Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the majority of instances acute viral hepatitis resolves totally without sequelae. Fulminant hepatitis is a highly lethal lesion but 20 to 25 per cent of patients, principally young patients, survive. Survivors do not appear to develop chronic liver disease. Persistent viral hepatitis follows acute icteric hepatitis, both type B and non-B, in 10 to 12 per cent of patients. Six long-term HBs Ag carriers demonstrated HBs Ag clearance after 14-73 months. Chronic active viral hepatitis often progresses to cirrhosis. This progressive hepatitis appeared as a sequelae of acute icteric type B hepatitis in 3 per cent of 429 patients. In patients with chronic active type B hepatitis, low titers of HBs Ag are common.
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PMID:Viral hepatitis: clinical aspects. 17 56

The clinical course of acute viral hepatitis may vary from asymptomatic to fulminant, and the final outcome can be complete recovery, chronic hepatitis or cirrhosis. The two main challenges this generally benign, self limiting infection has presented for may years have been to understand 1) the progression to fulminant hepatitis, and 2) the progression to chronic hepatitis or cirrhosis. Fulminant hepatitis may appear infrequently (1-2 % of patients with clinical hepatitis) in both type A and type B infections. Nearly 10% of patients with acute viral hepatitis type B develop either chronic hepatitis or cirrhosis. The exact figures for progression to chronicity in patients with type A infections are probably less,but are still not fully known. During the acute phase of the disease, the patients with later progression to chronicity differ significantly from those with subsequent resolution in a number of serological, biochemical and morphological variables. Persistence of HBS antigenaemia for more than 13 weeks, a high concentration of circulating Dane particles, and the presence in the serum of the "e" antigenic determinant seem to be reliable prognostic markers for pregression to chronic hepatitis or cirrhosis. Such markers are prerequisites for therapeutic trials with potent drugs which are only justified for patients with fulminant hepatitis and patients with progression to chronicity. If the different outcome of viral hepatitis is a result of the individual T-cell function, these two categories of patients may represent the opposite extremes in lymphocytic function. Controlled clinical trials are required to evaluate the clinical effect of immunosuppression in fulminant hepatitis and immunostimulation in chronic hepatitis.
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PMID:Clinical course and prognosis of acute hepatitis. 79 97

A radioimmunoassay for human alpha1-acid glycoprotein has been developed. 97.8% of 125I-alpha1-acid glycoprotein prepared for the assay were immunoprecipitable with specific anti-sera against the protein. alpha1-acid glycoprotein concentration in sera from normal adults was found to range between 70 and 114 mg/100 ml, with a mean of 93. Fulminant hepatitis, liver cirrhosis or chronic active hepatitis with sublobular necrosis caused a significant lowering of alpha1-acid glycoprotein concentration. Sera obtained from patients with acute hepatitis in convalescence, chronic inactive hepatitis or primary biliary cirrhosis gave normal concentration of the glycoprotein.
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PMID:Serum glycoproteins in the liver diseases. II. Radioimmunoassay of alpha-1 acid glycoprotein. 101 93

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

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

Hepatitis D virus appears to be endemic in the Middle East, but its distribution bears little relationship to that of HBV. Only in Jordan was an association between HDV-positive status and HBsAg-positive primary hepatocellular carcinoma found. Fulminant hepatitis and chronic sequelae were unusual in HDV-coinfection, while early mortality and a chronic outcome were commoner in HDV-superinfection. In established HBsAg-positive cirrhosis survival was not significantly different in the HDV-positive vs. the HDV-negative patients. In patients whose biopsies showed cirrhosis, severe necroinflammatory features were seen more often in the HDV-positive than in HDV-negative patients.
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PMID:The role of hepatitis D virus in liver disease in the Middle East. 202 Jul 22

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

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

The use of cadaveric organ donors with positive serologic tests for hepatitis C (HCV) has caused considerable debate. We have reviewed the clinical course of 43 EIA1 HCV-negative recipients who received kidney transplants from EIA1 HCV-positive donors (Study). We have attempted to define the rate of HCV-RNA transmission and to determine the frequency of HCV disease transmission as determined by abnormalities in liver function tests. Viral transmission was assessed using serologic assays for HCV antibody formation (EIA1, EIA2, and Matrix--an automated multiple antigen immunoblot assay) and with PCR testing for the presence of HCV-RNA on recipient sera. Liver function was followed longitudinally in the Study patients and compared with a group of 103 kidney recipients of organs from EIA1 HCV-negative donors (Control). Of the Study patients, 56% became PCR-positive for HCV-RNA, suggesting the transmission of HCV-RNA from the HCV-positive donor. Interpretation of serologic tests for HCV was complex. Currently available first (EIA1) and second (EIA2) generation serologic assays were always negative. The multiple antigen immunoblots assay (Matrix) had a high positive predictive value (93%) for the presence of HCV-RNA transmission, but one-third of Matrix-negative Study patients were PCR-positive (sensitivity = 66%). Currently, only 38% of recipients have HCV-RNA, suggesting that the virus may have been cleared by one-third of Study recipients who had circulating virus. Traditional tests of liver function (ALT, AST, AP, and GGT) were of limited use in predicting HCV-RNA transmission. Average AST, AP, and GGT were similar in the two groups. Average ALT was increased (93 I/U and 47 I/U) in Study and Control patients, respectively, but this difference was not significant. Episodes of abnormal liver function (ALT 60-99 IU for > or = 14 days) occurred in 22% of Study and 10% of Control patients (P = NS) and lasted longer in Study compared with Control patients (301 vs. 138 days; P < 0.02). Hepatitis (ALT > or = 100 IU for > 14 days) occurred with an equal frequency (6.5%) in both groups. The presence of HCV-RNA did not predict episodes of abnormal liver function. Fulminant hepatitis or rapidly progressive cirrhosis did not occur in the recipients of organs from HCV-positive donors. These data demonstrate a high efficiency of transfer of HCV-RNA by kidney transplantation from an HCV-positive donor to an HCV-negative recipient. A majority of the patients have asymptomatic HCV infection.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Transmission of hepatitis C by kidney transplantation--the risks. 815 29

Fulminant hepatitis is a rare complication of acute hepatitis A virus (HAV) infection. We report three cases of fulminant hepatic failure with death due to HAV infection in patients with pre-existing chronic liver disease. Data from the literature also indicate a high case fatality rate during HAV superinfection in patients with chronic hepatitis B, particularly those with cirrhosis, and in patients with alcoholic cirrhosis. In patients with chronic hepatitis C, results are conflicting with some reports indicating a high fatality rate of HAV superinfection and others not, irrespective of the presence or absence of cirrhosis. Based on our observations and this review of the literature, we suggest that patients with chronic liver disease should be vaccinated against hepatitis A.
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PMID:Fulminant hepatitis A in patients with chronic liver disease. 1092 41


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