Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fulminant hepatic failure (FHF) is a poorly understood condition in which total liver failure occurs and is thought to be caused by a variety of conditions including Reye's syndrome, hepatitis, drug overdoses, and vascular insufficiency. While this condition is an uncommon one, it carries with it a high fatality rate and must therefore be diagnosed as rapidly as possible. Six patients have been observed over a two-year period with biopsy and/or autopsy-confirmed FHF: one with acute hepatitis B-delta; three with histories of alcoholism, two of them with cirrhosis; one with acute tylenol overdose; and one with hepatic vascular insufficiency. All of these patients, except one, exhibited a rapid, fatal downhill course after onset of symptoms. In all of these patients, a consistent elevation was observed in serum levels of aspartate aminotransferase (AST) or serum glutamate oxaloacetate transaminase (SGOT) and alanine aminotransferase (ALT) or serum glutamate pyruvate transaminase (SGPT) such that the ratio of AST to ALT was significantly greater than 1 and in serum levels of ammonia. Other liver function tests were found to be abnormal but not in so consistent a pattern, although total protein and albumin were found to be significantly decreased in all of these patients. The stereotypical elevation of the transaminases with high AST-to-ALT ratios and the rise in ammonia appear to characterize this life-threatening illness most reliably.
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PMID:Serum analyte pattern characteristic of fulminant hepatic failure. 820 19

The cause of fulminant hepatic failure is reported to be unknown in more than half the cases in Japan. We recently reviewed 23 cases of fulminant hepatic failure that had been treated at our hospital. The cause of disease had been regarded as unknown before this study. It was found that seven of these patients had been under ecarazine hydrochloride therapy when they developed fulminant hepatic failure. We examined the reasons why fulminant hepatic failure in these seven patients had not been previously attributed to ecarazine, and found that it could be explained by the following factors: (1) the time from the start of ecarazine therapy to the onset of hepatic failure was long; (2) in all cases, hepatic failure developed more than 10 days after the clinical recognition of hepatitis; and (3) characteristic signs of drug-induced hepatic failure such as a skin rash and positive lymphocytes stimulation test with the drug were absent in all cases. Fulminant hepatic failure in these cases could be characterized by: (1) rapid decrease in serum alanine transaminase (ALT) level after discontinuation of ecarazine, (2) prolonged jaundice despite discontinuation of ecarazine, (3) high incidence of anti-nuclear antibody (ANA) (57%), and (4) histological findings of extensive hepatocellular necrosis ranging from bridging necrosis to massive necrosis. Of the seven patients, four died of fulminant hepatic failure. These four patients had received high doses of ecarazine hydrochloride for prolonged periods. Our data suggest that there may be many cases in which the cause of fulminant hepatic failure or acute hepatitis was not previously determined that can be attributed to long-term drug therapy for chronic diseases.
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PMID:Fulminant hepatic failure caused by ecarazine hydrochloride (a hydralazine derivative). 861 25

Fulminant hepatic failure (FHF) is an established indication for liver transplantation. A pretransplant diagnosis of FHF may be a risk factor for subsequent development of cytomegalovirus (CMV) infection, although the mechanism of this association is not understood. FHF is associated with very high levels of tumor necrosis factor alpha (TNF-alpha), and TNF-alpha may directly promote viral replication. We have used the polymerase chain reaction (PCR) to examine sequentially collected buffy coats from 106 consecutive adult liver transplant recipients. PCR evidence of CMV replication was found for 13 of 18 patients who underwent transplantation for FHF (c.f. 23/88 non-FHF patients; P < .01). Ten of 12 patients who received transplants transplanted for fulminant seronegative hepatitis were buffy-coat PCR-positive, sometimes during the first posttransplant week. TNF-alpha was measured by enzyme-linked immunosorbent assay in selected sera, and results were examined in the context of a quantitative PCR assay. Serum TNF-alpha levels increased and decreased in concert with viral titers. High levels of TNF-alpha were not found in the early posttransplant period. We conclude that FHF (in particular, seronegative hepatitis) is associated with enhanced CMV replication in the posttransplant period. Results also suggest that viral replication may be enhanced before transplantation. These patients may be at special risk for development of symptomatic CMV infection.
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PMID:Enhanced (cytomegalovirus) viral replication after transplantation for fulminant hepatic failure. 934

