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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new artificial liver support system (ALSS) consisting of plasma exchange (PE) in combination with hemodiafiltration (HDF) using high-performance membranes of polymethyl methacrylate (PMMA) and cellulose triacetate (CTA) was developed to efficiently remove middle molecules from plasma and treat fulminant hepatic failure (FHF) complicated by the onset of hepatic coma. Twenty-seven patients with FHF due to viral hepatitis, two with type A (HA), nine with type B (HB), and 16 with type non-A, non-B (NANB) underwent therapy with this new ALSS over the last five years. Three patients with an exacerbation of chronic HB and 15/16 with type NANB hepatitis were treated with interferon (IFN) also. Of these, 25 patients (92.6%) regained consciousness and 15 (55.6%) [1/2 (50%) with type A, 6/9 (66.7%) with type B and 8/16 (50%) with type NANB hepatitis] survived. Including four patients who survived with intensive care and plasma exchange alone, 19/31 (61.3%) patients survived. Because of its biocompatibility, both survivors and nonsurvivors could be sustained with the ALSS without complications for long periods (19.3 days for the survivors and 32.4 days for nonsurvivors). With this ALSS the ability to sustain life for such prolonged periods allows hepatic regeneration to occur and result in patient survival. It is anticipated that this new ALSS will not only be of value in cases of fulminant hepatic failure but that it may also play a role in sustaining life for those awaiting liver transplantation.
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PMID:Development of reliable artificial liver support (ALS)--plasma exchange in combination with hemodiafiltration using high-performance membranes. 844 78

The two most serious symptoms of fulminant hepatic failure are bleeding and hepatic coma. To overcome these problems, we developed an artificial liver support system comprising a combination of plasma exchange and hemodiafiltration using a high performance membrane. We treated 67 patients with fulminant hepatic failure. Of these, 65 patients (97.0%) regained normal consciousness, and 55 patients (80.9%) were kept alert as long as we continued to apply this system. All 7 patients (100%) with fulminant hepatitis caused by hepatitis A virus infection and 9 of 12 patients (75%) with fulminant hepatitis caused by acute hepatitis B (HB) virus infection survived. In addition, 7 of 15 HB virus carriers (46.7%) who developed fulminant hepatitis and 11 of 29 patients (37.9%) with fulminant hepatitis caused by non-A, non-B hepatitis viruses survived. The overall survival rate was 37 of 67 patients (55.2%). Our artificial liver support system allows as high a survival rate as liver transplantation.
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PMID:Favorable effect of new artificial liver support on survival of patients with fulminant hepatic failure. 890 26

The aim of this study was to develop in rats, a model of acute hepatic failure that mimics human fulminant hepatitis and to study the effect on survival of transplantation of isolated hepatocytes. This study showed that the mortality after 90% hepatectomy was reduced by the sole correction of hypoglycemia. On the other hand, 95% hepatectomy appeared as a reliable and reproductable model, associated with a period of hepatic coma, a deep disorder of coagulation, and a high mortality rate (> 80%) despite correction of hypoglycemia. In this model of acute hepatic failure, intraperitoneal transplantation of encapsulated isolated hepatocytes significantly reduced the mortality rate from 80% in the control groups to 31% in the transplanted group. A complete regeneration of the native liver was observed in all rats surviving. All animals survived after explantation of the hollow fibers. Well preserved hepatocytes were observed in hollow fibers two months after transplantation.
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PMID:[A good model of acute hepatic failure: 95% hepatectomy. Treatment by transplantation of hepatocytes]. 897 43

Between 1971 and 1989 we have treated 19 patients with hepatitis-associated aplastic anemia by marrow transplantation from their HLA-identical siblings following conditioning with 200 mg/kg cyclophosphamide (Cy) administered over a period of 4 days. One patient failed to engraft by day 34 and was given a second transplantation. He died from infection 15 days after the second transplantation. Eighteen patients had sustained engraftment. Six patients developed acute graft-vs.-host disease (GVHD) and two of these patients died 2.8 and 3.3 months after transplantation. Fifteen patients are surviving 4 to 24 (median 13) years after transplantation, while one patient died in a car accident 17 years after successful transplantation. Six of the surviving patients developed chronic GVHD. Two of the patients with chronic GVHD had preceding acute GVHD and four did not. Five of the six patients with chronic GVHD received donor buffy coat cells in addition to the marrow inoculum to prevent graft rejection. Twelve of the 15 surviving patients have Karnofsky performance scores of 100%. One patient, living more than 4 years after transplantation, has a Karnofsky score of 40% because of persistent cognitive deficits following non-A, non-B hepatitis with hepatic coma. Two patients developed hepatitis C infection 12 and 18 years after transplantation, respectively. Except for mild fatigue and mildly elevated liver function tests, these patients are doing well with Karnofsky performance scores between 95 and 100%. One patient developed severe coronary artery disease 10 years after transplantation, decreasing his Karnofsky performance score to 80%. Serum samples before and after transplantation from 13 patients were tested for hepatitis B virus (HBV) DNA and hepatitis C virus (HCV) RNA by polymerase chain reaction (PCR). Only one patient tested positive for HCV RNA before transplantation. Seven of 15 sera were hepatitis C RNA-positive posttransplantation, but only one of these patients has developed active hepatitis C. All 13 patients were were negative for hepatitis B surface antigen and HBV DNA. Only one patient had IgM antibodies against hepatitis A virus (HAV) before transplantation, which suggested HAV infection. Hepatitis-associated aplastic anemia apparently was caused in most patients by a non-A, non-B, non-C agent. HLA-identical marrow transplantation for hepatitis-associated aplastic anemia with Cy as conditioning regimen is well-tolerated and has a long-term event-free survival in excess of 80%, not different from results of marrow transplantations for aplastic anemia of other etiologies.
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PMID:Marrow transplantation for hepatitis-associated aplastic anemia: a follow-up of long-term survivors. 911 4

