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PubMed2003

Activin A and follistatin in acute liver failure.

BACKGROUND: Liver regeneration may be impaired in acute liver failure due to either inhibition of the proliferative response or ongoing liver cell death. Activin A, a member of the TGFbeta superfamily, inhibits hepatocyte DNA synthesis and induces apoptosis. METHODS: Levels of activin A and its binding protein follistatin in the serum of 23 patients with acute liver failure were determined by enzyme-linked immunosorbent assay. RESULTS: Serum activin A was significantly increased in acute liver failure patients (median 2.15 ng/ml, range 0.28-6.87 ng/ml) compared to normal controls (median 0.25 ng/ml, range 0.19-0.53 ng/ml; = 10; 0.001). However, this was not linked to the final disease outcome. Higher levels of activin A were found in the serum of patients with acute liver failure due to paracetamol overdose (median 2.87 ng/ml, range 0.72-6.87 ng/ml; = 17) than in patients with acute liver failure due to non-A to E hepatitis (median 1.10 ng/ml, range 0.28-2.70 ng/ml; = 6; 0.05). Serum follistatin was also increased in acute liver failure patients (median 2.84 ng/ml, range 0.57-13.24 ng/ml) compared to normal controls (median 0.68 ng/ml, range 0.32-3.70 ng/ml; 0.01). CONCLUSION: Serum activin A is increased in acute liver failure and could be a factor in the inhibition of liver regeneration.

Acetaminophen↗
PubMed2004

Kidney failure associated with liver transplantation or liver failure: the impact of continuous veno-venous hemofiltration.

BACKGROUND AND AIMS: The short-term outcome of critically ill patients with kidney failure combined with severe liver failure or orthotopic liver transplantation (OLTx) is poor. We sought to test the hypothesis that, with the exclusive use of continuous veno-venous hemofilration (CVVH) with minimal heparin-anticoagulation, the short and long-term outcomes of these patients would be improved. PATIENTS: Sixty-six consecutive patients with combined liver and kidney failure SETTING: Intensive Care Unit of tertiary hospital DESIGN: Retrospective interrogation of prospectively collected databases INTERVENTION: Treatment of all patients with continuous veno-venous hemofiltration (CVVH) by protocol with 2L/h of ultrafiltration rate and minimal use of circuit heparinization. Retrieval of specific information on demographic, clinical, therapeutic and outcome details. MEASUREMENTS AND MAIN RESULTS: From July 1995 to April 2004, 66 patients with combined liver and renal failure received continuous veno-venous hemofiltration (CVVH). Of these, 26 received liver transplantation and 40 did not. There were no significant differences in age, APACHE II score, bilirubin, ALT, INR or albumin on admission. The average duration of CVVH was 9.5 days for OLTx patients and 5 days for non-transplanted patients (p=0.013). Heparin anticoagulation was used in only 12% of OLTx patients and 20% of non-transplanted patients. ICU mortality was 15% in OLTx patients and 63% in non-transplanted patients (p<0.0005); hospital mortality was 23% compared to 70% (p<0. 001). Mean survival time at follow up was 1,120 days compared to 358 days (p<0.0001). CONCLUSIONS: ARF associated with OLTx has a much better outcome than ARF without OLTx. Furthermore, management based on a conservative anticoagulation policy and CVVH as the exclusive form of renal support was associated with the best ICU, hospital and long term survival reported so far.

Cause of Death↗
PubMed1994

Extracellular brain glutamate during acute liver failure and during acute hyperammonemia simulating acute liver failure: an experimental study based on in vivo brain dialysis.

