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 order to determine the differences in histological grade of activity and the stage of fibrosis in patients with chronic liver diseases due to multiple hepatitis virus infection and single infection of HBV and HCV we assessed the 68 liver biopsies samples according to Knodell and Scheuer scoring systems. Retrospectively, 216 liver biopsies reports from consecutive patients with chronic viral hepatitis were analysed. Histological activity index (HAI) in HBV/HCV coinfection was higher than in a single HCV infection; it did not differ in groups of HBV/HBC and HBV. The difference was due to the interface hepatitis; lobular activity and portal inflammation were the same. In HDV superinfection HAI was high due to both portal-periportal and lobular hepatitis. HAI depended mainly upon the presence of HBV replication; in patients with chronic hepatitis C with HBV-DNA HAI was also higher than in single HCV group. No difference in HAI between triple and dual hepatitis virus infection was found. In patients with HBV/HCV coinfection and especially with HDV superinfection the advanced stages occurred more than often than in patients with single infections.
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PMID:[An evaluation of the degree of the morphological activity and the stage of the process in patients with chronic liver diseases caused by coinfection with the hepatitis B, C and/or D viruses]. 994 4

HGV RNA was detected by Rt-nested PCR in sera from 49 patients with fulminant hepatitis. The results showed: a) HGV RNA positive rate was 16.3% (8/49) in patients with fulminant hepatitis including 4 subjects with HBV coinfection, 1 subject with HCV coinfection, 2 subjects with HBV and HCV coinfection and 1 subject with HGV infection alone. b) mortality in patients with fulminant hepatitis with HGV infection was 75% (6/8), suggesting that: a) both infection with HGV alone and superinfections of other types of hepatitis virus can result in fulminant hepatitis, b) clinical manifestations of fulminant hepatitis with HGV infection may appear to be more severe and with higher mortality.
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PMID:[Detection of HGV RNA in sera from patients with fulminant hepatitis in Shenyang]. 1032 39

Studies of the prevalence and clinical relevance of GB virus C (GBV-C) infection in 328 hemodialysis (HD) patients were done, and the possibility of nosocomial GBV-C transmission was explored by molecular epidemiology methods. For GBV-C viremic patients in a given HD unit, nucleotide sequences of the envelope region were analyzed by phylogenetic tree constructions. Of 328 HD patients, active hepatitis B virus, hepatitis C virus (HCV), and GBV-C infection were detected in 13%, 23%, and 17%, respectively. Except for a higher frequency of HCV coinfection, the demographic and clinical characteristics of patients with and without GBV-C infection were comparable. In contrast, patients with isolated HCV infection had significantly higher serum transaminase levels, longer time on HD, and more blood transfusions. Phylogenetic analysis showed several distinct clusters of closely related GBV-C isolates from one HD unit, suggesting the possibility of nosocomial transmission. These results suggest that GBV-C plays a minimal role in causing hepatitis in Taiwanese HD patients and in nosocomial transmission.
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PMID:GB virus C infection in hemodialysis patients: molecular evidence for nosocomial transmission. 1035 78

Hepatitis B (HBV) and C viral (HCV) dual-infection-associated liver disease is an uncommon indication for liver transplantation. The clinical and virologic outcomes in such patients have not been well studied. We retrospectively studied 13 patients with hepatitis B surface antigen (HBsAg) and antibody to HCV positivity who underwent orthotopic liver transplantation (OLT) and survived at least 30 days post-OLT. Antibody to hepatitis delta virus (HDV) was negative in 8 patients (group I) and positive in 5 patients (group II). Eleven of the 13 patients received standard hepatitis B immune prophylaxis, and they all remained HBsAg negative. All group I patients were HCV RNA positive after transplantation; in contrast, all group II patients were HCV RNA negative. Serum alanine aminotransferase levels were elevated in 88% (7 of 8) of the patients in group I compared with 20% (1 of 5 patients) in group II. None of the patients had graft loss from chronic rejection or recurrent hepatitis. Three patients had unsuspected hepatocellular carcinoma in the explant. We conclude that among liver transplant recipients with HBV and HCV coinfection, HDV infection is associated with the suppression of HCV replication and mild inflammatory activity after OLT.
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PMID:Clinical and virologic outcomes of hepatitis B and C viral coinfection after liver transplantation: effect of viral hepatitis D. 1064 84