Little information is available on acute liver failure (ALF) in the United States. We gathered demographic data retrospectively for a 2-year period from July 1994 to June 1996 on all cases of ALF from 13 hospitals (12 liver transplant centers). Data on the patients included age, hepatic coma grade on admission, presumed cause, transplantation, and outcome. Among 295 patients, 74 (25%) survived spontaneously, 121 (41%) underwent transplantation, and 99 (34%) died without undergoing transplantation. Ninety-two of 121 patients (76%) survived 1 year after transplantation. Acetaminophen overdose was the most frequent cause (60 patients; 20%), followed by cryptogenic/non A non B non C (NANBNC; 15%), idiosyncratic drug reactions (12%), hepatitis B (10%), and hepatitis A (7%). Spontaneous survival rates were highest for patients with acetaminophen overdose (57%) and hepatitis A (40%) and lowest for those with Wilson's disease (no survivors of 18 patients). The transplantation rate was highest for Wilson's disease (17 of 18 patients; 94%) and lowest for autoimmune hepatitis (29%) and acetaminophen overdose (12%). Age did not differ between survivors and nonsurvivors, perhaps reflecting a selection bias for patients transferred to liver transplant centers. Coma grade on admission was not a significant determinant of outcome, but showed a trend toward affecting both survival and transplantation rate. These findings on retrospectively studied patients from the United States differ from those previously gathered in the United Kingdom and France, highlighting the need for further study of trends in each country.
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PMID:Etiology and outcome for 295 patients with acute liver failure in the United States. 987 98

AIM:To assess the possible roles of cytokines (TNF-alpha, IFN-beta, IL-6 and IL-8) in liver damage of hepatitis B.METHODS:The serum TNF-alpha, IFN-beta, IL-6 and IL-8 were detected by ELISA in 66 patients with hepatitis B and 20 healthy blood donors.RESULTS:TNF-alpha and IL-6 in all types of clinical hepatitis B were significantly higher than those in healthy blood donors (P < 0.05); meanwhile the levels of TNF-alpha, IFN-beta, IL-6 and IL-8 in the patients with fulminant hepatitis B were much higher than those in the patients with acute hepatitis B (P < 0.05); the level of TNF-alpha was positively correlated with the levels of IFN-beta, Il-6 and IL-8 in all types of hepatitis B (r(IFN) = 0.24,r(IL6) = 0.35,r(IL8) = 0.44) and the TNF-alpha, IFN-beta, IL-6 and IL-8 were positively correlated with serum bilirubin (P < 0.05). Dynamic changes of these cytokines were observed in the course of acute and fulminant hepatitis. The level of IFN-beta peaked in the initial period of acute hepatitis and early stage of hepatic coma in fulminant hepatitis; TNF-alpha, IL-6 and IL-8 increased with exacerbation, and reached a peak when the liver damage was most serious, then decreased when patient conditions were improved.CONCLUSION:The increased cytokines were related to the inflammation of liver cells and multiple factors may play certain roles in liver damage.
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PMID:Detection of serum TNF-alpha,IFN-beta,IL-6 and IL-8 in patients with hepatitis B. 1181 82

