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)

Viral infection has been shown to induce aplastic anemia, unidentified types of hepatitis being the most common cause for aplastic anemia-associated viral hepatitis. The survival rate for this group of patients after bone marrow transplantation with stem cells from an HLA-matched sibling is not well known. The aim of this study was to determine the prevalence of hepatitis G virus (HGV) and transfusion transmitted virus (TTV) infection in non-A, non-B, non-C hepatitis associated-aplastic anemia (HAAA) patients, and to define the role of bone marrow transplantation (BMT) as a therapeutic modality for this disease. Sixty-eight patients (43 males and 25 females) with aplastic anemia, underwent allogeneic BMT at the Hadassah University Hospital between 1981 and 1997. Onset of hepatitis was defined as jaundice and elevated alanine aminotransaminase (ALT) levels. Onset of aplastic anemia was defined as the first date on which varying degrees of pancytopenia occurred: hemoglobin level below 10 g/dl, WBC below 2 x 10(9)/l and low platelet count 10 x 10(10)/l. Serial serum samples from HAAA patients were assayed for virological and/or serological markers of hepatitis A, B, C, D, E, G viruses, TTV and parvovirus B19. Seventeen of the 68 patients with aplastic anemia (25%) suffered from hepatitis, 12 males and five females, ages 5 to 36 years. The mean interval between onset of hepatitis and first indication of aplastic anemia was 62 days (range 14-225 days). The development of aplastic anemia was unrelated to age, sex or severity of hepatitis. Ten of the 17 patients (59%) achieved complete ALT recovery prior to the diagnosis of aplastic anemia. Serum samples were available for 15 patients; none had evidence of acute or active hepatitis A, B, C, D, E, G and TTV virus infection at the time of diagnosis. Parvovirus B19 DNA sequences were not detectable in 10 of 12 tested cases; two positive results were detected in serum samples obtained after blood transfusion, making the analysis of these positive results difficult. All 17 patients underwent BMT. The mean post-BMT follow-up period was 38 months (range 1 day-123 months), five patients (30%) died 1 to 160 days post BMT, and 12 (70%) are alive 31 to 123 months after BMT. Relapsing hepatitis was not observed in any of the patients. In conclusion, HAAA is a disease of the young and the etiologic agent associated with HAAA remains unknown. HGV, TTV and parvovirus B19 sequences were not detected in any of the HAAA cases. The survival rate after BMT with stem cells from an HLA-matched sibling is similar to that for patients with non-hepatitis-associated aplastic anemia.
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PMID:Lack of known hepatitis virus in hepatitis-associated aplastic anemia and outcome after bone marrow transplantation. 1128 88

Abnormal liver function in thyroid disorders may be secondary to thyrotoxicosis or to autoimmune injury to the liver. We report the case of a 36-year-old female who developed jaundice and pruritus with mild cholestasis and moderately elevated transaminase levels. The diagnosis of Graves' disease was made shortly thereafter. Laboratory findings were: alanine and aspartate aminotransferase 219 (IU/I (N: 9-50) and 102 IU/I (N: 10-15) respectively, alkaline phosphatase 336 IU/I (N: 40-135), bilirubin 24 micromol/I (N: 2-23), and gamma-glutamyl transpeptidase 232 IU/I (N: 9-43). Abdominal ultrasonography showed normal bile ducts; echocardiography ruled out heart failure; viral and autoimmune markers for hepatitis and cirrhosis were negative. Percutaneous liver biopsy showed moderate intrahepatic steatosis, anisokaryosis, lymphocyte infiltration in the portal areas, and Kupffer cell hyperplasia. Outcome was favorable after seven months of iodine therapy, confirming the diagnosis of thyrotoxicosis hepatitis.
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PMID:[Thyrotoxicosis hepatitis: a case report]. 1145 76

A coffee extract significantly suppressed lipopolysaccharide (LPS)-induced hepatitis in D-galactosamine-sensitized rats, as assessed by the plasma alanine and aspartate aminotransferase activities, when it was added to the diet (30 g/kg) and fed to rats for 14 days. Its effect was as strong as that of a green tea extract. The coffee extract suppressed LPS-induced hepatitis when singly force-fed (1.2 g/kg) 1.5 h prior to the injection of the drugs, whereas a decaffeinated coffee extract had no significant effect. The hepatoprotective effect of caffeine was stronger than that of theobromine. These results indicate that coffee can protect animals from LPS-induced hepatitis, and that the effect of coffee might be mainly due to caffeine.
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PMID:Suppressive effect of coffee on lipopolysaccharide-induced hepatitis in D-galactosamine-sensitized rats. 1157 46

