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Hyaluronic acid and endothelial damage due to paracetamol‐induced hepatotoxicity
Author(s) -
Williams Anna M.,
Langley Peter G.,
OseiHwediah Johnson,
Wendon Julia A.,
Hughes Robin D.
Publication year - 2003
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1034/j.1600-0676.2003.00808.x
Subject(s) - thrombomodulin , von willebrand factor , medicine , hyaluronic acid , endothelial stem cell , endothelial dysfunction , ingestion , endocrinology , endothelium , gastroenterology , liver function , platelet , chemistry , biochemistry , thrombin , in vitro , anatomy
Background: Damage to endothelial cells may be an important factor in the complications of acute liver failure, resulting in multi‐organ failure. The aim of this study was to assess endothelial cell function in patients with severe hepatotoxicity due to paracetamol ingestion. Patients and methods: Fifty‐eight patients with paracetamol‐induced hepatotoxicity were studied for up to 7 days. Serum hyaluronic acid (HA), as a marker of hepatic sinusoidal endothelial cell function, was determined using an enzyme‐linked binding assay. Plasma von Willebrand Factor, thrombomodulin and interleukin‐8 were also determined using ELISA. Results: Serum HA on admission was significantly increased (median 6777 ng/ml, range 24–50 967 ng/ml) as compared to normal controls ( n  = 10, median 21 ng/ml, range 0–50 ng/ml; P  < 0.001). In non‐survivors ( n  = 21) HA levels peaked on day 2 after admission ( P  = 0.044), and then decreased. In the survivors ( n  = 37) the levels of HA did not increase further. Plasma von Willebrand Factor, plasma thrombomodulin and serum interleukin‐8 were significantly increased in the patients as compared to the normal controls ( P  < 0.001). Serum interleukin‐8 was significantly higher in non‐survivors in the first 2 days. Conclusions: Endothelial function is abnormal in paracetamol‐induced hepatotoxicity. Damage to hepatic sinusoidal endothelial cells assessed by serum HA was greater in non‐survivors than survivors.

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