In Japan, living donor liver transplantation has been established as a therapeutic strategy for the rescue of terminal liver disease, including fulminant hepatic failure that shows no signs of recovery. We performed living donor liver transplantation for a subacute type fulminant hepatic failure patient, who had developed a hepatic coma of grade V (no right reflex, no response to pain stimuli). The electroencephalogram indicated almost flat waves. However, cranial computed tomography revealed that brain edema was not severe in this case. The recipient did not have hepatitis virus and had not taken medication that had been determined to cause hepatitis. The recipient was a 12-year-old boy, 165.5 cm in height and 45.5 kg in weight. The donor was his mother, who was 42 years old; her blood type, type B, was identical to that of the boy. The mother's right hepatic lobe was transplanted to her son (the recipient). The post-transplantation condition of recipient was quite excellent. He recovered consciousness 3 days after liver transplantation, and rapidly attained normal hepatic function. The donor was discharged on the 20th postoperative day without any problems. The recipient was discharged on the 79th postoperative day without any neurological deficits. This case suggests that deep coma without electroencephalogram waves may not be a contraindication for living donor liver transplantation in fulminant hepatic failure patients, if the brain edema is not severe.
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PMID:Complete recovery from fulminant hepatic failure with severe coma by living donor liver transplantation. 1274 61

AIM/BACKGROUND: There is an increasing evidence that certain hepatitis B virus (HBV) strains may contribute to the pathogenesis of fulminant hepatitis B (FHB). Recently, we reported that genotypes of HBV influence the clinical course of acute self-limited hepatitis B (AHB). In this study, we compared clinical features of FHB between different HBV genotypes and compared the prevalence of each genotype between FHB and AHB patients. METHODS: The subjects consisted of seven patients with FHB and 25 patients with AHB. The core promoter and precore region were directly sequenced following polymerase chain reaction, and genotype was determined by restriction fragment length polymorphism analysis of the S gene. RESULTS: Of the seven FHB patients, one had genotype A, one had genotype B, four had genotype C, and one had genotype D. Six of the seven FHB patients were infected by heterosexual contact; one FHB patient who was not infected by heterosexual contact had genotype C. All four FHB patients with genotype C had a short duration clinical course. In one patient with genotype A, the time from onset of hepatitis to hepatic coma was 30 days. These results are similar to those of the patients with AHB, in which clinical course was longer in patients with genotype A than in patients with genotype C. CONCLUSION: Viral genotype can be used to predict the clinical course of both FHB and AHB.
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PMID:Genotypic analysis of hepatitis B virus from patients with fulminant hepatitis: comparison with acute self-limited hepatitis. 1280 39

Fulminant hepatitis, or fulminant hepatic failure, is defined as a clinical syndrome of severe liver function impairment, which causes hepatic coma and the decrease in synthesizing capacity of liver, and develops within eight weeks of the onset of hepatitis. Several independent factors influence the survival of patients: age, the cause of liver disease, the degree and the duration of encephalopathy in relation to the onset of the disease, and the prevention of complications. Over the years many intensive treatments have been practiced. Liver transplantation is expensive, and patients who survive transplantation require life-long immunosuppression, clinical care and complications management. Without transplantation fulminant hepatitis and hepatic failure might be completely recovered spontaneously, and the patient could expect a normal life. Two cases of fulminant B hepatitis with intensive care treatment, and their survival despite unfavorable prognosis are presented in this paper. The management of patients with fulminant hepatitis required intensive monitoring and therapeutic measures, including corticosteroids. The prognosis for survival without transplantation in fulminant hepatitis is limited by the measures of medical treatment and new specific therapeutic modalities which must be developed through basic research.
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PMID:[Fulminant hepatitis B]. 1289 32

Fulminant hepatic failure, which is represented by fulminant hepatitis, is fatal in most cases unless prompt liver transplantation is performed. Even if liver transplantation is performed, irreversible neurological damage is often complicated. In this case report, we describe two cases of fulminant hepatitis induced by acute hepatitis B virus infection, both of which were successfully rescued by living related liver transplantation without significant complications. The case 1 was a 45-year-old Japanese male. He complained general malaise and anorexia. His local physician diagnosed him as acute hepatitis B, and referred to our hospital. Due to severe coagulopathy, plasma exchange was performed 3 times. However, his hepatic coma progressed rapidly along with rapid decrease of both his direct/indirect bilirubin (D/T) ratio and serum blood urea nitrogen (BUN) levels. Living related liver transplantation was performed under the diagnosis of acute fulminant hepatitis B. The case 2 was a 34-year-old Japanese male. His complaints were fever and skin rush. He was referred to our hospital under the diagnosis of acute hepatitis B. On the second day after admission, he developed grade II hepatic coma, which deteriorated into grade III in spite of intensive therapy including plasma exchange. He also demonstrated rapid decrease of both D/T ratio and serum BUN level. Living related liver transplantation was performed on the next day. Both cases recovered without any evidence of neurological sequelae. In general, it is extremely difficult to rescue fulminant hepatitis by conservative treatments, particularly in cases with rapid progression. Although emergency liver transplantation may be an only option to rescue in such a case, living related liver transplantation has an advantage in view of urgent organ donation over cadeveric transplantation.
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PMID:Living related liver transplantation for acute fulminant hepatitis B: experience from two possible hyper-acute cases. 1567 78


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