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PubMed2003

Bridging a patient with acute liver failure to liver transplantation by the AMC-bioartificial liver.

Recently a phase I clinical trial has been started in Italy to bridge patients with acute liver failure (ALF) to orthotopic liver transplantation (OLT) by the AMC-bioartificial liver (AMC-BAL). The AMC-BAL is charged with 10 x 10(9) viable primary porcine hepatocytes isolated from a specified pathogen-free (SPF) pig. Here we report a patient with ALF due to acute HBV infection. This patient was treated for 35 h by two AMC-BAL treatments and was bridged to OLT. There was improvement of biochemical and clinical parameters during the treatment. No severe adverse events were observed during treatment and follow-up of 15 months after hospital discharge. Possible porcine endogenous retrovirus (PERV) activity could not be detected in the patient's blood or blood cells up to 12 months after treatment.

Adult↗
PubMed1999

A predictive model for the development of hepatocellular carcinoma, liver failure, or liver transplantation for patients presenting to clinic with chronic hepatitis C.

OBJECTIVE: Chronic infection with hepatitis C may lead to the development of cirrhosis, liver failure, and hepatocellular carcinoma. However, not all patients progress to these endpoints. Ideally, clinicians could improve their capability of stratifying the risk and the time frame within which their patients will progress to these endpoints. The purpose of the present study was to construct statistical models predicting disease progression for individual patients. METHODS: Study endpoints were the development of hepatocellular carcinoma, liver transplantation, or death due to liver disease. The study cohort was 256 patients with hepatitis C acquired from either blood transfusion or use of intravenous drugs. During follow-up, 17 patients developed hepatocellular carcinoma, seven received liver transplantation, and 12 died from liver disease. RESULTS: On multivariate analysis a history of decompensation (relative risk [RR] 4.321, 95% confidence interval [CI] 1.777-10.511) and the serum albumin (RR 0.253, 95% CI 0.136-0.474) were independently associated with the study endpoints. Patients without a history of decompensation and with a serum albumin > or = 4.1 mg/dl had a 3.2% chance of developing the study endpoints within 5 yr. Patients with a history of decompensation and a serum albumin < 4.1 mg/dl had a 40% chance of developing a study endpoint within 5 yr. Baseline genotype and quantitative RNA were not associated with development of the clinical endpoints, with the exception of patients coinfected with two or more genotypes. CONCLUSION: Thus, the serum albumin and a history of decompensation are useful for predicting the development of hepatocellular carcinoma, liver transplantation, and death due to liver disease among patients with hepatitis C.

Adult↗
PubMed2006

Primary herpes simplex virus type-2 infection as a cause of liver failure after liver transplantation.

We report a case of fatal primary herpes simplex virus type-2 (HSV-2) infection following liver transplantation, which manifested with fever and liver failure in the absence of muco-cutaneous disease. The infection was characterized by high levels of HSV DNA in blood and the patient's inability to mount HSV-specific T-cell responses while showing preserved T-cell responses against cytomegalovirus. The donor was HSV-1 immunoglobulin G (IgG) seronegative and HSV-2 IgG seropositive, whereas the recipient was HSV-1 and HSV-2 IgG seronegative, suggesting that the graft may have been the source of the infection. In HSV-seronegative recipients of grafts from HSV-seropositive donors, HSV infection should be included in the differential diagnosis of a febrile illness, regardless of the absence of muco-cutaneous disease. In this setting, real-time polymerase chain reaction applied to blood samples provides a sensitive, rapid, and quantitative diagnostic tool.

Adult↗
PubMed1999

Treatment of acute liver failure: hybrid liver support. A critical overview.

Hybrid liver support systems, which combine living cells of the liver in an extracorporeal circuit, have entered the first clinical trials in patients with acute liver failure. The goal of the different developments is to provide within a few hours a biological support of the patient's failing liver. Different technical solutions can be found to provide a sufficient functional mass of liver cells to the patient. Within this article, the biotechnical and clinical backgrounds of these developments are discussed, initial clinical results are summarized and an evaluation of this method as experimental treatment is given.

