Removal of endotoxin and cytokines by plasma exchange in patients with acute hepatic failure

Iwai, Hiroko; Nagaki, Masahito; Naito, Tomoo; Ishiki, Yoshihide; Murakami, Nobuo; Sugihara, Junichi; Muto, Yasutoshi; Moriwaki, Hisataka

doi:10.1097/00003246-199805000-00021

Cited by 111 publications

(85 citation statements)

References 23 publications

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“…This concept is supported by Knaus et al [21], who state that changes in the APACHE III score on each subsequent day of ICU therapy provide daily updates in the risk estimates. Both clinical and experimental studies have shown that plasmapheresis lowers circulating levels of endotoxin and cytokines such as tumor necrosis factor α and interleukin 1β [10,18,28,29,30]. Most authors claim that the beneficial effect of plasmapheresis is due to the removal of these mediators.…”

Section: Discussionmentioning

confidence: 99%

Plasmapheresis in severe sepsis and septic shock: a prospective, randomised, controlled trial

et al. 2002

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Objective: To determine the therapeutic efficacy and safety of plasmapheresis in the treatment of patients with severe sepsis and septic shock. Design: Prospective, randomised, clinical trial with a planned, midstudy, interim analysis. Setting: Intensive care unit in a university hospital in Archangels, Russia. Patients: Consecutive patients with severe sepsis or septic shock. Interventions: One hundred and six patients were randomised to receive either standard therapy or an add-on treatment with plasmapheresis. Measurements and results:The primary endpoint was 28-day survival. Septic shock was diagnosed in 57% of the plasmapheresis-treated patients and 54% of the control patients. Mean APACHE III score at entry was 56.4 in the plasmapheresis group and 53.5 in the control group. The 28-day, all-cause mortality rate was 33.3% (18/54) in the plasmapheresis group and 53.8% (28/52) in the control group. This represents a relative risk for fatal outcome in the plasmapheresis group of 0.61, an absolute risk reduction of 20.5% and a number of patients needed to treat of 4.9. Apart from six transient episodes of hypotension and one allergic reaction to fresh frozen plasma, no adverse reactions were attributable to the plasmapheresis treatment in this study. Conclusions: Plasmapheresis may be an important adjuvant to conventional treatment to reduce mortality in patients with severe sepsis or septic shock. Plasmapheresis is a safe procedure in the treatment of septic patients. A prospective randomised multicentre trial is warranted to confirm our results and to determine which subgroups of septic patients will benefit most from this treatment modality.

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Section: Discussionmentioning

confidence: 99%

Plasmapheresis in severe sepsis and septic shock: a prospective, randomised, controlled trial

et al. 2002

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“…[1][2][3] Multiorgan dysfunction in ALF is believed to derive from oxidative stress due to reactive oxygen species and reactive nitrogen species 4 and from immunological injury mediated by cytokines. [5][6][7][8] N-acetylcysteine (NAC) is a thiol-containing agent that scavenges free oxygen radicals and replenishes cellular mitochondrial and cytosolic glutathione stores. [9][10][11] NAC has also been shown to directly scavenge reactive oxygen species and reactive nitrogen species.…”

Section: See Editorial On Pagementioning

confidence: 99%

Safety and efficacy of N-acetylcysteine in children with non-acetaminophen-induced acute liver failure

