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)

Three patients suffered from fulminant hepatitis within 23, 59 and 22 weeks after having ingested a total dose of 16, 26 and 15 g, respectively, of amodiaquine for the prophylaxis of malaria. Amodiaquine administration was continued for 44, 21 and 25 days after the onset of jaundice, respectively. One patient underwent emergency orthotopic liver transplantation and survived. The other two died. Fulminant hepatitis threatens patients in whom amodiaquine administration is protracted for several months and not interrupted when jaundice occurs.
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PMID:Amodiaquine-induced fulminant hepatitis. 334 31

A 36-year-old man developed fulminant hepatitis and acute renal failure with profound hyponatremia (116 mEq/L). Emergent hemodialysis corrected the serum sodium to 136 mEq/L within 24 hours. He developed generalized convulsions 11 days later. Magnetic resonance imaging (MRI) revealed a single large symmetrical lesion in the pons and extensive white matter lesions in the bilateral occipital, temporal, parietal and right frontal regions. These lesions showed marked resolution as the patient recovered. Fulminant hepatitis and acute renal failure could induce extensive edema in the cerebral white matter. Therefore, not all MRI abnormalities in the white matter after correction of hyponatremia necessarily reflect myelinolysis.
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PMID:Reversible white matter lesions in a patient with fulminant hepatitis and acute renal failure. 791 24

A 19-year-old male healthy hepatitis B virus (HBV) carrier developed fulminant hepatitis following allogenic bone marrow transplantation (BMT) from his brother, who was also a healthy HBV carrier, during the first complete remission of acute myelogenic leukemia (M1, FAB classification). Serum markers related to both HBV and hepatitis C virus (HCV) were elevated during active liver injury when a point mutation in the precore (pre-C) region occurred in the HBV. The patient received low-dose interferon alpha (IFN-alpha), while the dose of cyclosporin A was tapered; the patient eventually recovered from the liver injury. Fulminant hepatitis due to HBV and/or HCV following BMT is rare, and it is considered to have a very poor prognosis. The rationale for the use of low-dose IFN-alpha with cyclosporin A (CyA) is discussed.
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PMID:Fulminant hepatitis following bone marrow transplantation in hepatitis B virus carrier siblings. 800 May 16

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

A 14-year-old girl with acute lymphoblastic leukemia in second remission received an allogeneic marrow graft from her HLA identical brother. Cyclosporine A and short term methotrexate were given for prophylaxis against graft versus host disease. On day 42 post transplantation elevation of SGOT and SGPT was recognized, rising the next day to 8,560IU and 2,590IU, respectively. Prothrombin activity dropped below 10%. HCV antibody and HBs antigen were both negative. Fulminant hepatitis was diagnosed, therefore plasma exchange was initiated. However, hepatic encephalopathy developed and she died on day 57. The postmortem liver appearance was consistent with early changes of veno-occlusive disease. Such atypical cases of VOD with late onset are difficult to distinguish from fulminant hepatitis but should be kept in mind.
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PMID:[Fulminant hepatitis-like veno-occlusive disease of the liver after allogeneic bone marrow transplantation in acute lymphoblastic leukemia]. 831 37

Perinatal transmission of hepatitis B virus (HBV) occurs in about 10%-20% of anti-HBe seropositive mothers. The babies are at risk of developing fulminant hepatitis. In most cases no viral DNA has been detected in the sera of mothers and children by conventional hybridisation techniques. Thus, the aim of our investigation was to demonstrate HBV DNA in three children with liver failure and their anti-HBe positive mothers by more sensitive molecular hybridisation techniques. The babies were healthy at birth and did not receive vaccination. At 3 months of age they developed acute liver failure and died from liver insufficiency. Only in one child serum HBV DNA was detected by dot blot hybridisation, but polymerase chain reaction (PCR)-detectable HBV DNA was present in all sera. The liver specimen was negative for HBV DNA by Southern blot hybridisation, but showed a focal distribution of viral sequences as determined by in situ hybridisation. This finding was confirmed by PCR. Our results prove that chronic anti-HBe positive HBsAg carrier mothers and their babies show a low level virus replication. Fulminant hepatitis is due to vertical transmission of very small amounts of viral DNA, only detectable by most sensitive techniques like PCR and in situ hybridisation. Our findings underline the necessity to vaccinate all babies of HBsAg positive mothers regardless of HBeAg/anti-HBe status.
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PMID:Low level virus replication in infants with vertically transmitted fulminant hepatitis and their anti-HBe positive mothers. 835 18

