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)

In this symposium, the speakers have discussed the progress of the current diagnostic methods available for the diagnosis of viral hepatitis type C, and the accuracy and reproducibility at hand now, or which should be attained in the near future. Since the first appearance of ELISA (Ortho) and RIA (Dainabot) kit, the screening of infected blood with HCV from donors has been very successful. Posttransfusion hepatitis following infected blood transfusion has clearly decreased. The carrier rate of HCV in the Ehime prefecture is reported to be 1.85% in males and 1.25% in females. Diagnostic methods of the second generation such as ELISA and RIBA using C200 and C22 (core) protein as antigens yield 92.6 to 100% positive results in a diagnosis of NANB hepatitis following anti-hemophilic sera injection or hemodialysis. Detection of HCV RNA by RT-PCR procedure promised accurate diagnosis. Using such diagnostic methods, the majority of the patients with NANB chronic hepatitis were diagnosed as having CH type C. IgM anti-C 100-3 antibody was not useful for early diagnosis of patients infected with HCV, but the titer was useful for determining the therapeutic response of patients on INF therapy. The route of infection was concluded to be mostly horizontal rather than vertical (maternal-child), though a few cases were present suggestive of maternal transmission. Interferon therapy against patients with CH type C was effective in CAH 2A, but only a poor response was observed in patients with CAH 2B.
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PMID:[Symposium: Current evaluation of diagnostic methods on viral hepatitis type C and consequent clinical features]. 165 58

The levels of beta 2-microglobulin (beta 2m) in peripheral blood mononuclear cells (PBMC) and livers from patients with chronic liver diseases type B were measured. Beta 2m of liver and PBMC in chronic active hepatitis was higher than those of controls (p less than 0.01, p less than 0.01). beta 2m of PBMC are directly proportional to those of livers (r = 0.746), beta 2m levels of PBMC in patients with chronic active hepatitis during the exacerbation of hepatitis was higher than those of remission of hepatitis. The levels of beta 2m in PBMC in vivo, was significantly increased during either interferon alpha or beta administration. Interferon-gamma positive cells in the liver were exacted in the beta 2m increased group of chronic hepatitis type B. INF-gamma production in the lymphocyte of livers, may play an important role in the occurrence of liver injury in patients with chronic hepatitis type B.
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PMID:[Increased levels of beta 2-microglobulin in peripheral blood mononuclear cells and hepatocytes in patients with chronic hepatitis type B]. 190 79

HBV and HCV cause most of chronic hepatitis; the HDV is a co-infectious virus and it rend the help of HBV to duplicate; HAV and HEV do not induce chronic hepatitis. Etiology is not the same, without apparent reasons, in all the world and the distinction between persistent chronic hepatitis and active idiopathic chronic hepatitis is meaningless, because one can shift in the other. Diagnosis is possible using serologic tests and by determination of the DNA of the HBV and RNA of the HCV. Interferon is a good therapeutic tool either for B hepatitis than for C hepatitis in about 50% of case. On the contrary, the results obtained with liver transplantation are disappointing and those achieved with ribavirin have not been conclusive yet. The treatment with INF for more than one year and with full dosages, gives good results in about 50% of patients with hepatitis D. In the other patients it is not useful a second cycle with INF or the introduction of pure antiviral drugs alone or in association with INF.
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PMID:[Chronic viral hepatitis: diagnosis and treatment]. 876 73

Twenty-five per cent of haemodialysed patients carry anti-HCV antibodies; these antibodies are associated with detectable viraemia in 85% and chronic hepatitis in 90% of subjects, despite normal transaminases in more than half of them. This underlines the importance of antiviral therapy. We evaluated the tolerance and effectiveness of a classic interferon (IFN) treatment (3 MU three times a week for 6 months, subcutaneously) in 19 haemodialysis patients presenting with anti-HCV antibodies and chronic (n = 16) or acute (n = 3) hepatitis. Thirteen of those 19 patients had elevated transaminases. Viraemia C was detected by genome amplification (PCR) and by the bDNA test before and after interferon therapy as well as 6 months at least after the end of INF treatment. Response (defined as liver enzyme normalization) was noted in 11 (84.6%) of the 13 patients with elevated transaminases; at the end of follow-up, six exhibited long-term response and five had relapsed, HCV-RNA was detected in 15 of the 19 patients before IFN therapy and remained positive in 7/15 initially viraemic patients at the end of treatment. Hepatitis C RNA was detected at the last follow-up visit (mean follow-up duration 18 +/- 9 months) in 12 of the 15 initially viraemic patients. Liver histology was improved in most patients, regardless of their biological response. One patient could not complete the 6-month course because of clinical and haematological adverse events. In the six patients with strictly normal transaminases, HCV RNA was detectable in 4/6 patients before treatment, in 2/4 viraemic patients at the end of treatment, and in 4/4 at the last follow-up visit. All pathological signs disappeared in four of the five patients who had no detectable HCV-RNA before IFN therapy. To conclude: (i) interferon-alpha exhibits satisfactory effectiveness and tolerance in haemodialysed patient; (ii) HCV replication recurs in most of these patients despite histological improvement; (iii) interferon-alpha can be effective even in patients with chronic hepatitis and no detectable HCV-RNA.
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PMID:Effectiveness and tolerance of interferon-alpha 2b in the treatment of chronic hepatitis C in haemodialysis patients. 891 58