Fulminant hepatic failure is a life-threatening condition associated with a mortality of approximately 80 per cent. Liver transplantation may be the only life-saving recourse in such cases. The condition can be caused by any of a number of different agencies such as viral infection, or toxic, circulatory or metabolic factors, though in a large proportion of cases the aetiology is unknown. Recently, knowledge has accumulated of a new hepatitis virus, hepatitis GB virus (HGBV), a Flavivirus remotely related to hepatitis C. The clinical significance of this virus is unclear. It is found in 3-4 per cent of blood donors, and most HGBV-positive patients are asymptomatic though some develop fulminant hepatic failure. The article consists in a case report of fulminant hepatic failure in a 17-year-old woman where no possible aetiological factor could be identified, other than her HGBV-positivity. The patient underwent a successful liver transplantation and is now, 18 months later, in excellent condition. She is still HGBV-positive but manifests no hepatic effects. Whether HGBV infection was responsible for the hepatic failure remains unclear, however.
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PMID:[Hepatitis GBV isolated in acute liver failure. Successful outcome after liver transplantation]. 941 Oct 92

Most cases of acute hepatitis are caused by hepatitis viruses A, B or C. Diagnosis rests on the risk factor history and serological tests. In seronegative cases, consider other agents, such as Epstein-Barr virus and cytomegalovirus, drug reactions and autoimmune hepatitis. Hepatitis A and B can be prevented by appropriate use of highly effective, safe vaccines. Acute liver failure is an uncommon, devastating complication of acute viral hepatitis; continued vomiting, prolongation of prothrombin time and clouding of consciousness are indications for urgent transfer to a liver transplant unit. Hepatitis A is a simple, enterically transmitted illness that does not cause chronic hepatitis. 95% of adults recover from acute hepatitis B, whereas infection with hepatitis B virus acquired in childhood usually becomes chronic.
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PMID:Acute viral hepatitis. 964 Mar 8

Autoimmune hepatitis is a chronic inflammatory liver disorder of unknown etiology associated with serum autoantibodies and hypergammaglobulinemia. This disease has a broad spectrum of presentations ranging from asymptomatic to fulminant hepatic failure. A 36 year old female with past history of hypothyroidism developed jaundice 2 months prior to admission. Outpatient evaluation revealed ANA and anti-SMA antibodies in high titers, negative viral markers for hepatitis, and hypergammaglobulinemia. A presumptive diagnosis of autoimmune hepatitis was made; steroids were recommended but the patient did not take them. She was admitted to the University Hospital due to increased jaundice, general malaise and ascites 5 weeks later. She deteriorated developing coagulopathy, encephalopathy and increasing hyperbilirubinemia. Intravenous corticosteroids were started. The patient improved and was discharged 3 weeks after admission. Fulminant hepatic failure has a high mortality and may require liver transplant. Our patient survived fulminant hepatic failure that resolved after corticosteroid therapy. It is important to identify and distinguish autoimmune hepatitis from other forms of liver disease because of the high percentage of response to immuno-suppressive therapy. Early diagnosis and treatment of this condition could improve survival, quality of life, and defer liver transplantation.
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PMID:Steroid therapy in fulminant hepatic failure secondary to autoimmune hepatitis. 988 78

Acute hepatic failure develops as a disease entity of rather diverse origin. With disease progression, toxic bilirubin levels may cause severe complications which include AV-nodal blockage, cardiac arrhythmia, impaired consciousness, generalized seizures, and status epilepticus. Treatment choices to prevent clinical deterioration comprise of costly and limited available orthotopic liver transplantation, utilization of extracorporeal bioartificial liver support devices and haemoperfusion/plasmaperfusion treatment with activated charcoal/anion exchange filters. Here, we present a patient with acute drug-induced cholestatic hepatitis. Excessively elevated bilirubin levels were accompanied by cardiac and cerebral complications. Extracorporeal resin perfusion treatment (Plasorba, BR-350) was successfully performed over a 50-day period without activation of the coagulation system or side effects. Bilirubin levels were lowered to a minimum of 225 micromol/l, with concurrent clinical improvement. In conclusion, extracorporeal anion exchange plasmaperfusion may be a viable long-term treatment for hyperbilirubinaemic side effects in overt cholestatic hepatitis.
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PMID:Long-term extracorporeal bilirubin elimination: A case report on cascade resin plasmaperfusion. 1034 81

Fulminant hepatic failure (FHF) is a clinical syndrome resulting from massive death of liver cells or sudden and severe impairment of liver function. The causes of FHF are diverse and the overall mortality is very high. Recently, it became clear that apoptosis of hepatocytes is the critical cause of acute hepatic failure in FHF. It is well known that a family of cysteine proteases called caspase is one of the key mediators of the apoptotic pathway. Thus, caspases are attractive potential targets for the treatment of disorders resulting from excessive apoptosis. In this report, we examined the activity of a new caspase inhibitor, Xyz 033 mp. This nonpeptide inhibitor showed broad-spectrum caspase-inhibiting activity and protected primary rat hepatocytes from apoptotic death. In a mouse model of FHF induced by concavalin A (Con A), Xyz 033 mp suppressed elevated AST and ALT and specifically reduced IL-1 beta concentration. Also, Xyz 033 mp rescued mice from lethal experimental hepatitis induced by Con A. In addition, histological examinations indicated that Xyz 033 mp protected hepatocytes from the fatal apoptogenic effect of Con A. These results suggest that Xyz 033 mp may be a candidate therapeutic agent for FHF caused by massive apoptotic death of hepatocytes.
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PMID:A broad-spectrum caspase inhibitor blocks concanavalin A-induced hepatitis in mice. 1111 61

