-R).These results are consistent with an increased activation of coagulation (increased FPA and shortened FPA-R) during normal pregnancy, which is compensated for by a concomitant rise in fibrinolytic activity (increased D-dimer and B beta 15-42). In 2 patients who miscarried and 2 patients who developed hypertension during pregnancy changes indicative of a non compensated hypercoagulable state could be seen. The study shows that the progress of pregnancy is associated with increased activation of coagulation and a concomitant rise in fibrin(ogen) degradation products. This data shows that a combination of these tests may be capable of detecting changes in the haemostatic balance that occur before the onset of clinical signs of gynaecological problems.


1975 ◽  
Vol 28 (11) ◽  
pp. 872-874 ◽  
Author(s):  
J A Rennie ◽  
D Ogston

1981 ◽  
Vol 26 (2) ◽  
pp. 133-134
Author(s):  
E. James Anthony

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