Thromb Haemost 1987; 58(01): 078
DOI: 10.1055/s-0038-1643069
Abstracts
LIVER DISEASE
Schattauer GmbH Stuttgart

SUBSTITUTION THERAPY WITH ANTITHROMBIN III: CLINICAL EXPERIENCE WITH DECOMPENSATED LIVER CIRRHOSIS AND HEMORRHAGIC COMPLICATIONS

R Lorenz
II. Med. Klinik und Poliklinik der TU Munchen, Klinikum rechts der Isar
,
M Holweger
II. Med. Klinik und Poliklinik der TU Munchen, Klinikum rechts der Isar
,
GE Vogel
II. Med. Klinik und Poliklinik der TU Munchen, Klinikum rechts der Isar
,
M Classen
II. Med. Klinik und Poliklinik der TU Munchen, Klinikum rechts der Isar
› Author Affiliations
Further Information

Publication History

Publication Date:
23 August 2018 (online)

Preview

In patients with decompensated liver cirrhosis, the coagulation disorder requires therapy only when bleeding complications occur. As therapy involves the risk of triggering a consumption coagulopathy, the discussion here examines the beneficial effect of boosting the inhibitor Potential by supplementing the administration of fresh plasma with substitution of AT III concentrate. To investigate this question, we conducted a retrospective study on the clinical course in 19 patients with decompensated liver cirrhosis, hepatic encephalopathy and bleeding complications.

The following treatment scheme was employed uniformly in all 19 cases: substitution of vitamin K 20 mg/d, heparin 100 - 300 U/h and fresh plaspna 2-4 bags/d. AT III concentrate (3 - 8 × 500 U/d Ky-bemin HS ) was administered additionally in group 1 (n=8), but was omitted in group 2 (n= 11). Both groups were statistically comparable with regard to initial laboratory findings (e.g. bilirubin, group 1: 11.7 ± 3.6 mg/dl; bilirubin, group 2: 10 ± 2.9 mg/dl) and encephalopathy Tcoma stages 1-2), with the exception of the two survivors in group - who had been in a precomatose stage (stages 0-1) and had bilirubin levels of 3 ± 1.5 mg/dl.

A comparison oT both collectives shows a lethality of 62.5 % (n=5) for group 1, and of 81 % (n=9) for group 2. Clinically, the incidence of hemorrhagic complications in group 1 was 61 %, but 100 % in group 2, although laboratory analysis showed no differences in the parameters of systemic coagulation. As regards the other laboratory values, including the transaminases and blood count, there were only differences in the development of the bilirubin values which, in group 1, rose to -3 ± 4 mg/dl only during the terminal phase, but which, in group 2, began to rise continuously from the second day of treatment onwards 2nd reached values of 28 ± 8.6 mg/dl.

It follows that, in patients with decompensated liver cirrhosis and bleeding complications, the administration of AT III concentrate (Ky-bernin HS ) as a supplement to conventional coagulation therapy, increases the survival rate and reduces the incidence of further bleeding. It is, however, not possible tc explain the cause of this effect from the analysis of the laboratory data for the systemic coagulation. Therefore, one may hypothesize that the effect is due to beneficial effect of AT III within microcirculation.