Animals↗
PubMed1999

Hepatitis A-induced diabetes mellitus, acute renal failure, and liver failure.

A 38-year-old otherwise healthy man presented with hepatic failure (aspartate aminotransferase of 7212 U/L, alanine aminotransferase of 6629 U/L, total and direct bilirubin of 10.7 mg/dL) and acute renal failure (creatinine of 11.6 mg/dL and blood urea nitrogen of 42 mg/dL), which required hemodialysis when the creatinine increased to 21 mg/dL, with a blood urea nitrogen of 115 mg/dL, and the patient became oliguric. On admission, this patient also had a lipase of 1833 U/L, amylase of 211 U/L, glucose of 210 mg/dL, and reactive IgM antibody for acute hepatitis A. The hepatitis and acute renal failure resolved in 3 months, but this patient continues to have type II diabetes mellitus 7 years after the hepatitis A infection. This case illustrates that hepatitis A infection may be severe with liver failure, acute renal failure, and permanent diabetes mellitus as sequale of this infection.

Acute Kidney Injury↗
PubMed2005

Ma huang associated acute liver failure requiring liver transplantation.

An ever increasing number of herbal remedies are recognized as potentially hepatotoxic. We report a case of fulminant hepatic failure requiring liver transplantation associated with the use of Ma huang, a traditional Chinese remedy containing ephedrine-type alkaloids. The literature surrounding the potential liver toxicities of Ma huang is reviewed and the proposed pathogenetic mechanisms are critically examined.

Drugs, Chinese Herbal↗
PubMed1988

[Orthotopic liver transplantation in Wilson's disease and acute liver failure].

Liver histology demonstrated progressive cirrhosis in a 19-year-old girl with a subacute form of Wilson's disease. Despite D-penicillamine administration her liver functions rapidly deteriorated further. Orthotopic liver transplantation was performed. Postoperatively there were two mild rejection episodes, an organic psychiatric syndrome and generalized tremor. Copper metabolism and clinical symptoms became normal postoperatively. Five months after the transplantation she was in a good general condition, able to continue her education.

Acute Disease↗
PubMed1973

Liver biopsy and prognosis in acute liver failure.

Liver biopsy was performed in 38 patients with fulminant hepatitis and coma and repeated in 22. Stereological estimation of hepatocyte volume was correlated with levels of clotting factors. Early liver biopsy allowed prognosis in 55% of the cases. All patients with a hepatocyte volume of <35% and thromboplastin time </=10% died; all patients but two with hepatocyte volume >/=35% and thromboplastin time >10% recovered consciousness (n = 9) or at least showed evidence of marked liver regeneration (n = 2). On serial liver biopsy a significant increase in hepatocyte volume and clotting factors was only observed in patients who recovered consciousness. The estimated liver cell mass after regeneration in patients who recovered consciousness was >/=45% and <45% in the patients who did not.

Acute Disease↗
PubMed2000

Troglitazone-induced fulminant hepatic failure. Acute Liver Failure Study Group.

The three reported cases demonstrate that troglitazone is an idiosyncratic hepatotoxin that can lead to irreversible liver injury. Thus, troglitazone should be prescribed with caution and should not be used as a first-line agent in the treatment of type II DM when potentially less toxic alternatives are available. It remains to be seen whether the hepatotoxicity associated with troglitazone is a drug-class effect or specific to troglitazone. Other thiazolidinediones currently in clinical trials may be able to provide the therapeutic benefits of troglitazone without significant hepatotoxicity. If troglitazone is used, frequent monitoring of serum aminotransferases and symptoms is mandatory. However, as illustrated by these and other cases reported to date, the onset of troglitazone-induced liver injury is insidious and temporally variable. Thus, the value of close monitoring and when, if ever, it is safe to stop such monitoring are currently unclear.

Chromans↗
PubMed2005

Comparison of pioglitazone with other antidiabetic drugs for associated incidence of liver failure: no evidence of increased risk of liver failure with pioglitazone.