Hyperammonemia is thought to be important in the pathogenesis of hepatic encephalopathy. However, the mechanism leading to ammonia toxicity is still not known. Since the metabolism of the most important excitatory neurotransmitter, glutamate, is closely linked to that of ammonia, it has been postulated that hyperammonemia lowers the availability of the neurotransmitter glutamate. To study this hypothesis, we used brain dialysis to measure glutamate levels in extracellular cerebral fluid from rabbits with acute ischemic liver failure or acute hyperammonemia. The basal glutamate concentration was found to be increased during both acute liver failure (start of experiments 4.9 +/- 1.7 mumol/l; end of experiments 9.5 +/- 2.1 mumol/l, n = 6, difference p < 0.05) and acute hyperammonemia (start of experiments 4.4 +/- 1.2 mumol/l; end of experiments 7.3 +/- 1.8 mumol/l, n = 7, difference p > 0.05) (mean +/- SEM). Both the veratridine- and the potassium-evoked glutamate release were increased during acute liver failure but appeared normal during hyperammonemia. We conclude that during acute liver failure and acute hyperammonemia in the rabbit there is no decreased glutamate availability in the extracellular space of the cortical brain; on the contrary, we found evidence for increased extracellular glutamate concentrations in the cortical brain, which were more pronounced in acute liver failure. Experimental hepatic encephalopathy is thus not due to cerebral glutamate deficiency.

Ammonia↗
PubMed2006

MELD score as a prognostic model for listing acute liver failure patients for liver transplantation.

OBJECTIVES: The King's College Hospital (KCH) criteria are widely used for listing patients with acute liver failure (ALF) for liver transplantation (LT). Recent reports have suggested that the Model for End-Stage Liver Disease (MELD) score may be useful in assessing prognosis in ALF (nonparacetamol). This study compares prognostic accuracy of the two systems in patients with paracetamol (POD)-induced ALF treated in this unit. METHODS: Seventy-two patients (average age 38 years; F:M ratio 2:1) admitted from 1994 to 2005 with POD-related ALF were studied. Clinical and biochemical parameters were recorded. The effect of applying a MELD score of greater than 30 as listing criteria for LT was calculated and compared with the KCH criteria. Outcomes were defined as LT, death, or full recovery. RESULTS: Thirty-one patients (43%) recovered with medical therapy, 29 (40%) patients died, and 12 (17%) underwent LT. Sixty five percent of patients had a MELD > 30 and therefore could potentially be listed on admission; however, using KCH criteria only 24% patients were listed immediately. Sensitivity and negative predictive value of MELD was higher then KCH; however, we found KCH to have much higher specificity and positive predictive value. CONCLUSION: MELD has higher sensitivity and negative predictive value for POD-induced ALF than the KCH criteria. However, the high false-positive rate associated with MELD limits its clinical utility. The high negative predictive value of MELD score may allow it to be used in conjunction with KCH criteria to avoid unneeded LT in patients who will likely recover spontaneously.

Adult↗
PubMed2003

Molecular neurobiology of acute liver failure.

Acute liver failure results in encephalopathy and brain edema that is characterized by astrocytic cell swelling. Molecular biological techniques have led to the identification of alterations in expression of several genes coding for key astrocytic proteins in acute liver failure. Such proteins include amino acid transporters, structural proteins, the endothelial cell glucose transporter GLUT-1, the mitochondrial "peripheral-type" benzodiazepine receptor, and the water channel protein aquaporin IV. Magnetic resonance spectroscopic studies reveal increased brain lactate concentrations that are positively correlated with severity of encephalopathy and brain edema in acute liver failure, suggesting a deficit of cellular oxidative capacity and impending brain energy failure. Mild hypothermia prevents brain edema in acute liver failure, and mechanisms responsible for this beneficial effect include reduced blood-brain ammonia transfer as well as normalization of astrocytic amino acid transport and brain energy metabolism. Further elucidation of the molecular mechanisms responsible for brain edema and encephalopathy in acute liver failure will undoubtedly lead to novel treatment strategies for these complications.

Astrocytes↗
PubMed2000

Prognostic value of abdominal CT scanning and hepatic histopathology in patients with acute liver failure.

