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  • Aggressive anticoagulation  (1)
  • Antibodies, inhibiting  (1)
  • Biochemical bone markers  (1)
  • 1
    ISSN: 1432-0584
    Keywords: Intracoronary stenting ; Aggressive anticoagulation ; Subacute occlusion ; Bleeding complication ; Prothrombin fragment 1+2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Patients with intracoronary stent implantation are treated with aggressive anticoagulant and antiplatelet therapy consisting of high-dose heparin, phenprocoumon, acetylsalicylic acid, dipyridamole, and the infusion of dextran to prevent a subacute thrombotic occlusion of the stented segment. In an effort to optimize this treatment by reducing both imminent bleeding complications and subacute thrombotic occlusion, the concentrations of prothrombin fragment 1+2 (F1+2) were determined after intracoronary Palmaz-Schatz stent implantation in 19 consecutive patients. The F1+2 concentrations after stent implantation and before the initiation of oral anticoagulant therapy (OAT) were 0.35 nm/l and 0.25–0.53 nm/l (median and 25th–75th percentile), versus 0.74 nm/l and 0.52–0.78 nm/l, in healthy subjects and 0.61 nm/l and 0.30–1.02 nm/l in 15 patients with ongoing proximal DVT. Nine days after initiation of OAT, F1+2 concentrations in both patient groups had not yet reached levels observed in patients with OAT in the stable state (0.16 nm/l, 0.12–0.26 nm/l;n=76;P〈0.0001 compared with healthy subjects; INR 2.0–4.5). Despite an INR greater than 2.0, accompanying heparinization was terminated on day 9. In two stented patients a minor bleeding complication arose after the removal of the arterial catheter. Subacute thrombotic occlusions were not observed. Since F1+2 concentrations did not exceed the upper limit of normal range (1.11 nm/l) in any of the 19 patients, the therapeutic regimen was not changed. Monitoring F1+2 may thus be helpful in introducing a more individual treatment if aggressive anticoagulation has to be performed.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0827
    Keywords: Bone density measurement ; Dual energy X-ray absorptiometry ; Collagen type I ; Biochemical bone markers ; b-quotient
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Abstract In contrast to medical imaging, the biochemical markers allow a more frequent determination and are not as invasive as histomorphometric methods. We investigated biochemical markers of type I collagen compared with bone density measurements in 85 females between 41 and 89 years of age (median: 57 years). The bone density measurements were performed by dual-energy X-ray absorptiometry (DXA) on the lumbar spine (L1–4). The bone density measurements were stated as percentage of the norm. All patients were divided into three groups: I=〈80%; II=80–120%; III=〉120%. Based on this classification the median concentration of the I-carboxyterminal propeptide of type I procollagen in serum (S-PICP) as an anabolic marker of type I collagen increased significantly with rising bone density: I 65.0* μg/liter (interquartile range: 52.1–78.0 μg/liter); II 85.9* μg/liter (52.1–115.5 μg/liter); III 81.4 μg/liter (62.0–101.0 μg/liter); * P〈0.05. The concentration of urinary pyridinolines (U-PYR) as a marker for degradation of type I collagen decreased. The I-carboxyterminal telopeptide (S-ICTP) and osteocalcin (S-BGP) did not change. The multivariate regression analysis showed no relationship between bone density measurement and biochemical bone markers. Only the age significantly correlated negatively with bone density measurement. For a better assessment of type I collagen metabolism we created a “b-quotient” by dividing the sum of S-PICP and S-BGP by U-PYR. The median b-quotient increased significantly: I 1.55*+ (0.97–2.04); II 2.09* (1.57–2.86); III 2.46+ (1.58–3.22);*+ P〈0.05. Changes in bone metabolism cannot be identified by the determination of a single marker. However, the improved biochemical diagnostic measurement using the b-quotient may provide early information about the progression of a metabolic disorder within the interval of imaging.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Creatine kinase, isoenzymes ; Creatin kinase, isoenzyme-MB ; Antibodies, inhibiting ; Kinetic enzyme activity determination ; Myocardial infarction ; Creatinkinase-Isoenzyme ; Creatinkinase-Isoenzym MB ; Antikörper, inhibierende ; Enzymaktivitäts-Bestimmung, kinetische ; Myokardinfarkt
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Es wird über eine neue Methode zur quantitativen Bestimmung der Creatinkinase MB-Aktivität im Serum berichtet. Die Methode beruht auf einer direkten Messung der Aktivität der Creatin-kinase-Untereinheit B nach Hemmung der Aktivität der Creatinkinase-Untereinheit M durch inhibierende Antikörper und benötigt zur Durchführung 15 min. Bei allen 83 untersuchten Patienten mit klinisch gesichertem Myokardinfarkt konnten zwischen der 6. und 28. Stunde nach Infarkteintritt Creatinkinase MB-Aktivität gemessen werden. Der Creatinkinase MB-Anteil zum Zeitpunkt der höchsten Creatinkinase-Gesamtaktivität betrug 6–17%, im Mittel 8%. Diese Methode ermöglicht daher in der Notfalldiagnostik eine Differentialdiagnose unklarer Creatinkinase-Gesamtaktivitäts-Erhöhungen.
    Notes: Summary A new method for the determination of creatine kinase-MB activity in the serum is presented. The principle of this method is the direct measurement of the activity of creatine kinase M subunits by inhibiting antibodies. The total test procedure takes 15 min. In the sera of all the 83 patients tested, who have clinically proven myocard infarction, creatine kinase-MB activity can be measured between the 6th and 28th hour after infarction. At the time of maximum total creatine kinase activity the percentage of creatine kinase-MB activity is between 6 and 17%, the mean value being 8%. In cases of emergency this method can be used for the differential diagnosis of elevated total creatine kinase activities of unknown origin.
    Type of Medium: Electronic Resource
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