AIM: The aim of this study was to assess the incidence of liver failure in association with antidiabetic treatment using pioglitazone vs. other oral antidiabetic medications. METHODS: The study was a retrospective analysis of claim data from the PharMetrics Patient-Centric Database that had over 1.12 million enrollees with type 2 diabetes. All patients, > or =18 years of age with type 2 diabetes, who had initiated treatment either with a thiazolidinedione (pioglitazone and rosiglitazone), sulfonylurea or metformin were identified and matched on the basis of propensity scores, which served as a proxy for severity of disease. The primary measure of interest was the incidence of liver failure or hepatitis post-index date. In addition to unadjusted comparisons, Cox proportional hazard models were employed to estimate the risk of developing liver failure or hepatitis. RESULTS: There was no significant difference in the 1- and 2-year incidence rates of liver failure or hepatitis (primary and secondary diagnoses) between the pioglitazone monotherapy group and the respective comparator groups. In Cox proportional hazard models controlling for age, pre-index total healthcare costs, Charlson comorbidity index, procedures and a hospitalization or Emergency room (ER) visit for pre-index hyperglycaemia, and pioglitazone were not associated with an increased risk of liver failure or hepatitis, compared to all other defined groups. Furthermore, no primary or secondary diagnosis of liver failure was reported in the pioglitazone group during the follow-up period. CONCLUSIONS: Results of retrospective data analysis demonstrate no evidence of increased risk of liver failure or hepatitis for patients initiating therapy on pioglitazone, compared to other oral antidiabetic agents. Pioglitazone therapy was not associated with an increased risk of liver failure at 2 years relative to other oral antidiabetic therapies.

Administration, Oral↗
PubMed2001

Relevance of two-stage total hepatectomy and liver transplantation in acute liver failure and severe liver trauma.

Emergency liver transplantation frequently is the only life-saving procedure in cases of acute liver failure. It remains unclear whether emergency hepatectomy with portocaval shunt followed by liver transplantation as a two-stage procedure should be performed in cases in which a donor organ is not yet available. It has been stated that "toxic liver syndrome" could be treated by means of this strategy. From 1990 to 1995 we performed emergency hepatectomies in eight cases of acute liver failure or traumatic liver rupture with exsanguinating bleeding. In six cases we were able to perform a subsequent liver transplantation. Five of the six patients who underwent an emergency hepatectomy died. Emergency hepatectomy led to a significant increase in epinephrine dosage until the transplantation was performed. Only after transplantation did the need for epinephrine therapy decrease. The need for oxygen support did not change during the entire observation period. Plasmatic coagulation was stabilized by substitution, showing significantly higher values at 24 h after transplantation than at 48 h before transplantation. Fibrinogen increased significantly after transplantation in this group of patients. The experiences gathered at our clinic, however, do not show advantages that would allow a recommendation of emergency hepatectomy and subsequent liver transplantation as a two-stage procedure except for situations of severe and uncontrollable hepatic bleeding. Considering the progressive destabilization of our patients, fast procurement of donor organs seems to be of imminent importance for the outcome.

Acute Disease↗
PubMed1999

Acute liver failure.

Acute liver failure is a rare but potentially fatal disease. Adult definition of fulminant hepatic failure, which includes the development of hepatic necrosis and encephalopathy within 8 weeks of onset of liver disease does not apply to acute liver failure in children particularly if secondary to autoimmune or metabolic liver disease. The etiology of acute liver failure varies with the age of the child. In neonates, infection or an inborn error of metabolism are common, while viral hepatitis and drug induced liver failure are more likely in older children. The clinical presentation of acute liver failure includes jaundice, coagulopathy and encephalopathy. In neonates, encephalopathy may be subclinical. The management of acute liver failure includes assessment of prognosis for liver transplantation; prevention and treatment of complications while awaiting hepatic regeneration or a donor liver and hepatic support. The major complications of acute liver failure are sepsis, gastro-intestinal bleeding, cerebral edema, renal and cardiac failure. Selection for liver transplantation depends on the etiology of the disease, prognostic factors, the presence or absence of multisystem disease and/or reversible brain damage. Prognostic factors for survival are less well established in children than in adults but children with metabolic liver disease, prothrombin time > 50 seconds, rising bilirubin and falling transaminase, grade II or higher grade of hepatic coma indicate poor prognosis. Most children receive a reduced or split liver graft. Living related donations for acute liver failure are also carried out by some centres. Survival post liver transplantation for acute liver failure has improved and most recipients can expect a 70% five year survival.

