H Nakae1, K Narita, S Endo. 1. Department of Emergency and Critical Care Medicine, Akita University School of Medicine, Akita, Japan.
Abstract
PURPOSE: The Fas ligand (FasL)/Fas system is an apoptosis induction system that plays an important role in homeostasis and biophylaxis. We measured tumor necrosis factor alpha (TNF-alpha), soluble FasL (sFasL), and soluble Fas (sFas) in patients with acute hepatic failure to determine the relation between such failure and apoptosis. MATERIALS AND METHODS: We assayed 21 blood samples from patients with acute hepatic failure and 8 from patients with sepsis but without acute hepatic failure. Serum TNF-alpha, sFas, and sFasL levels were determined by enzyme-linked immunosorbent assay. RESULTS: sFasL levels were significantly higher in the patients with acute hepatic failure than in the patients with sepsis (0.68 +/- 0.42 ng/mL vs. 0 ng/mL, P =.0001). No significant differences were observed in sFas levels between the two groups. A significant correlation was observed between TNF-alpha and sFas levels (r = 0.657, P =.0008); a negative correlation was observed between TNF-alpha and sFasL levels (r = 0.454, P =.038). CONCLUSIONS: Our results suggest that pathologic aggravation of acute hepatic failure are related to changes in the FasL/Fas system and that TNF-alpha and sFasL, in particular, may play hepatoprotective roles. Copyright 2001 by W.B. Saunders Company
PURPOSE: The Fas ligand (FasL)/Fas system is an apoptosis induction system that plays an important role in homeostasis and biophylaxis. We measured tumor necrosis factor alpha (TNF-alpha), soluble FasL (sFasL), and soluble Fas (sFas) in patients with acute hepatic failure to determine the relation between such failure and apoptosis. MATERIALS AND METHODS: We assayed 21 blood samples from patients with acute hepatic failure and 8 from patients with sepsis but without acute hepatic failure. Serum TNF-alpha, sFas, and sFasL levels were determined by enzyme-linked immunosorbent assay. RESULTS: sFasL levels were significantly higher in the patients with acute hepatic failure than in the patients with sepsis (0.68 +/- 0.42 ng/mL vs. 0 ng/mL, P =.0001). No significant differences were observed in sFas levels between the two groups. A significant correlation was observed between TNF-alpha and sFas levels (r = 0.657, P =.0008); a negative correlation was observed between TNF-alpha and sFasL levels (r = 0.454, P =.038). CONCLUSIONS: Our results suggest that pathologic aggravation of acute hepatic failure are related to changes in the FasL/Fas system and that TNF-alpha and sFasL, in particular, may play hepatoprotective roles. Copyright 2001 by W.B. Saunders Company
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