Thromb Haemost 1989; 62(02): 651-653
DOI: 10.1055/s-0038-1646877
Original Article
Schattauer GmbH Stuttgart

Plasminogen Activators and Plasminogen Activator Inhibitors in Liver Deficiencies Caused by Chronic Alcoholism or Infectious Hepatitis

Chiên Tran-Thang
Policlinics and Laboratory of Hematology, Department of Internal Medicine, University Hospital, Lausanne, Switzerland
,
Josette Fasel-Felley
Policlinics and Laboratory of Hematology, Department of Internal Medicine, University Hospital, Lausanne, Switzerland
,
Gerard Pralong
Policlinics and Laboratory of Hematology, Department of Internal Medicine, University Hospital, Lausanne, Switzerland
,
Jean-René Hofstetter
Policlinics and Laboratory of Hematology, Department of Internal Medicine, University Hospital, Lausanne, Switzerland
,
Fedor Bachmann
Policlinics and Laboratory of Hematology, Department of Internal Medicine, University Hospital, Lausanne, Switzerland
,
Egbert K O Kruithof
Policlinics and Laboratory of Hematology, Department of Internal Medicine, University Hospital, Lausanne, Switzerland
› Institutsangaben
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Publikationsverlauf

Received 21. Dezember 1988

Accepted after revision 17. März 1989

Publikationsdatum:
30. Juni 2018 (online)

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Summary

Plasma concentrations of tissue-type plasminogen activator (t-PA), urokinase (u-PA), plasminogen activator inhibitor 1 (PAI-1) and PAI-2 were studied in 53 patients with liver deficiency caused by chronic alcoholism (n = 40), viral hepatitis (n = 10) or malignant disease of the liver (n = 3) and compared to that of a control group (n = 20) of healthy subjects. u-PA and PAI-1 levels were significantly increased in all patients with chronic alcoholism, whereas high t-PA was only observed in combination with disturbed liver function tests or with liver cirrhosis (two and sixfold above control values, respectively). A good correlation was observed between t-PA and gamma glutamyl transferase (r = 0.615; p <0.001). In patients with infectious hepatitis or with malignant disease of the liver t-PA was normal whereas u-PA and PAI-1 were increased.

PAI-2 levels were close to or below the detection limit (15 ng/ml) in the control group and in most patients. However, in two patients with alcohol induced cirrhosis PAI-2 levels were approximately 45 ng/ml and in one patient with hepatocarcinoma even 66 ng/ml. Thus, in liver disease, marked elevations of t-PA, u-PA and PAI-1 levels may occur, with increased PAI-1 as an early marker of liver defects and t-PA a marker of severe liver defects.