Reactivation of hepatitis B virus (HBV) infection in subjects receiving cytotoxic treatment for non-Hodgkin's lymphoma (NHL) is well documented. This report describes the case of a 69-year-old male chronic HBV carrier who developed severe flare-up of hepatitis B following chemotherapy for large B-cell NHL. Prior to chemotherapy, the patient had normal liver function tests and was negative for HBV DNA by polymerase chain reaction (PCR) assay. HBV reactivation consisted of a rise in hepatic transaminases (peak alanine aminotransferase=1178 IU/ml), hyperbilirubinemia (7.1 mg/dl), and high levels of serum HBV DNA (63.6 x 10(6) copies/ml). A liver biopsy revealed highly active hepatitis and confluent necroses. Lamivudine treatment (100 mg daily) resulted in rapid loss of hepatitis B virus DNA, resolution of hepatitis, and clinical recovery. The patient is still in remission for NHL. Lamivudine is effective in the control of HBV reactivation following chemotherapy.
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PMID:Successful treatment with lamivudine for reactivated hepatitis B infection following chemotherapy for non-Hodgkin's lymphoma. 1180 36

Free-radical-mediated oxidant damage can contribute to acute hepatitis. Vitamin E, a classic antioxidant, has been tested as a therapy for rodent acute hepatitis, but the protection achieved has not been complete. This study demonstrated that in rats, sodium diethyldithiocarbamate (DDC), a potent antioxidant, strongly depressed galactosamine-induced hepatitis in terms of serum alanine amino transferase activities and bile acids, though not in terms of serum beta-glucuronidase activities. A potential limitation for DDC use in humans, inhibition of copper metalloenzyme activities, did occur at the DDC dose used here. However, these effects were not severe. Thus, DDC could make a useful short term therapeutic drug for acute hepatitis.
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PMID:Diethyldithiocarbamate inhibition of galactosamine-induced hepatitis in rats. 1188 24

Proteolytic processing of the mouse hepatitis virus strain A59 (MHV-A59) replicase gene product, pp1a, results in polypeptides p28, p65, p50, and p240 in infected cells. Based on previously identified p28 and p65 cleavage sites, a p50 cleavage site was proposed to occur between Ala-1262 and Ala-1263. Results of mutagenesis and in vitro cleavage assays show that PLP-1 was able to cleave in trans when the proposed p50 cleavage sequence replaced the p28 cleavage sequence. Mutagenesis was also used to investigate cleavage between Gly-904 and Val-905, a cleavage site predicted to produce a precursor of p65, p72, that was detected in cells infected with MHV strain JHM, but not with MHV-A59. No cleavage could be detected using substrate that carried both the p65 site and the predicted p72 cleavage sequence. Thus, it appeared that PLP-1 could recognize the proposed p50 sequence but not the predicted p72 site under the in vitro conditions used.
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PMID:Further in vitro characterization of mouse hepatitis virus papain-like proteinase 1: cleavage sequence requirements within pp1a. 1193 66

The conformational nature of the B cell epitopes on the hepadnavirus surface antigens makes its characterization difficult. Here, a new approach by DNA vaccination with plasmids expressing chimeric hepadnavirus surface antigens was explored to determine B cell epitopes on the surface antigens of woodchuck hepatitis virus (WHsAg). A series of chimeric genes consisting of complementary fragments of WHsAg and hepatitis B virus surface antigens (HBsAg) was constructed. These plasmids expressed the following: (i) middle chimeric surface antigens (MCSAgs), including pre-S2 region and small surface antigens; (ii) small chimeric surface antigens (CSAgs); (iii) a mutated WHsAg with two amino acid substitutions, the Leu 136 to Thr and Ala 140 to Asp, within the central immunogenic region. The mutated region from amino acid 135 to 143 within WHsAg mimics the second loop of the HBsAg a-determinant. MCSAgs and CSAgs were expressed in transiently transfected mammalian cells and were reactive to anti-HBsAg and anti-WHsAg, as shown by indirect immunofluorescence staining and ELISA. Vaccination with plasmids encoding MCSAgs induced strong antibody responses to the pre-S2 region. Anti-pre-S2 antibodies were directed to a linear, immunodominant region within the amino-terminal region of the pre-S2 region and were able to precipitate serum WHsAg. Vaccinations with the plasmids expressing the CSAgs led to the conclusion that an extended region aa 116-169 of WHsAg, analogous to the HBsAg a-determinant, was sufficient for the induction of anti-WHsAg antibodies. The mutated WHsAg with the second loop of the HBsAg a-determinant efficiently induced anti-WHsAg antibodies, but also a low titer of anti-HBsAg. Thus, multiple B cell epitopes of a linear and conformational nature are present on WHsAg. We presented an efficient and broadly applicable strategy for analysis of complex immunogenic determinants of natural or mutated viral antigens.
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PMID:Characterization of complex B cell epitopes on woodchuck hepatitis virus surface antigens by using plasmids encoding chimeric proteins and DNA immunization. 1200 76