Focal segmental glomerulosclerosis (FSGS) associated with type C virus (HCV) hepatitis has not been described in the literature to date. However, we experienced a 30-year-old man, who had had HCV hepatitis, developed nephrotic syndrome and was admitted to our hospital. The first renal biopsy showed FSGS which was diagnosed by light, immunofluorescent, and electron microscopic study. FSGS diagnosis was based upon the findings of focal segmental glomerular sclerosis associated with hyalinosis and foam cells, segmental deposition of IgM and C3 on glomeruli, and epithelial cell vacuolization in the Bowman's space. HCV hepatitis was treated with interferon-alpha (INF-alpha) over 6 months. The treatment brought the disappearance of not only HCV-RNA from the blood, but also the manifestation of nephrotic syndrome. Therefore, the second renal biopsy was performed, but did not reveal any great pathological improvement. Five months later after the remission, he again had an elevated HCV-RNA level and a relapse of nephrotic syndrome. He was retreated with the same therapy and achieved a second remission of nephrotic syndrome. FSGS associated with HCV hepatitis is described first and the implication of INF-therapy in the improvement of proteinuria is discussed.
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PMID:[Focal segmental glomerulosclerosis associated with type C virus hepatitis and decrement of proteinuria by interferon-alpha therapy]. 1036 24

A 21-year-old man was admitted to our hospital for acute hepatitis of unknown cause. His liver function improved with rest, but worsened 2 months later. He developed a high fever and pancytopenia. The serum level of cytokines including TNF-alpha, IFN-gamma, IL-6, and M-CSF was elevated, and hemophagocytes were seen in bone marrow. These findings suggested a hemophagocytic syndrome-like state. With prednisolone, gamma-globulin, and G-CSF, the high fever disappeared and the patient's liver function gradually recovered. However, the severe pancytopenia persisted. The bone marrow became acellular with a small number of hemophagocytes, and hepatitis-associated aplastic anemia was diagnosed. After immunosuppressive therapy with ATG, CyA and G-CSF was started, and the patient showed hematopoietic reconstitution. The bone marrow CD4+/CD8+ lymphocyte ratio recovered to within the normal range, and the serum cytokines including TNF-alpha and IFN-gamma decreased. The increase in serum cytokines, particularly TNF-alpha and INF-gamma, as well as the presence of activated T cells associated with the preceding hemophagocytic syndrome-like state may have predisposed this patient to aplastic anemia.
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PMID:[Hepatitis-associated aplastic anemia preceded by a hemophagocytic syndrome-like state]. 1463 47

Interferon-alpha (IFN-alpha) is a potent suppressor of hepatitis B virus (HBV) replication in the HBV-transgenic mouse, depleting virus replication intermediates from infected hepatocytes via pathways mediated by interferon-gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha). It has also been hypothesized that cytokines induce curing of infected hepatocytes via non-cytolytic pathways during resolution of transient hepadnavirus infections. We have therefore evaluated therapy of chronic woodchuck hepatitis virus (WHV) infections using treatment with the nucleoside analog clevudine [L-FMAU; 1-(2-fluoro-5-methyl-b-L-arabinofuranosyl) uracil] and therapy with adenovirus vectors expressing INF-gamma, TNF-alpha, and beta-galactosidase. Before their use in vivo, expression of IFN-gamma and TNF-alpha from the adenovirus vectors was evaluated in vitro. Conditioned media from adenovirus-infected WC-3 cells was shown to inhibit WHV replication in baculovirus-transduced cells. Adenovirus super-infection of the liver in woodchucks led to declines in the percentage of hepatocytes with detectable core antigen and nucleic acids, and in levels of covalently closed circular DNA (cccDNA) and total WHV DNA, but a major long-term benefit of adenovirus super-infection during clevudine treatment was not demonstrated. Moreover, the effect took at least 2 weeks to develop suggesting that the declines in the percentage of WHV-infected cells, ccc, and total WHV DNA resulted from induction of the adaptive immune response by the adenovirus super-infection, and only indirectly from the expression of cytokines by the vectors.
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PMID:Adenovirus-based gene therapy during clevudine treatment of woodchucks chronically infected with woodchuck hepatitis virus. 1532 95