Acute liver failure has extremely high mortality without liver transplantation. We attempted to determine the value of abdominal CT scanning and liver biopsy in its management. A retrospective analysis of patients with acute liver failure was performed; demographic, clinical, radiologic and histopathologic features were noted. Over a period of 13 years, 177 patients were evaluated. The mean age was 39 years and 63% were females. The patients were divided into three groups. Fourteen percent survived with medical management (group I), 37% died (group II), and 49% had liver transplantation (group III). Most patients showed diffuse low density of the liver on CT scanning and the proportions were similar in the three groups. Moderate to large ascites was not present in group I but occurred in 31% of patients in group II and in 15% in group III. Mean hepatic volumes were similar in the three groups; however, 97% of the patients with a liver volume of less than 1000 ml either died or required liver transplantation. Liver biopsies among patients with spontaneous recovery (group I) were distinguished by the presence of regenerative changes and a hepatic parenchymal necrosis of less than 50%. These results suggest that in patients with acute liver failure a liver volume of less than 1000 ml and/or hepatic parenchymal necrosis of greater than 50% is indicative of a poor prognosis. This information may assist decision making in such patients, in particular, regarding the need for liver transplantation.

Adolescent↗
PubMed2005

Drug-induced acute liver failure.

Acute liver failure is the most severe expression and represents the first cause of fatalities related to drugs. As a consequence, it is also the first cause of drug withdrawal from the pharmaceutical market. The incidence of drug-induced hepatotoxicity in the general population has been recently estimated to be around 14/100,000 inhabitants in a Western country. Drugs appear to be responsible for 10-52% of all causes of acute liver failure. In Western countries, paracetamol (acetaminophen) represents the first cause of all liver failures. The contribution of non-paracetamol drugs given at normal doses is equivalent to that of combined viral hepatitis A and B. The natural prognosis varies between drugs. The spontaneous mortality rate ranges from 32% to 50% for paracetamol intoxication and more than 75% for other drugs. The preventive occurrence of drug hepatotoxicity and the course to acute liver failure is rather limited. It is recommended to stop the administration of a suspected drug when alanine aminotransferase levels increase to more than 3-5 times the upper limit of normal. In paracetamol intoxication, the rapid administration of N-acetylcysteine is a classical antidote. At the stage of liver failure, treatment is mostly supportive. Since irreversible damage is unpredictable, early transfer to a transplantation centre should be considered.

Acetaminophen↗
PubMed1996

Management of acute liver failure.

Acute liver failure (ALF) constitutes a medical emergency requiring the prompt response of experienced clinicians. As it is relatively infrequent, and tends to evolve rapidly, decisions concerning care and prognosis must be made promptly. Determining etiology is vital since prognosis is largely determined by the cause of the illness, and the use of antidotes may be lifesaving. Estimating the severity of the liver failure is also important, because if liver transplantation is necessary, it must be undertaken quickly. No treatment thus far is better than good general care of the comatose patient, with attention to the special problems associated with acute liver failure: cerebral edema, infection, circulatory collapse. A number of issues have been debated recently, including use of prostaglandins and N-acetylcysteine for treatment of all forms of acute liver failure, and the use of extracorporeal liver assist machines, however, the efficacy of non-specific treatments for this complex syndrome has not been proven.

Drug-Related Side Effects and Adverse Reactions↗
PubMed2003

Advances in extracorporeal detoxification by MARS dialysis in patients with liver failure.

Although liver transplantation has become standard procedure for patients with liver failure, a number of issues in the management of these patients remains to be addressed. Alternative approaches have been tested, such as hepatocytes containing liver-support systems and filtration devices. However, the replacement of detoxification has been difficult, as the majority of toxins accumulating in liver failure is albumin-bound. Albumin dialysis (MARS system) is characterized by the specific removal of albumin-bound toxins through an innovative membrane transport. In particular, the albumin acts as a specific molecular adsorbent that is regenerated on line in a recycling system. Nowadays MARS represents the most frequently used liver support system. This treatment has been shown to remove albumin-bound molecules, such as bilirubin, bile acids, aromatic amino acids and copper. The removal of these toxins is clinically accompanied with an improvement of liver, cardiovascular and renal functions and hepatic encephalopathy. In several trials MARS was found to improve the clinical situation in patients with acute exacerbation of chronic liver failure and acute hepatic failure, but also in hepatorenal syndrome and primary graft non function or chronic rejection after liver transplantation. In summary, a critical analysis of the literature confirms that MARS device can be a safe therapeutic choice to achieve a better clinical outcome, and, sometimes, a survival advantage in patients with liver failure, even if a multi-center randomized trial is the only reliable way to enforce today's results. Further advances in the MARS components will definitively state whether albumin dialysis may represent the future in the field of artificial liver devices.

