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Stauffer's syndrome in renal cell carcinoma evidence for intravascular coagulation

Latente Verbrauchskoagulopathie als mögliche Ursache des Stauffer-Syndroms bei Hypernephrom

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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.

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.

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Authors and Affiliations

  1. Medizinische Universitätsklinik, Bergheimer Str. 56a, D-6900, Heidelberg, Germany

    K. Andrassy, H. Gärtner, E. Ritz & R. Zimmermann

  2. Zentrallaboratorium, Zentrum der Inneren Medizin, Klinikum der J.W. Goethe-Universität, Theodor-Stern-Kai 7, D-6000, Frankfurt/Main

    W. H. Siede

  3. Urologische Abteilung, Chirurgische Universitätsklinik, D-6900, Heidelberg

    G. Riedasch & K. Möhring

  4. Urologische Klinik, Städt. Krankenanstalten, D-7500, Karlsruhe

    E. Matouschek

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  1. K. Andrassy
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Andrassy, K., Gärtner, H., Siede, W.H. et al. Stauffer's syndrome in renal cell carcinoma evidence for intravascular coagulation. Klin Wochenschr 58, 91–97 (1980). https://doi.org/10.1007/BF01477193

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  • DOI: https://doi.org/10.1007/BF01477193

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