Worsening of hepatic dysfunction as a consequence of repeated hydroxyethylstarch infusions

被引:67
作者
Christidis, C
Mal, F
Ramos, J
Senejoux, A
Callard, P
Navarro, R
Trinchet, JC
Larrey, D
Beaugrand, M
Guettier, C
机构
[1] Jean Verdier Hosp, Dept Hepatogastroenterol, Bondy, France
[2] Inst Mutualiste Montsouris, Dept Hepatogastroenterol, Paris, France
[3] Gui De Chauliac Hosp, Dept Pathol, Montpellier, France
[4] Hop Tenon, Dept Pathol, F-75970 Paris, France
[5] Hop Lapeyronie, Dept Hematol & Med Oncol, F-34059 Montpellier, France
[6] Hop Lapeyronie, Dept Hepatogastroenterol, F-34059 Montpellier, France
[7] Jean Verdier Hosp, Dept Pathol, Bondy, France
关键词
liver; hydroxyethyl starch; tissue storage;
D O I
10.1016/S0168-8278(01)00200-8
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background/Aims: Due to its apparent safety and low cost, hydroxyethylstarch (HES) is increasingly used as a volume expander. The aim of this retrospective study was to highlight the risk of hepatic dysfunction after iterative HES infusions. Methods: Between April 1996 and April 1998, nine patients were referred for worsening of their clinical condition after repeated HES infusions. Six patients had previous chronic liver disease, cirrhosis in four cases. All patients underwent a liver biopsy. Results: All post-HES liver biopsies showed diffuse microvacuolization of Kupffer cells, which was associated with focal hepatocyte vacuolization in seven cases. The vacuoles contained periodic acid Schiff positive material at their margins and were lysosomal by electron microscopy. The clinical symptoms of hepatic disease, although difficult to interpret in cirrhotic patients, worsened after HES infusions. Portal hypertension was noted in three non-cirrhotic patients. Serum alkaline phosphatase and gammaglutamyl transferase activities were increased when compared with previous values. Eight patients died, six of them within 1-4 weeks of hepatic failure or septic shock. In the only living patient, symptoms improved after HES withdrawal. Conclusions: Repeated administration of HES could favour severe portal hypertension, liver failure and sepsis, particularly in the setting of chronic liver disease. The basis of these adverse effects is the lysosomal storage of HES in Kupffer cells and hepatocytes. (C) 2001 European Association for the Study of the Liver. Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:726 / 732
页数:7
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