Fulminant hepatitis due to herpes simplex virus (HSV) in adults is a rare and deadly disease. We describe a 23-year-old woman with a 20-year history of Crohn's disease (CD) who was hospitalized with an acute febrile illness and diarrhea. A computed tomography (CT) scan of the abdomen demonstrated an intramural sigmoid colon abscess and multiple abscesses in the liver. Despite high-dose parenteral corticosteroids and broad-spectrum antibiotics, the patient remained acutely ill, with high fever and markedly elevated serum transaminase levels, but no jaundice. Sigmoid resection and wedge liver biopsy were performed at laparotomy. Histologic examination documented HSV-type intranuclear inclusions and inflammation with necrosis in both the sigmoid colon and liver specimens. The patient subsequently died despite parenteral acyclovir treatment. Although rare, fulminant hepatitis due to HSV simplex virus should be considered in the differential diagnosis of all patients with severe hepatitis. Of special note, the necrotizing liver lesions may be mistaken for pyogenic abscesses on CT scan.
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PMID:Fulminant herpes hepatitis mimicking hepatic abscesses. 842 Nov 51

GBV-C might be a causative agent of fulminant hepatitis of unknown etiology. Fulminant hepatitis is an indication for liver transplantation. However, in Japan, because of the legal difficulties associated with cadaveric donation, patients with fulminant hepatitis are still treated by plasmapheresis and multiple transfusions of fresh frozen plasma. So, the possibility that GBV-C might be transmitted by transfusions after the onset of fulminant hepatitis is real. Therefore, we have examined the possible role of GBV-C in non-A-E fulminant hepatitis. Nine patients with non-A-E fulminant hepatitis and one with non-A-E late onset hepatic failure were examined. Sera were obtained from the patients at admission before any blood or blood products were given, and again after transfusions. GBV-C RNA was detected by nested reverse transcription polymerase chain reaction with primers based on the reported sequence. GBV-C RNA was negative in all 10 pretransfusion patients with non-A-E fulminant hepatitis or late onset hepatic failure. Then, fresh frozen plasma was transfused to these patients, and four of them became seropositive. GBV-C is unlikely to be a major etiologic agent for non-A-E fulminant hepatitis in Japan.
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PMID:Detection of GBV-C RNA in patients with non-A-E fulminant hepatitis by reverse-transcription polymerase chain reaction. 914 49

Hepatitis E virus (HEV) is a major cause of clinical hepatitis in regions of endemicity, affecting primarily young adults and travelers to these areas. We present 5 cases of acute HEV infection in travelers and review 143 cases of HEV infection found by a literature search that were contracted in areas of endemicity. Fulminant hepatitis occurred in 2.7% of the reported cases; 2 of these were fatal. The destination of most of the travelers with acute HEV infection was the Indian subcontinent. The overall risk of contracting HEV infection for travelers appears to be lower than the risk for hepatitis A virus infection. Pregnant women and individuals with underlying liver disease may be a risk for severe infection.
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PMID:Hepatitis E virus infection in travelers. 1052 82

A TIMELY TOPIC: Liver toxicity remains a common problem despite adequate information for physicians and drug watch programs. The number of recent publications reporting severe drug-induced liver disease emphasizes the need for prudence. ACUTE AND CHRONIC HEPATOTOXICITY: Cases of acute drug-induced liver disease have been described for nearly all drug classes: a few examples concern hepatitis subsequent to administration of fluoxetin, acarbose, riluzole, coumarin, or orlistat. Fulminant hepatitis is fortunately an exceptional event but has been described after administration of ketoprofene, nimesulid, and clarithyromycin. Chronic liver disease has also resulted from the use of mesalazine, minocyclin or fibrates. Nevirapin prescribed for HIV infection can cause severe liver disease. OTHER AGENTS: Certain herbal agents, such as chelidoin for example, can cause cholestasis. Certain excipients can also be toxic for the liver. Ecstasy appears to be a frequent cause of sometimes severe liver disease in younger subjects.
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PMID:[Hepatotoxicity of medications]. 1136 Jul 29


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