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

Controversy surrounds the indication of liver transplantation in patients with hepatitis B virus infection. The major problem is the very high risk of infection of the graft. Some investigators have suggested that the presence of HBsAg is a contraindication to liver transplantation. Between February 1975 and December 1990, 178 HBs positive patients were transplanted at Paul Brousse Hospital in Professor H. Bismuth's Department, 137 for post hepatitis cirrhosis and 41 for fulminant hepatitis. Since April 1984 we have decided long term immunoprophylactic therapy for all patients with HBs infection. But only from August 1987 our supply of purified anti HBs immunoglobulin has been adequate to treat all our patients according to the following protocol: 10.000 IU during the peroperative phase, 10.000 IU immediately after intervention, 10.000 IU every day for the first 6 days, 10.000 IU when the anti HBs levels were under 150 IU/l. One hundred thirty-nine patients were treated by this method. 110 cleared HBs antigen from their sera and their liver were biologically and histologically free of B virus infection. 29 patients showed reappearance of HBs antigen in their sera and nearly all of them developed objective, histologically confirmed, graft lesions. These lesions are those of classical infection: acute hepatitis, active chronic hepatitis and cirrhosis. So 79% of patients were successfully treated with a follow up of 45 months to 6 months. We also studied the prognostic factors under treatment. The study shows: in the case of fulminant hepatitis, 93% success versus 77% in post hepatitis cirrhosis; in the case of Delta superinfection, 94% success versus 66% with pure B infection; in the absence of HBVDNA in the patient's sera before transplantation, 92% success versus 20% in the presence of HBVDNA. For a better understanding of the overall results, the two following parameters have to be considered: some patients relapsed after stopping their treatment, some other patients, despite repositivation of HBs antigen in their sera showed a paradoxal good evolution. These considerations enable us to obtain HBVDNA positive patients: 10% success, HBVDNA negative patients: Fulminant hepatitis: 100% success B Delta post hepatitis cirrhosis: 100% success B post hepatitis cirrhosis: 92% success.
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PMID:[Relapse prevention in liver transplant patients treated for liver involvement due to hepatitis B virus]. 163 19

Twenty-seven children with non-A, non-B hepatitis were studied with regard to their clinical, serologic, and histologic features. In contrast to adult patients, non-A, non-B hepatitis developed in most pediatric patients (19 out of 27) in the absence of identifiable parenteral exposure, probably because of fewer chances for exposure of children to blood or blood-contaminated products. Perinatal transmission was considered possible in one of the patients. Fulminant hepatitis had occurred in six patients, two of whom died. It is noteworthy that fulminant hepatitis usually occurred in children with sporadic non-A, non-B hepatitis. The progression to chronic hepatitis after acute illness is less likely in children than in adults. Chronic hepatitis developed in four patients. Two of these were asymptomatic at presentation, suggesting that in some patients, non-A, non-B hepatitis infections may remain undetected and progress to chronic hepatitis. Liver histologic examination was performed in 11 patients. There were no characteristic histologic findings which could differentiate non-A, non-B from B hepatitis. Antibodies to hepatitis C virus (anti-HCV) were tested in 22 of the 27 patients and 8 (36%) were seropositive for anti-HCV.
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PMID:Non-A, non-B hepatitis in children: a clinical, histologic, and serologic study. 165 19

The Acute Hepatic Failure Study Group (AHFSG) has conducted a double-blinded, randomized evaluation of hydrocortisone in patients with acute hepatic failure. From July 1975 through August 1978, a 38-month period, 18 medical centers in the United States and one in Canada participated in this trial. A total of 64 patients were accessed and found eligible to participate in the study; two of them were subsequently eliminated from our analysis. Eighteen patients received placebo; 23 received 400 mg hydrocortisone per day, and 21 patients were administered 800 mg hydrocortisone per day. We did not observe any therapeutic effect of hydrocortisone, and the survival rates for placebo versus 400 mg and versus 800 mg hydrocortisone per day were 22%, 9%, and 24%, respectively. Fulminant hepatitis associated with drug hepatotoxicity or non-A, non-B hepatitis seemed to have a worse prognosis than fulminant B, although these differences were not significant. Serum alpha-fetoprotein had a modest prognostic value of survival and seemed to be limited to fulminant B. The AHFSG recommends, therefore, that corticosteroid use in acute hepatic failure with hepatic encephalopathy be discontinued.
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PMID:A double-blinded, randomized trial of hydrocortisone in acute hepatic failure. The Acute Hepatic Failure Study Group. 171 46