TT virus (TTV) has recently been identified in patients with post-transfusion non-A, non-G hepatitis. It is reported to be common in patients with a variety of liver diseases and with history of transfusion. Its pathogenesis in chronic liver diseases remains unclear. In this study, we have determined the prevalence of TTV in a continuous ambulatory peritoneal dialysis (CAPD) population and related its prevalence with history of previous hemodialysis, transfusion, HCV positivity and serum alanine amino-transferase (ALT) levels. TTV was detected in 44% of 63 CAPD patients and 30% of 43 healthy controls (p = 0.15). Frequency of TTV was similar in previously hemodialysed and never hemodialysed (8/14, 57% vs. 20/40, 41%, p = 0.15) and previously transfused and non-transfused (7/19, 37% vs. 15/44, 34%) CAPD patients. Prevalence of TTV was also similar in HCV(+) and HCV(-) patients. Serum ALT levels were 19 +/- 16 and 20 +/- 12 U/l in TTV(+) and TTV(-) patients, respectively. These results indicate that prevalence of TTV in a CAPD population is similar to healthy controls, and other routes of transmission in addition to parenteral routes might be involved in the transmission of TTV.
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PMID:Prevalence of TT virus in a CAPD population. 1205 78

During more than 104 weeks of treatment with lamivudine (3TC) in chronic woodchuck hepatitis virus (WHV) carrier woodchucks, viral recrudescence occurred. Analysis of WHV DNA polymerase from woodchuck serum samples by PCR followed by DNA sequencing demonstrated that all samples were wild type at the conserved YMDD motif in domain C. Four of the six 3TC-treated woodchucks showed a mixture of the wild-type Ala (GCT) and the mutant Thr (ACT) at the conserved amino acid residue 566 (FLLA) in domain B of the WHV polymerase region. The appearance of the A566T mutation was temporally associated with viral recrudescence. This change is analogous with the amino acid 181 (FLLA) in HBV where 3TC selects for a change from Ala to Thr in humans. In the woodchuck, the Ala to Thr change in the polymerase gene results in a mutation of the WHV surface protein (amino acid 377) from Trp (TGG) to an opal codon (TGA), which may prematurely terminates the polypeptide. Three WHV molecular infectious clones were constructed to study this mutation in greater detail in vitro: A566T, analogous to A181T in HBV; M589V, analogous to the M204V in HBV; and the double mutant A566T/M589V, analogous to A181T/M204V in HBV. These mutants exhibited drug-sensitivity and replication profiles that paralleled those reported for analogous HBV variants. In transfected Huh7 cells, WHV containing the M589V mutation conferred at least 100-fold increased resistance to 3TC, but replicated approximately 5-fold less efficiently than wild-type virus as judged by both extracellular virus production and intracellular DNA replicative forms. In contrast, A566T mutant was approximately 10-fold more resistant to 3TC, replicated intracellularly as well as wild type, but produced 10-fold lower levels of virions than wild type. These findings are consistent with the observation that the A566T mutation alters the overlapping WHV surface antigen reading frame. WHV carrying mutations in the conserved YMDD motif, while not directly selected during lamivudine therapy in WHV carrier woodchucks, are replication competent in cell culture indicating the potential for their emergence in treated animals. These results further illustrate the utility of the WHV/woodchuck model to studies of HBV-drug resistance.
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PMID:Mutations in the conserved woodchuck hepatitis virus polymerase FLLA and YMDD regions conferring resistance to lamivudine. 1207 58

Hepatitis A virus (HAV) is a worldwide disease; in most cases, it causes an acute self-limited illness that does not lead to a chronic state. The course of HAV viremia in a homosexual male with human immunodeficiency virus type 1 (HIV-1) and the correlation between HIV and HAV viral load, alanine aminotranferase (ALT) level, and CD4(+) lymphocyte count were investigated during the course of the infection. HAV RNA was detected quantitatively up to 256 days after clinical onset. To our knowledge, this specific case is the first report of a prolonged infection with hepatitis A in a male with HIV-1. The ALT levels decreased gradually; however, 286 days after clinical onset of hepatitis, ALT levels were three times higher than normal values. HIV viral load was not affected by the infection with HAV and CD4(+) cell count was stable during the course of the co-infection. The duration and the high-titer viremia of hepatitis A virus in an immunodeficient patient constitute a serious risk of the spread of hepatitis A within this population. As inactivated HAV vaccine is safe in HIV-positive subjects, it would be wise to establish a strategy of preventive vaccination in this high-risk group.
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PMID:Prolonged hepatitis A infection in an HIV-1 seropositive patient. 1221 Apr 24


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