Adsorption↗
PubMed2002

Nimesulide-induced severe hemolytic anemia and acute liver failure leading to liver transplantation.

We present the case of a 63-year-old woman who had undergone 7 months of treatment with Nimesulide (100 mg/b.i.d.) for symptomatic osteoarthritis. The patient was admitted to our unit with a clinical picture of progressive jaundice over 3 weeks. Clinical and analytical studies revealed acute liver failure, this being confirmed by liver biopsy, which showed submassive necrosis. Serological tests for different viral agents causing hepatitis were all negative. In addition, she presented a picture of severe haemolytic anaemia resistant to several treatments and needed multiple transfusions. Twenty-three days after admission, the patient presented hepatic encephalopathy and received an orthotopic liver transplant on day 25. The evolution after transplantation was good and the patient continues in good health with no evidence of haemolysis almost 2 years later. Liver toxicity due to Nimesulide is well known, but to our knowledge the occurrence of haemolytic anaemia has not been related to this drug previously. For these reasons, Nimesulide has been restricted or removed from the market in several countries in recent months.

Anemia, Hemolytic↗
PubMed1998

[Prognostic factors in acute liver failure].

Acute liver failure is defined as acute severe, potentially reversible hepatic failure complicated by cerebral dysfunction. The high mortality rate of between 50% and 90% justifies early transfer to a specialised centre with the possibility of orthotopic liver transplantation to ensure adequate intensive care monitoring and treatment, 57 patients with acute liver failure (34 female, 23 male, aged 6 to 87 years, median 33 years) treated at our intensive care unit during the past 10 years were analysed retrospectively. Various factors and laboratory data were analysed in respect to their prognostic value. Depending on the aetiology, the survival rate in acute liver failure under conservative treatment ranges from 79% (amanita intoxication) to 10% (cryptogenic genesis). The most important predictive parameter is the extent of cerebral dysfunction. The extent of cerebral dysfunction is a determining factor of the survival rate under conservative treatment; it ranges from 94% (patients with hepatic encephalopathy grade I) to 11% (patients with hepatic encephalopathy grade IV). The occurrence of complications such as infections, cerebral oedema, respiratory failure or renal failure is also associated with an unfavourable outcome. Additionally, various laboratory parameters have a predictive ability. The mortality rate of our patients with acute liver failure has decreased from 56% to 32% since early intensive care monitoring and treatment and the possibility of acute orthotopic liver transplantation were established.

Adolescent↗
PubMed2005

Liver failure in transplanted liver due to Amanita falloides.

Two patients underwent liver transplantation due to Amanita falloides poisoning. In one of them the clinical symptoms, signs, and laboratory findings related to liver failure were similar to the findings before the transplantation. The patient died and the pathological examination of the liver was similar to the patient's earlier explanted liver.

Adult↗
PubMed1994

Acute liver failure.

Acute liver failure is a multiorgan syndrome with dramatic clinical features and, often, a fatal outcome. It is characterized by the onset of coma and coagulopathy within 6 months, and usually in < 6 weeks, from onset of illness. Viral hepatitis, drug-related liver injury, and the alcohol-acetaminophen syndrome are the most common etiologies. Altered mental status accompanied by jaundice is a hallmark of acute liver failure. A unique feature is the evolution of increased intracranial pressure due to cerebral edema. The resulting cerebral ischemia and brainstem herniation account for approximately 50% of deaths in patients with acute liver failure. Mannitol therapy may successfully treat most patients with high intracerebral pressure. Most patients demonstrate features of the multiple organ failure syndrome, including a shock-like state, renal failure, and occasionally respiratory distress syndrome. Close monitoring of volume status is necessary, since administration of large quantities of fluid may be required. Infection is also common; most pathogens are gram-positive, and fungal infections are also seen. Because an optimum therapy for acute liver failure does not yet exist, liver transplantation should be considered early, before advanced levels of coma develop. Alternative, experimental treatment modalities include heterotopic liver grafting, administration of hepatocyte growth factor, use of an extracorporeal liver-assist device, and liver cell transplantation, but none of these has attained widespread use.