The purpose of the present paper was to asses the values of plasminogen (PLg) as severity index in viral hepatitis (VH). The results were compared with serum bilirubin (SB) and prothrombin time. The following groups of patients were investigated: I- VH (n-672); II- Fulminant hepatitis (FH)(n-53); III-Liver cirrhosis (n-52); IV- Cholangiohepatitis (21); Toxic hepatitis (n-22); V- Gall stone (n-56) VI- Neoplasms with jaundice (n-56); VII- Healthy subjects (n-137). PLg was found to be diminished in parenchymal liver diseases, especially in VH's patients according to the severity and the stage of the diseases. The most impressive decline was observed in FH--more than 50% of the tests showed Plg activity less than 10% (reverence values 83-126% activity). In VH, PLg was superior to SB and prothrombin time when evaluating the severity of the disease at the time of admission in the hospital. We proposed PLg as valuable criterion for the severity of VH. The range being as follows: Light forms of VH- PLg activity above 70%; Medium forms-from 69 to 50%; Severe forms-from 49 to 20% and patients with high risk of liver coma-PLg activity below 20%.
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PMID:Bilirubin or plasminogen--which is better in the assessment of the severity of viral hepatitis? 175 47

Two distinct forms of non A non B viral hepatitis are now distinguished: (a) parenterally transmitted non A non B hepatitis, mainly due to hepatitis C virus, (b) enterically transmitted non A non B hepatitis, mainly due to hepatitis E virus. Hepatitis C virus is an enveloped, 50 to 60 nm in diameter, single stranded RNA virus. Its transmission is essentially parenteral and resembles that of hepatitis B virus. Individuals at risk are those in contact with blood products. Sexual transmission is uncommon. C virus hepatitis is characterized by a frequent course to chronic hepatitis, cirrhosis and hepatocellular carcinoma. Fulminant hepatitis is rare. Chronic forms are associated with the presence of anti-HCV antibodies in the serum. These antibodies are rarely present in the acute stage of the disease. Hepatitis E virus is a non-enveloped, 30 nm in diameter, single stranded RNA virus. Its transmission is faecal-oral, thus similar to that of hepatitis A virus. The disease is almost exclusively encountered in developing countries. It is not observed in France, apart from imported cases. Like A virus hepatitis, chronicity never occurs. Fulminant hepatitis is possible in pregnant women in the third trimester of pregnancy. There is no routine serological test. Development of vaccines against these two viruses can be expected.
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PMID:[Non-A non-B acute hepatitis]. 211 1

Hepatitis due to viruses other than A, B, C, D, E are numerous but uncommon in adults. Among the group of Herpesviridae (HSV, CMV, EBV, VZV), clinical hepatitis is usually suggestive of disseminated viral infection. Fulminant hepatitis occasionally observed in immunocompromised hosts are due to HSV, and VZV, but exceptionally to EBV. Many new techniques using specific monoclonal antibodies permit an accurate and fast diagnosis. Three drugs (vidarabine, acyclovir, ribavirine) have been shown to be efficient in the treatment of severe forms of the disease. Hepatitis due to exotic viruses (Amaril, Ebola, Lassa) are exceptional in France, but require specific prophylactic measures.
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PMID:[The other types of viral hepatitis]. 216 4