Background: Rebound hepatitis is a potentially life-threatening complication of withdrawal from immunosuppressive therapy in patients with chronic Hepatitis B viral (HBV) infections. Objectives: To document the incidence of rebound hepatitis and determine whether the hepatitis is associated with serologic evidence of immunological rebound or the appearance of specific mutations in the HBV genome. Methods: Serum cytokines (IL-6, IL-10, TNF-alpha and INF-gamma) were documented by enzyme linked immunoassays and previously described HBV mutants (surface, core, pre-core and basal core promoter) by signal probe hybridization analysis in chronic HBV carriers treated with either 6 weeks of prednisone followed by 6 weeks of acyclovir (PR/AC, n = 20) or placebo/placebo (PL/PL, n = 20). Results: Rebound hepatitis (serum ALT > 2X baseline) occurred in 6/20 (30%) PR/AC patients versus 2/20 (10%) PL/PL recipients (P = 0.24). Serum cytokine levels were similar in those who developed rebound hepatitis compared to those who did not. HBV mutants were absent prior to and during treatment but developed in the follow-up period in three patients. All three patients were PR/AC recipients and in each case, the HBV mutation was in the basal core promoter gene. In two of the three patients, the mutant appeared just prior to the onset of rebound hepatitis while in the third, rebound hepatitis did not occur. Conclusions: The results of this study indicate an association exists between some cases of rebound hepatitis and the development of HBV mutants.
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PMID:Rebound hepatitis following withdrawal of immunosuppressive therapy in patients with chronic Hepatitis B viral infections. 1534 68

Liver cirrhosis main related to hepatitis C virus constitutes the main indication of liver transplantation in Europe and the USA, representing as many as 50% of the indications in adults, while cirrhosis associated with hepatitis B virus represents around 10%. The indications for transplantation in patients with infection by both viruses are fulminant hepatitis, decompensated cirrhosis and hepatocellular carcinoma. Both injections may relapse after transplantation. The evolution of the relapse in the graft is variable and can include non-significant alterations of the liver junction tests, chronic active hepatitis and cirrhosis. Less frequently, a particularly severe form called "fibrosing cholestatic hepatitis" can develop, which rapidly evolve to graft failure. The immunoglobin against the B virus and lamivudine reduce the risk of reinfection. The principal factor associated with reinfection is active viral replication before the transplantation, thus it is considered a contraindication for liver transplantation. INF-alpha has been used in the treatment of hepatitis B virus reinfection with discouraging results. More recently, lamivudine and adefovir have been used. Post-transplantation recurrence of hepatitis C is universal and its evolution towards cirrhosis is more rapid than in immunocompetent patients, with graft dysfunction being the most frequent cause of mortality and of indication for retransplantation. Different factors have been related to the severity of the recurrence including factors related to the donor, the recipient, the virus, immunosuppression and surgery. There are no preventive treatments against recurrence of post-transplantation hepatitis C. In the treatment of the hepatitis C virus recurrence, INF-alpha and rivabirin have been used in single form or in combination with variable results, with the combined therapy being more effective. Recently, encouraging results have been described with the combination of pegylated interferon and rivabirin without a higher incidence of rejection. Finally, the results of retransplantation in patients with recurrent hepatitis B or C have not been encouraging.
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PMID:[Liver transplantation in patients with cirrhosis secondary to hepatitis B virus and hepatitis C virus infections]. 1538 47

Recent studies have indicated that cytokines can be used as markers for disease progression in hepatitis C virus (HCV)-infected patients, therefore this study was conducted to determine the influence of pegylated IFN vs standard IFN on interleukin-2 receptor (IL-2R), IL-6R, IL-8, TNFR-I, TNFR-II, sFas, and sFas-L in Egyptian patients with chronic hepatitis C genotype 4, as no previous studies have been performed on this genotype. We also aim at establishing a possible relationship between these cytokines and the response to INF to determine whether they can be used as noninvasive markers for the response to INF therapy and as monitors for the outcome of treatment. Thirty-eight patients with chronic HCV hepatitis were investigated for the serum levels of the previously mentioned cytokines in a randomized opened controlled trial (22 patients treated with pegylated IFN and 16 patients treated with standard IFN). Cytokine levels were measured by ELISA at 0, 1 and 12 months of IFN therapy. There was marked increase in the serum levels of IL-2R and IL-6R in nonresponders to pegylated interferon, IL-8, TNFR-I and II were significantly higher in nonresponders to standard interferon but were also high in responders of pegylated interferon. sFas and sFas-L showed high levels among responders to pegylated interferon but the standard interferon was again less effective in this regard. Serum levels of TNFR-II, sFas and sFas-L have the potential to be used as serological markers for response to pegylated IFN therapy, and IL-8 is a predictor for nonresponse. Moreover, TNFR-I and II have the potential to be used as markers of response to standard IFN treatment. The persistent correlation between sFas and TNFR-II may elaborate the possible role of pegylated IFN in the induction of apoptosis as a possible new mechanism of viral clearance during treatment with pegylated interferon treatment.
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PMID:Immunomodulators, sFas and Fas-L as potential noninvasive predictors of IFN treatment in patients with HCV genotype-4. 1757 88


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