Effect of anticoagulant treatment measured by fibrinopeptide a (fpA) in patients with venous thrombo-embolism

Peuscher, F.W.; Aken, W.G. van; Flier, Odilia Th.N; Dalen, E. A. Stoepman-Van; Cremer-Goote, Thea M; Mourik, Jan A. van

doi:10.1016/0049-3848(80)90168-1

Cited by 44 publications

(24 citation statements)

References 24 publications

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“…1). This value is within the reported normal (24) and is consistent with previous reports ofrapid normalization ofFPA levels after heparin therapy for venous thromboembolic disease (33,34). In contrast, the mean plasma value for desarginine FPB before rt-PA infusion was 5.6 nM, whereas normal levels are < 0.6 nM (29).…”

Section: Methodssupporting

confidence: 93%

Human tissue-type plasminogen activator releases fibrinopeptides A and B from fibrinogen.

Weitz

Cruickshank²,

Thong³

et al. 1988

J. Clin. Invest.

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In five patients with venous thromboembolic disease treated with recombinant tissue-type plasminogen activator (rt-PA), there was a marked increase in the mean concentrations of fibrinopeptide A (from 0.6 to 5.9 nM; P < 0.0001) and desarginine fibrinopeptide B (from 5.6 nM to 24.1 nM; P < 0.01) 30 min after a bolus of rt-PA (0.6 mg/kg). Thrombin was unlikely to be responsible because the levels of desarginine fibrinopeptide B exceeded those of fibrinopeptide A and the changes occurred despite concomitant heparin therapy. The purpose of this study therefore, was to determine whether rt-PA directly releases the fibrinopeptides from fibrinogen. Incubation of rt-PA with heparinized plasma or purified fibrinogen resulted in time and dose-dependent release of both fibrinopeptide A and B. Contaminating thrombin was not responsible for this activity by the following criteria: the rate of rt-PA mediated fibrinopeptide B release was considerably faster than that of fibrinopeptide A, and fibrinopeptide release was unaffected by heparin, hirudin, or a monospecific antithrombin IgG. Aprotinin also had no effect on fibrinopeptide release, indicating that this activity was not plasmin mediated. Fibrinopeptide release was shown to be due to rt-PA because this activity was completely blocked by a monoclonal antibody against the enzyme. Further, the specificity of rt-PA for the thrombin cleavage sites on fibrinogen was confirmed by the demonstration that rt-PA released fibrinopeptide A or fibrinopeptide B from fibrinopeptide A or B-containing substrates, respectively. These studies thus demonstrate that (a) rt-PA releases fibrinopeptides A and B from fibrinogen thereby indicating that this enzyme is not specific for plasminogen, and (b) plasma fibrinopeptide A and desarginine fibrinopeptide B levels are not specific markers of thrombin action on fibrinogen in patients receiving rt-PA.

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Section: Methodssupporting

confidence: 93%

Human tissue-type plasminogen activator releases fibrinopeptides A and B from fibrinogen.

Weitz

Cruickshank²,

Thong³

et al. 1988

J. Clin. Invest.

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“…Although the prothrombin and partial thromboplastin times were fully corrected by the in vitro addition of normal plasma, the effect of plasma transfusions on clinical bleeding and circulating factor X levels was suboptimal or entirely absent [21,23]. All cases manifested a complete sponta neous recovery as did ours.…”

Section: Discussionmentioning

confidence: 67%

“…The first such case involved a man who devel oped severe spontaneous bleeding within 4 h following heavy exposure to methylbromide and chlorpicrin [21], A second case occurred in a 10-year-old child in the absence of antecedent illness or documented exposure to drugs or toxins [22]. Other cases were associated with mycoplasma infection [23], viral pneumonia [24], and a right upper lobe pneumonia of unspecified etiology [25].…”

Section: Discussionmentioning

confidence: 99%

Progressive Systemic Sclerosis with the Nephrotic Syndrome and Acquired Factor X Deficiency

Eiser¹,

Zilversmit²,

Neff³

et al. 1986

Am J Nephrol

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A patient with progressive systemic sclerosis (PSS) involving skin, digit, esophagus, and lung developed the nephrotic syndrome and rapidly progressive renal insufficiency. Renal pathology revealed capillary collapse, cellular crescents, arteriolar hyaline deposition, and mesangial proliferation. On immunofluorescence IgM, C3, and fibrinogen were present in mesangium and capillary walls. Prebiopsy coagulation screening revealed a factor X deficiency which caused substantial prolongation of the partial thromboplastin time without an overt bleeding diathesis. The acquired factor X deficiency resolved after fresh frozen plasma and vitamin K administration, although some spontaneous improvement was noted. Nephrotic syndrome may occasionally be seen in the acute fulminant form of PSS and should not deter diagnosis of PSS.

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“…Owing to its high rate of elimination from plasma (halflife from 3 to 5 min) Fibrinopeptide A can be considered a sensitive parameter for the indication of fibrin formation in vivo (3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19). However, all the radioimmunological procedures described so far are time-consuming (2,(13)(14)(15)(16)(17)22).…”

Section: Intf Pductionmentioning

confidence: 99%

Fibrinopeptide A Radioimmunoassay: A Rapid and Sensitive Measurement of Fibrin Generation in vivo

Stehle¹,

Harenberg²,

Schmidt-Gayk³

et al. 1983

CCLM

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Summary: Fibrinopeptide A is cleaved from fibrinogen by thrombin. One niole of fibrinogen releases two moles of fibrinopeptide A during coagulation. In the present paper we describe a rapid and sensitive inethod to detect human fibrinopeptide A immunoreactivity in plasma.Double-antibody precipitation with a preincubation of first and second antiserum was used.The limits of detection were extended to fibrinopeptide A levels between 0.3 g/l and 160 g/l and the time spent on the assay procedure was shortened from 14 hours to 2 hours.Fibrinopeptide A levels in healthy volunteers were below 2.5 |ig/l. This new technique correlates with our previously described method (r = 0.96; comparative determination of 100 patient plasmas). Radioimmunassay für Fibrinopeptid A: Eine schnelle und empfindliche Bestimmung der Fibrinbildung-in vivoZusammenfassung: Fibrinopeptid A wird vom Fibrinogenmolekül durch Thrombin abgespalten.Ein Mol Fibrinogen gibt zwei Mol Fibrinopeptid A während des Gerinnungsprozesses ab.

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Effect of anticoagulant treatment measured by fibrinopeptide a (fpA) in patients with venous thrombo-embolism

Cited by 44 publications

References 24 publications

Human tissue-type plasminogen activator releases fibrinopeptides A and B from fibrinogen.

Human tissue-type plasminogen activator releases fibrinopeptides A and B from fibrinogen.

Progressive Systemic Sclerosis with the Nephrotic Syndrome and Acquired Factor X Deficiency

Fibrinopeptide A Radioimmunoassay: A Rapid and Sensitive Measurement of Fibrin Generation in vivo

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