Fulminant hepatitis is associated with an 80% mortality rate. Surviving patients do not develop chronic liver disease. Failure to produce adequate amounts of interferon and to achieve an antiviral state seem to be the basic defects in this condition. Tumor necrosis factor (TNF) has been shown to be induced by viruses. By rapid lysis of virus infected cells, it also prevents optimal viral replication thus reducing the viral yield and the infection rate and extent. On the other hand, it has growth promoting characteristics. We postulate that TNF has a dual role in fulminant hepatitis: (a) It acts as an antiviral agent by eliminating virus infected cells thus reducing viral yields and limiting spread of infection; (b) it may be the signal for hepatocyte regeneration. Only those patients, in whom the regeneration rate exceeds lysis of infected hepatocyte by TNF, survive.
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PMID:Does tumor necrosis factor play a role in the pathogenesis of fulminant hepatitis? 246 60

Fulminant hepatitis was observed in a 44-year-old patient with cirrhosis, 38 days after the beginning of a treatment by disulfiram. Hepatitis was associated with fever and hypereosinophilia. Liver transplantation was performed with success. We reviewed 15 previously published cases of disulfiram-induced hepatitis. They occurred from 10 to 180 days after the beginning of the treatment by disulfiram, aminotransferases were increased whereas alkaline phosphatases were not markedly changed; there was either focal or widespread necrosis. Fulminant hepatitis was observed mainly in patients with alcoholic chronic liver disease or in patients who continued to ingest disulfiram while jaundice was already present. An immunoallergic mechanism is thought to be responsible for disulfiram-induced hepatitis.
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PMID:[Fulminant hepatitis induced by disulfiram in a patient with alcoholic cirrhosis. Survival after liver transplantation]. 262 87

Eleven male fulminant hepatitis (FH) patients (mean age: 47.7 +/- 16 years) positive for hepatitis B surface antigen (HBsAg) but negative for IgM antibody to hepatitis B core antigen (IgM anti-HBc) were admitted consecutively to the Athens Hospital for Infectious Diseases between May 1981 and November 1983. Because of the absence of IgM anti-HBc, determined by an enzyme immunoassay, these patients were considered to be HBsAg carriers with a superimposed acute hepatitis. Three of the 11 patients received immunosuppressive chemotherapy during the six months before the onset of the acute hepatitis. None of the patients was homosexual or a drug addict. Infection with hepatitis A virus (HAV), hepatitis B virus (HBV), or hepatitis delta virus (HDV) was detected with serologic markers and/or molecular hybridization techniques. Fulminant hepatitis was attributed to spontaneous reactivation of chronic hepatitis B in four patients, chemotherapy-induced reactivation of chronic hepatitis B in three patients, HDV superinfection in one patient and possible superinfection by non-A, non-B agent(s), HDV, or HDV-like agents in three patients. Reactivation of chronic hepatitis B was an important cause of apparent acute hepatitis in heterosexual male HBsAg carriers from an area with a high prevalence of HBV infection.
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PMID:Fulminant hepatitis in asymptomatic hepatitis B surface antigen carriers in Greece. 309 15

This study describes the aetiology and clinical course of fulminant viral hepatitis in 34 patients. Sixteen of 34 (47%) patients presented with serological evidence that indicated that hepatitis B virus (HBV) was the cause of fulminant hepatitis, while in 13 of 34 (38%) non-A, non-B (NANB) virus was implicated as the cause. Further, in three cases (9%) and two cases (6%) the patients' serological data indicated that hepatitis A (HAV) and the delta agent superinfection, respectively, were the cause. Forty-seven per cent of cases with fulminant viral hepatitis were among those aged between 21 and 40 years. Fulminant hepatitis due to HAV was confined to children less than five years of age, while the two patients who had delta infection were 40 years or older. Fulminant hepatitis occurred with equal frequency among males and females, and with the exception of one case, who had a NANB virus infection, the outcome of fulminant viral hepatitis in this study was invariably fatal.
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PMID:Fulminant viral hepatitis in Kuwait. 315 28


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