There have been conflicting reports of the clinical outcome of acute hepatitis A virus (HAV) infection in patients with chronic hepatitis C virus (HCV) infection. A prospective study evaluated 432 patients with chronic hepatitis C (183 with cirrhosis) over a 7-year period. Of the 17 patients with concurrent HAV infection, seven developed fulminant hepatitis and six died. None of these patients had cirrhosis; however, the HLA phenotype (A1; B8:DR3) appeared to be a significant factor in the development of fulminant hepatitis. Patients with this phenotype had high titres of antinuclear antibodies, antismooth muscle antibodies and antiasialoglycoprotein-receptor antibodies, possibly reflecting the induction of autoimmune hepatitis in this group. The high frequency of fulminant hepatitis in patients with HAV/HCV coinfection contrasts with other surveys, although a large Centers for Disease Control and Prevention (CDC) survey demonstrated that HAV infection in patients with pre-existing chronic liver disease (CLD) is associated with increased mortality. It is likely that CLD has some importance as an underlying factor in the development of fulminant hepatitis following HAV infection. Further prospective studies are needed to clarify this issue.
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PMID:Fulminant hepatitis associated with hepatitis A virus superinfection in patients with chronic hepatitis C. 1086 37

Patients with hepatitis B virus (HBV) infection may be coinfected with other viral diseases, such as hepatitis C virus (HCV) and/or D virus (HDV), or have serious diseases secondary to the hepatitis, such as hepatocellular carcinoma. These coexisting conditions have an impact on the success of treatment and of liver transplantation. Patients with HBV and HDV are at lower risk for HBV recurrence than are patients with HBV alone; likewise, patients with HBV/HCV coinfection appear to have a higher 5-year survival rate posttransplantation. Treatment of coinfection is similar to that used for HBV alone. Hepatitis B immune globulin and interferon have been found to be effective in varying degrees. Recurrence or reinfection of disease after liver transplantation presents many clinical problems that will require new therapeutic approaches. Future studies will help to begin solving these challenges.
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PMID:Hepatitis B transplantation: special conditions. 1089 41

The interactions among hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis delta virus (HDV) were studied by measuring HBV-DNA and HCV-RNA levels and by determining the influence of viral genotypes and mutations in HBV basal core promoter (BCP) and precore regions. We included 65 consecutive patients, 25 HBV/HCV, 18 HBV/HDV, and 22 HBV/HCV/HDV. Controls consisted of 55 patients with chronic HBV and 55 with chronic HCV infection. HBV-DNA and HCV-RNA levels were lower in coinfections than in single infections (P <.05). HBV/HCV coinfection was associated with lower HBV viremia (8.2 x 10(4) copies/mL) and lower HCV-RNA levels (7 x 10(5) IU/mL), than the corresponding control group (P <.05), with more marked decrease in HBV replication (P <.05). Moreover, in HBV/HCV coinfection and in triple coinfection we observed an inverse relationship between HBV-DNA and HCV-RNA levels (P <.05). HBV/HDV coinfection was associated with lower HBV viremia (2.5 x 10(4) copies/mL) than that found in HBV infection (P <.05). Patients with triple coinfection showed lower HBV-DNA and HCV-RNA levels than control groups (P <.05). Prevalence of precore mutations was lower in HCV coinfections (P <.05). No significant association was observed between HCV-RNA levels and HBV precore mutations, BCP mutations or HBV genotypes, or between HBV-DNA levels and HCV genotypes (P <.05). In conclusion, HCV exhibited stronger inhibitory action in the reciprocal inhibition seen in HBV/HCV coinfection. HDV was the dominant virus in HBV/HDV coinfection and in triple coinfection, and had a greater unfavorable influence on HCV than on HBV replication. The reciprocal inhibition of viral replication seemed to be little influenced by the inherent genomic factors studied.
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PMID:Role of hepatitis B, C, and D viruses in dual and triple infection: influence of viral genotypes and hepatitis B precore and basal core promoter mutations on viral replicative interference. 1148 26

