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  • 1
    ISSN: 1432-1440
    Keywords: Hypernephrom ; Gamma-GT ; Alkalische Phosphatase ; Isoenzyme der alkalischen Phosphatase ; Prothrombinzeit ; Thrombinkoagulasezeit ; Alkoholtest ; Fibrinmonomerkomplexe ; Fibrinspaltprodukte ; Renal cell carcinoma ; Gamma-GT ; Alkaline phosphatase and isoenzymes ; Disseminated intravascular coagulation (DIC) ; Prothrombin time ; Thrombin coagulase time ; Ethanol gelation test ; Soluble fibrin monomer complexes ; Fibrin degradation products
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary In 40 patients with non-metastasising (n=31) and metastasising (n=9) renal cell carcinoma, evidence of Stauffer's syndrome (increase in alkaline serum phosphatase and prolongation of prothrombin time) was found in 18 patients. Prolongation of prothrombin time was not due to depletion of vitamin K-dependent coagulation factors or manifest fibrinolysis, but due to the presence of circulating fibrinogen fibrinmonomer-FDP complexes. Ethanol gelation test was found to be positive in 28/40 subjects and soluble fibrin monomer complexes were increased in 38/40 patients. The resulting disturbance of fibrinogen-fibrin conversion was reflected by an increase in thrombin coagulase time and reptilase time. These findings suggests a state of latent compensated intravascular coagulation (presumably triggered within the vascular tumor). For diagnostic purposes the most sensitive indicator is thrombin coagulase time. Thrombin coagulase time normalised after tumor resection and was positive in patients with recurrent metastases. The increase in alkaline serum phosphatase was due to an increase in the hepatic isoenzyme. Such an increase was much more common than the elevation of total alkaline serum phosphatase. Regan's isoenzyme was only found in 1 subject. In parallel, gamma-GT was elevated in 24 patients. The study shows that Stauffer's syndrome occurs more frequently than commonly assumed when thrombin coagulase time, gamma-GT and the hepatic isoenzyme of alkaline serum phosphatase are determined in patients with renal cell carcinoma. DIC and low grade fibrinolysis may account for the coagulation abnormalities of the syndrome.
    Notes: Zusammenfassung Ein Stauffer-Syndrom (erhöhte alkalische Phosphatase und verlängerte Prothrombinzeit) wurde bei 18 von 40 Hypernephrom-Patienten gefunden. Es konnte gezeigt werden, daß die verlängerte Prothrombinzeit nicht auf eine Verminderung Vitamin K-abhängiger Gerinnungsfaktoren, sondern auf zirkulierende Fibrinogen-Fibrinomer-Fibrinspaltproduktkomplexe zurückzuführen ist. Der Alkoholtest nach Godal war bei 28 von 48 Patienten positiv und erhöhte Mengen an zirkulierenden Fibrinmonomeren wurden bei 38 von 40 Patienten gefunden. Eine gesteigerte Fibrinolyse ließ sich in 19 von 40 Patienten nachweisen. Die Verlängerung der Thrombinkoagulase-und Reptilasezeit wird auf die zirkulierenden Fibrinmonomer-Fibrinspaltproduktkomplexe zurückgeführt, die die gestörte Umwandlung von Fibrinogen in Fibrin verursachen. Die vorliegenden Befunde sprechen für eine latente kompensierte intravasale Verbrauchskoagulopathie, die wahrscheinlich innerhalb des gefäßreichen Tumors ausgelöst wird. Als empfindlicher Indikator für diagnostische Zwecke erwies sich die Thrombinkoagulasezeit. Die Thrombinkoagulasezeit normalisierte sich nach chirurgischer Entfernung des Tumors und wurde nach Auftreten von Metastasen wieder pathologisch. Die Erhöhung der alkalischen Phosphatase war in der Regel nur auf einen Anstieg des hepatischen Isoenzyms zurückzuführen. Zum Nachweis des Stauffer-Syndroms erwiesen sich das hepatische Isoenzym der alkalischen Phosphatase und die Gamma-GT empfindlicher als die Gesamt-alkalische Phosphatase.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 179 (1981), S. 269-274 
    ISSN: 1433-8580
    Keywords: Rat ; Alkaline phosphatase isoenzyme in serum and liver homogenate ; Cholestasis ; Bile duct ligation ; Intoxication with: ANIT, CCL4, phenobarbital
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Alkaline phosphatase isoenzymes (API) in serum of rats during cholestasis are investigated. For comparison different membrane systems in liver are damaged. Proliferation of bile canaliculi, sinusoidal area, and endoplasmic reticulum, respectively, is induced by different toxic conditions. It is found that in cholestasis an API5 in serum arises which is not present in serum of normal rats, but can be detected in normal rat liver. Thus, it is not a de novo synthesis of this API. Under the condition connected with a proliferation of bile canaliculi we find this API5 in serum. Under different conditions without proliferation of bile canaliculi we do not find an increase of this API5. We assume, therefore, that API5 in cholestasis is produced by cells of the bile canaliculi rather than by liver parenchymal cells in the sinusoidal area. No difference is found in intra- or extrahepatic cholestasis.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1433-8580
    Keywords: Somatostatin ; Phalloidin ; Shock ; Liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of somatostatin in phalloidin-intoxicated rats was studied. Animals were given phalloidin i.p. 1.2 mg/kg (LD 90–100). Somatostatin, 250 µg/animal, was administered i.p. in saline 5 min prior and s.c. in protamine-sulphate/ZnCl2 suspension 30 min prior and 30 min after intoxication, unless stated otherwise. In vivo and in vitro uptake studies of the toxin were performed. Liver enzymes (GPT, GLDH) and kallikrein-like activities were determined in blood obtained by orbital venipuncture. Light and electron microscopy was carried out. Somatostatin treatment led to an increase in survival rate. Of the 20 treated rats six died whereas of the 20 untreated animals 18 died. A dose dependency was proven effective when half of the initial dose of somatostatin was given. In vivo and in vitro uptake studies of the toxin demonstrate that somatostatin does not alter toxin uptake rate by rat livers. Liver enzymes remained elevated in treated and control rats. Kallikrein-like activities showed a 61% decline in treated animals whereas they rose up to 120% in controls as compared to pretreatment conditions. Light and electron microscopy reveals less severe lesions in somatostatin-treated animals. A possible interaction of somatostatin in shock development is discussed, phalloidin seems to be a suitable tool for further investigations concerning cell protection by somatostatin.
    Type of Medium: Electronic Resource
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