et al. 2007

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Acute liver failure (ALF) carries a high mortality in children. N-acetylcysteine (NAC), an antioxidant agent that replenishes mitochondrial and cytosolic glutathione stores, has been used in the treatment of late acetaminophen-induced ALF and non-acetaminophen-induced ALF. In our unit, NAC was introduced as additional treatment for non-acetaminophen-induced ALF in 1995. The aim of this study was to evaluate the safety and efficacy of NAC in children with ALF not caused by acetaminophen poisoning. A retrospective review of medical records of 170 children presenting with nonacetaminopheninduced ALF between 1989 and 2004 was undertaken. ALF was defined as either international normalized ratio of prothrombin time (INR) Ͼ 2 and abnormal liver function or INR Ͼ1.5 with encephalopathy and abnormal liver function. Children were divided into the following groups: Group 1 (1989)(1990)(1991)(1992)(1993)(1994), standard care (n ϭ 59; 34 [58%] male; median age 2.03 yr, range 0.003-15.8 yr); and Group 2 (1995)(1996)(1997)(1998)(1999)(2000)(2001)(2002)(2003)(2004), standard care and NAC administration (n ϭ 111; 57 [51%] male; median age 3.51 yr, range 0.005-17.4 yr). NAC was administered as a continuous infusion (100 mg/kg/24 hours) until INR Ͻ 1.4, death, or liver transplantation (LT). The median duration of NAC administration in Group 2 was 5 (range, 1-77) days. Complications were noted in 8 (10.8%) children: rash in 3, arrhythmia in 3, and dizziness and peripheral edema in 1. One child had an allergic reaction (bronchospasm) and NAC was stopped. A total of 41 (71%) children in Group 1 vs. 85 (77%) in Group 2 required admission to intensive care, P ϭ not significant (ns). The length of intensive care stay was 6 (range, 1-58) days in Group 1 vs. 5 (range, 1-68) days in Group 2, P ϭ ns and length of hospital stay was 25 (range, 1-264) days vs. 19 (range, 1-201) days, P ϭ 0.05. The 10-yr actuarial survival was 50% in Group 1 compared to 75% in Group 2, P ϭ 0.009. Survival with native liver occurred in 13 (22%) in Group 1 vs. 48 (43%) in Group 2, P ϭ 0.005; 15 (25%) in Group 1 died without transplant vs. 21 (19%) in Group 2, P ϭ ns; and LT was performed in 32 (54%) vs. 42 (38%), P ϭ ns. Death after transplantation occurred in 15 (39%) in Group 1 vs. 8 (16%) in Group 2, P ϭ 0.02. In conclusion, NAC is safe in non-acetaminophen-induced ALF. In this retrospective study NAC was associated with a shorter length of hospital stay, higher incidence of native liver recovery without transplantation, and better survival after transplantation. Liver Transpl 14: [25][26][27][28][29][30] 2008 See Editorial on Page 7Acute liver failure (ALF) in children is a rare but often fatal condition without liver transplantation (LT). [1][2][3] Multiorgan dysfunction in ALF is believed to derive from oxidative stress due to reactive oxygen species and reactive nitrogen species 4 and from immunological injury mediated by cytokines. 5-8 N-acetylcysteine (NAC) is a thiol-containing agent that scavenges free oxygen radicals and replenishes cellular mitochon...

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“…10 A variety of toxins accumulating in the body as a result of liver injury and cytokines released directly from the necrotic liver into the circulation are considered to be responsible for the deterioration of the condition. 11 It is also reported that activated leukocytes and their proteases can contribute to the pathogenesis of liver injury. 12,13 Furthermore, severe liver injury develops both impaired productive and consumptive coagulatory disturbance resulting in DIC and fatal outcomes.…”

mentioning

confidence: 99%

Urinary trypsin inhibitor protects against liver injury and coagulation pathway dysregulation induced by lipopolysaccharide/D-galactosamine in mice

Takano

Inoue

Shimada

et al. 2009

Laboratory Investigation

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Urinary trypsin inhibitor (UTI), a serine protease inhibitor, has been widely used for patients with inflammatory disorders including disseminated intravascular coagulation, shock, and pancreatitis in Japan. Our recent studies using UTI-null (À/À) mice have shown that UTI protects against systemic inflammatory responses and acute lung injury. However, the role of UTI in liver injury has not been elucidated. This study determined the contribution of UTI to liver injury and coagulatory disturbance induced by lipopolysaccharide and D-galactosamine (LPS/D-GalN) using UTI (À/À) and wild-type (WT) mice. LPS/D-GalN treatment caused severe liver injury characterized by neutrophilic inflammation, hemorrhagic change, necrosis, and apoptosis, which was more prominent in UTI (À/À) than in WT mice. In both genotypes of mice, LPS/D-GalN challenge caused elevations of aspartate amino-transferase and alanine amino-transferase, prolongation of the prothrombin and activated partial thromboplastin time, and decreases in fibrinogen and platelet counts, as compared with vehicle challenge. These changes, however, were significantly greater in UTI (À/À) than in WT mice. Circulatory levels of tumor necrosis factor (TNF)-a (Po0.05) and interferon (IFN)-g were also greater in UTI (À/À) than in WT mice after LPS/D-GalN challenge. These results suggest that UTI protects against severe liver injury and subsequent coagulatory disturbance induced by LPS/D-GalN, which was mediated, at least partly, through the suppression of TNF-a production along with its antiprotease activity.

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Removal of endotoxin and cytokines by plasma exchange in patients with acute hepatic failure

Abstract: TNF-alpha and IL-6 may be important in the pathogenesis of the clinical symptoms that differentiate fulminant hepatitis from the severe form of acute hepatitis, and plasma exchange removes these inflammatory mediators from the circulation of patients with severe liver disease.

Cited by 111 publications

References 23 publications

Plasmapheresis in severe sepsis and septic shock: a prospective, randomised, controlled trial

Plasmapheresis in severe sepsis and septic shock: a prospective, randomised, controlled trial

Safety and efficacy of N-acetylcysteine in children with non-acetaminophen-induced acute liver failure

Urinary trypsin inhibitor protects against liver injury and coagulation pathway dysregulation induced by lipopolysaccharide/D-galactosamine in mice

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