Age Distribution↗
PubMed1999

Renal failure in acute liver failure.

Renal failure develops in approximately 55% of all patients referred to specialized centres with acute liver failure. The renal failure may be secondary to the liver failure itself (and is termed the hepatorenal syndrome) or the renal failure may be a secondary insult that directly affects both liver and kidney alike (for example paracetamol overdose). The pathogenesis of the hepatorenal syndrome involves the development of a hyperdynamic circulation, with a lowering of renal perfusion pressure, the activation of the sympathetic nervous system, which renders the kidneys more susceptible to modest decreases in perfusion pressure, and increased synthesis of a variety of vasoactive mediators. These mediators can cause renal vasoconstriction, but more importantly they can also decrease the glomerular capillary ultrafiltration coefficient (Kf), thus causing a decline of glomerular filtration rate over and above that caused by renal vasoconstriction alone. The treatment of the renal failure in acute liver failure involves the optimization of renal haemodynamics and haemofiltration. Renal failure will always recover when there is recovery of liver function, and in the absence of a spontaneous hepatic recovery, liver transplantation will reverse the hepatorenal syndrome.

Acute Kidney Injury↗
PubMed2002

Splanchnic circulation and metabolism in patients with acute liver failure.

Acute liver failure is associated with mortality of around 50%. The aim of the present studies was to examine the circulatory and metabolic state of the splanchnic region in acute liver failure. This had not been studied previously and it could be expected that improved understanding of the pathophysiology of acute liver failure could lead to improved therapy. Hepatic plasma flow was estimated in patients with acute liver failure after development of hepatic encephalopathy grade III, by the use of liver vein catheterization and continuous infusion of sorbitol. The method was evaluated against the prerequisites of Fick's principle. Hepatic plasma flow could be estimated with sorbitol but not in all patients and the standard error of the estimated hepatic blood flow was higher than in other patient groups. In 20 patients with acute liver failure, mean hepatic blood flow was increased. At the same time, the systemic and the peripheral hemodynamics were examined. The ratio hepatic blood flow/cardiac output was increased in many patients. Lower extremity blood flow was within normal limits. Thus, low systemic vascular resistance index in acute liver failure was likely to be a consequence of vasodilatation in the muscular resistance vessels and, in particular, in the splanchnic resistance vessels. Intervention with high-volume plasmapheresis changed systemic and splanchnic hemodynamics differently, suggesting that the splanchnic vasodilatation in liver failure may by caused by a specific mechanism different from the one that leads to peripheral vasodilatation. Infusion of dopamine increased mean arterial pressure, cardiac output, and hepatic blood flow in acute liver failure. The splanchnic exchange of substrates for oxidative metabolism was examined. Splanchnic oxygen consumption was increased. The ratio splanchnic oxygen consumption/systemic oxygen consumption indicated that 1/3 of the oxygen used in the whole body in acute liver failure was used in the splanchnic region. The splanchnic metabolism of fuel substrates was abnormal. Lactate and pyruvate was released and there were no detectable gradients of free fatty acids or of the sum of amino acids. There was a small release of ketone bodies. The data suggested that the energy needs of the failing liver was covered by intracellular fat. The hypothesis of splanchnic tissue hypoxia was examined from different approaches. The normal hepatic venous oxygen saturation, the splanchnic release of both lactate and pyruvate, and a normal hepatic venous pyruvate/lactate ratio in the presence of low acetoacetate/hydroxybutyrate ratio rather indicated high substrate turnover than splanchnic tissue hypoxia. Amino acid and ammonia metabolism was examined. It was observed that arterial ammonia concentration measured after institution of mechanical ventilation was associated with cerebral herniation 1-5 days later. The background for hyperammonemia was that ammonia was released from the splanchnic circulation. The data implied that glutamine was deamidated in the gut and alanine and ammonia was released into the portal vein as during normal circumstances. Then due to severely decreased hepatic function the liver was unable to remove ammonia and alanine as it normally would. Further, the data implied that urea synthesis was impaired. Exchange of ammonia in muscle tissue was studied in 7 patients with acute liver failure and muscle tissue seems to play a major role in ammonia detoxification in acute liver failure. Treatment with high-volume plasmapheresis decreased arterial ammonia, which was likely due to increased urea production or stimulation of glutamine synthesis in muscle tissue. These findings add to our understanding of the pathophysiology and have implications for the management of acute liver failure.