Liver transplantation has been recognized as an effective therapeutic method for end-stage liver disease in Japan. Fulminant hepatic failure is also an indication for liver transplantation, and the number of patients undergoing liver transplantation has been increasing. Reversibility and urgency are characteristics of fulminant hepatitis. If given appropriate critical support, many patients recover spontaneously. However, many patients develop cerebral edema or multiorgan failure before the liver can regenerate. Indications, operative procedures, and outcome of liver transplantation for fulminant hepatitis are discussed here. At Shinshu University, 23 of 169 cases of liver transplantation were for fulminant hepatitis. One transplantation was from a cadaveric donor and 22 from living donors. The actuarial 5-year patient and graft survival rate was 85.4%. Although some problems remain in liver transplantation for fulminant hepatitis, the results are better than those of conventional therapy. Therefore patients with fulminant hepatic failure should be listed for liver transplantation when grade 2 hepatic encephalopathy develops. Moreover, in cases of severe acute hepatitis, i.e., before patients develop grade 2 encephalopathy, liver transplantation should be considered among choices of therapy in the near future.
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PMID:[Liver transplantation for fulminant hepatitis]. 1204 75

As reported in the literature, the mortality rates for patients with Acute Hepatic Failure (AHF) approaches 80% in cases in which liver transplantation is not possible. Post-transplant mortality mostly depends on the severity of the neurological condition at the time of the operation (20% in I-II degree coma patients and 44% in III degree coma patients). The primary indications for liver transplantation in AHF are Fulminant Hepatitis (FH)(93%), Subfulminant Hepatitis (5%) and other indications (2%). Other causes of AHF are Primary Non-Function (PNF) and Delayed Function (DF), which occur in 7-10%. Therefore it becomes necessary to monitor the patients with a Liver Support Device to be able to improve the clinical condition of the patients before liver transplantation (LT). In our experience we used the Molecular Adsorbent Recirculating System (MARS) (MARS Monitor; Teraklin AG, Rostock Germany), which enables the selective removal of albumin-bound substances accumulating in liver failure by the use of albumin-enriched dialysate. The system is used as a bridging device to orthotopic liver transplantation (OLT) of patients with FHF. We studied 34 patients, including 16 males and 18 females: 9 were affected by Primary-Non-Function (PNF), nine by Fulminant Hepatitis (FH), six by Delayed-Non-Function (DNF), and ten by Acute on Chronic Hepatic Failure (AOCHF). The average age of the patients was 41.8 years and the average number of applications was 6.4; the median length of application was about eight hours. The parameters that we monitored, before and after each treatment, were neurological status (EEG, cerebral CT, Glasgow Coma Score), haemodynamic parameters, acid base equilibrium, and blood gas analysis. We also monitored hepatic and renal function. In addition, the clinical conditions of the patients were monitored using kidney and liver ultrasound/ultrasonography (US). Inclusion criteria were bilirubin > 15 mg/dL, ammonia > 160 micro g/dL and a Glasgow Coma Score between 6 and 11. The reduction of bilirubin and ammonia were very significant (P < 0.01), whereas the changes of International Normalized Ratio (INR) were not significant. Also the modifications of albumin, total protein, sodium, potassium and calcium were not significant. In conclusion, four out of nine patients with PNF are alive without a second transplantation and were discharged after about 48 days; four out of nine underwent OLT, while one out of nine died; five out of six patients with DF are alive without a second transplantation, and they were discharged after an average time of 55.5 days, one out of six died; six out of nine patients with fulminant hepatitis underwent OLT and four of these are alive, while two died due to sepsis; three patients are alive without OLT. Four patients with AOCHF underwent OLT and are alive, three patients are alive and on a waiting list, two died while on a waiting list and one patient who experienced reactivation of HBV infection during chemotherapy for non-Hodgkin's lymphoma is alive. In spite of the limited number of cases of our study, we believe that MARS can be applied with high tolerance for a very long period of time. In addition, its repeatability allows it to be used in patients with DNF and FH as a bridge to transplant. In patients with DNF, it is used while waiting for complete recovery of the transplanted organ.
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PMID:MARS (Molecular Adsorbent Recirculating System): experience in 34 cases of acute liver failure. 1222 Mar 3


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