Humans↗
PubMed2002

Etiology and outcome of acute liver failure: experience from a liver transplantation centre in Montreal.

BACKGROUND: Acute liver failure is a rare condition in which massive liver injury is associated with the rapid development of hepatic encephalopathy. Although viral hepatitis and drug-induced liver injury are the most common causes, no specific etiology is found in a substantial proportion of cases reported from Europe and the United States. AIM: To determine the etiology and outcome of patients with acute liver failure in the authors' institution. PATIENTS AND METHODS: The charts of 81 consecutive patients admitted to Saint-Luc between 1991 and 1999 were reviewed. RESULTS: The etiology was viral in 27 cases (33.2%), toxic or drug-induced in 22 (27.2%), of unknown origin in 22 (27.2%) and due to various causes in 10 (12.3%) (autoimmune, vascular, cancer). Of the 81 patients, 16% survived without liver transplantation, and 84% died or underwent liver transplantation. Survival without liver transplantation differed according to the mode of presentation: the survival rate was 27% in patients with hyperacute liver failure, 7% in those with acute liver failure and 0% in those with subacute liver failure. Among the 38 patients who underwent liver transplantation, survival one year after transplantation was 71%. In the 30 patients who died without liver transplantation, the main causes of death were cerebral edema and sepsis. CONCLUSIONS: Acute liver failure is associated with a high mortality, and liver transplantation is the treatment of choice. In a significant proportion of cases, the etiology remains undetermined and is probably related to yet unidentified hepatotropic viruses.

Adult↗
PubMed2003

Successful MARS treatment in severe cholestatic patients with acute on chronic liver failure.

Extracorporeal liver devices have gained great attention as a complementary approach to liver transplantation in patients with acute on chronic liver failure. Among others, Molecular Adsorbent Recycling System (MARS) is a hemodiafiltration against albumin able to remove low molecular weight toxins. We aimed to validate the use of MARS in patients presenting with acute on chronic liver failure with severe cholestasis. We enrolled 7 patients with acute on chronic liver failure, presenting with bilirubin >25 mg/dl and hepatorenal syndrome and/or hepatic encephalopathy grade >II. Liver biochemistry, coagulation, blood cell count, electrolytes, ammonia, lactate, blood urea nitrogen, creatinine, bile acids, Fischer ratio, and encephalopathy grade were assessed before and after each MARS treatment. MARS can represent a safe therapeutic choice to achieve a quick improvement of neurological status, a hemodynamic stability, and a better clinical outcome. In particular, our encouraging results suggest that also, patients with severe cholestasis may represent in the future a good indication for MARS treatment.

Adult↗
PubMed2004

Molecular adsorbent recycling system in treating patients with acute liver failure: a bridge to liver transplantation.

BACKGROUND: Acute liver failure is still a life-threatening disease although it can be treated by liver transplantation. This study was conducted to assess the molecular adsorbent recycling system (MARS), which may bridge acute liver failure patients to liver transplantation. METHODS: Biochemical indexes and other clinical data were analyzed of 8 patients with acute liver failure, who had been treated by MARS for 34 times and subsequent Piggyback liver transplantation. RESULTS: After treatment with MARS, the levels of transaminase and total bilirubin decreased markedly, but coagulation function remained unimproved. All patients survived and discharged from the hospital. CONCLUSION: MARS is effective in bridging patients with acute liver failure to liver transplantation.

Acute Disease↗