Amino Acids↗
PubMedDate not supplied

[Acute liver failure].

Acute liver failure, also called fulminant hepatic failure, is characterized by sudden hepatic synthetic dysfunction associated with coagulopathy and hepatic encephalopathy. Acute liver failure has most recently been defined based on the timing from onset of jaundice to encephalopathy as follows: 1) hyperacute (1-7 days); 2) acute (8-28 days), and 3) subacute (29-60 days). Rapid onset of encephalopathy in hyperacute liver failure is paradoxically associated with highest rate of spontaneous recovery, and subacute liver failure is associated with worst prognosis. The etiology of liver failure is established by history, serologic assays, and exclusion of alternative causes. Acute liver failure is most frequently caused by drug hepatotoxicity, including acetaminophen toxicity and idiosyncratic drug reactions, with viral hepatitis playing a lesser role in recent surveys. A substantial number of cases have an indeterminate etiology. Major complications of acute liver failure that require active intervention include metabolic disorders, coagulopathy, cerebral edema, renal failure, and infection. The focus of management of acute liver failure is comprehensive supportive care in an intensive care unit and assessment of the need for liver transplantation.

Humans↗
PubMed2005

Evaluation of plasma ammonia levels in patients with acute liver failure and chronic liver disease and its correlation with the severity of hepatic encephalopathy and clinical features of raised intracranial tension.

OBJECTIVES: The present study was designed to (a) evaluate and compare plasma ammonia levels (PAL) in patients with acute liver failure (ALF) and chronic liver disease (CLD) with or without hepatic encephalopathy (HE); (b) correlate the severity of HE with PAL; and (c) correlate PAL with clinical features of raised intracranial tension in ALF. DESIGN AND METHODS: A total of 40 patients, comprised of 20 patients with ALF (Group A) and 20 patients with CLD (Group B, which was comprised of 8 patients with HE (subgroup B1) and 12 patients without HE (subgroup B2)), were studied. PAL was estimated using an enzymatic UV-method (RANDOX). The clinical and biochemical profile of all the patients was recorded. Correlation between the grade of HE and PAL was derived using Pearson's correlation coefficient. The mean PAL of ALF patients with and without raised intracranial tension was compared using the standard error of difference between the two means. RESULTS: The mean PAL (micromol/L) +/- SD was as follows: Group A: 172.1 +/- 52.55, subgroup B1: 58.75 +/- 29.38, subgroup B2: 42.17 +/- 18.19 (normal levels = 10-47 micromol/L). All patients with ALF showed PAL more than the upper limit of the normal range, and there was good correlation between the severity of HE and PAL [r = 0.91 at P < 0.05]. In subgroup B1 (CLD with HE), 3/8 patients (37.5%), and in subgroup B2 (CLD with HE), 4/12 patients (33.3%) patients had PAL more than the upper limit of normal range. Within Group A, 14 patients had clinical features of raised intracranial tension/cerebral edema, and the mean PAL of these patients (188.21 +/- 49.15 micromol/L) was significantly higher than those who did not have features of raised intracranial tension (134.5 +/- 42.36 micromol/L) (SE of difference between two means). CONCLUSIONS: Raised PAL appears to be an important laboratory abnormality seen in patients with ALF, and there seems to be a significant correlation between the severity of encephalopathy and PAL in these patients. However, among patients with CLD, the proportion of patients with PAL more than the upper limit of normal range is not significantly different between those with or without HE. Our study also suggests that high PAL in ALF patients appears to correlate with clinical features of cerebral edema and raised intracranial tension.

Adult↗