HIV-hepatitis C virus (HCV) coinfection is common and affects more than one-third of all HIV infected persons worldwide. Prevalence among risk categories varies according to shared risk factors for transmission, mainly intravenous drug use (IDU) and hemophiliacs. Chronic HCV infection seems to accelerate the course of HIV disease, resulting in a worsened clinical and immunological progression. At the same time, several studies suggest that HIV disease modifies the natural history of HCV infection, leading to a faster course of progression from active hepatitis to cirrhosis, to end stage liver disease and death. HCV infection mimics opportunistic diseases because its natural history is significantly accelerated in HIV patients. Since highly active antiretroviral therapy (HAART) has slowed the progression of HIV disease and decreased the rate of HIV associated mortality, the prognosis of HIV disease has been modified, and the need to treat HCV coinfection become a significant issue. Because of the poor response rate obtained by either interferon alone or interferon thrice weekly plus ribavirin, the combination of pegylated interferon and ribavirin will probably become the standard of care, although the clinicians should be aware of the overlapping toxicity of nucleoside analogues and ribavirin. Many selected categories of patients pose particular challenges to physicians treating HCV infection: nonresponders to interferon, cirrhotic patients, and patients infected with both HCV and HBV. Liver transplantation in HIV patients is currently under evaluation, but should become the rescue therapy for HIV patients with end stage liver disease.
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PMID:HCV chronic hepatitis in patients with HIV: clinical management issues. 1213 7

Coinfection with HIV and the hepatitis C virus (HCV) or hepatitis B virus (HBV) is a growing public health concern. Because the diseases are spread in similar ways--notably through shared use of needles to inject drugs and sexual activity--many people are coinfected with HIV and HCV, HIV and HBV, or even all three viruses. Hepatitis C and hepatitis B are viral infections of the liver; over time they can lead to serious consequences including liver cirrhosis and liver cancer. Most studies show that HIV infection leads to more aggressive hepatitis C or hepatitis B and a higher risk of liver damage. Studies of how HCV and HBV affect HIV disease are less clear. Most research shows that HCV does not accelerate HIV disease progression, but HIV/HCV coinfection may impair immune system recovery after starting antiretroviral therapy. Coinfection can complicate treatment. People with liver damage due to chronic hepatitis are more likely to experience hepatotoxicity (liver toxicity) related to anti-HIV drugs. In addition, drugs used to treat HIV and hepatitis can interact and side effects may be exacerbated. Most experts recommend that HIV should be controlled first before a person begins HCV treatment. With careful management, most people with HIV/HCV or HIV/HBV coinfection can be successfully treated for both diseases. In fact, several recent studies suggest that HIV/HCV-coinfected people with well-controlled HIV disease and relatively high CD4 cell counts may do as well as those with HCV alone.
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PMID:HIV and hepatitis C coinfection. 1269 Oct 36

To evaluate the interference between HBV, HCV and HDV and the clinical impact of coinfection as compared with single HBV or HCV infection, we unrolled 618 HBsAg and/or anti-HCV positive subjects (337 with liver biopsy and 281 without liver biopsy) at their first observation at one of the seven Italian Liver Units from 1993 to 1997 (Padova, Rome, Sassari, Naples, Bari, Messina, Palermo). Serum HBV-DNA by dot-blot was found more frequently in patients with HBV infection alone (52% of 133 cases) than in those with HBV-HCV coinfection (28% of 64 cases, p<0.005) or in those with HBV-HDV-HCV coinfection (12% of 25 cases, p<0.0005) or with HBV-HDV coinfection (13% of 8 cases, p<0.05). We observed a higher prevalence of HCV-RNA positive cases in the patients with HCV infection alone (91.2% of 114 cases) than in those with HBV-HCV coinfection (64.5% of 62 cases, p<0.0001) or with HBV-HDV-HCV infection (19% of 21 cases, p<0.0001). These observations suggest a reciprocal inhibition of HBV and HCV genome in multiple hepatitis viral infection. A severe liver disease was more frequently observed in patients with HBV-HCV coinfection (66%) than in those with a single HBV infection (43%, p<0.05) or HCV infection (46%, p<0.05). Anti-HCV positive/anti-HBc positive patients, lacking both HBsAg and anti-HBs, compared with the anti-HCV positive/anti HBc negative ones, more frequently showed severe clinical presentation and less frequently had a sustained response to a-IFN treatment.
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PMID:[Virological and clinical aspects of multiple hepatitis virus infections: preliminary data of an italian multicentre study] 1275 87


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