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)

A study of anti-HCV in the sera of different populations of Beijing was conducted. Of the general population, 2.1% (9/438) were anti-HCV positive, and of the patients that underwent blood transfusion 11.1% (6/54) were anti-HCV positive. Among patients with chronic liver diseases, anti-HCV was positive in 10.5% (36/342) of patients with chronic persistent hepatitis (CPH), 12.1% (13/107) of those with chronic active hepatitis (CAH), 42.6% (63/148) of those with liver cirrhosis (LC) and 38.4% (20/52) of those with hepatocellular carcinoma (HCC). HBsAg and anti-HCV were both positive in none of the general population, in 6.7% (23/342) of patients with CPH, in 8.4% (9/107) of those with CAH, in 31.1% (46/148) of those with LC and in 28.9% (15/52) of those with HCC. In the development of hepatitis into chronicity, detection of anti-HCV is of great significance. It was found that HBV-HCV coinfection made the condition of the patients with hepatitis worsened and it had close relations with hepatocellular carcinoma. Investigation in subjects below the age of 35 in the general population and in patients with chronic hepatitis indicate that besides the mother-to-infant route or the route of blood transfusion, HCV has other routes of propagation.
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PMID:[Investigation of anti-hepatitis C virus in the sera of different populations of Beijing]. 137 86

Recently, a novel virus, tentatively designated GB virus (GBV-C) was identified in patients with hepatitis. The frequency of this novel virus infection was therefore investigated in 58 patients with chronic hepatitis B virus (HBV) infection and in 74 patients with chronic hepatitis C virus (HCV) infection who had received orthotopic liver transplantation (OLT) because of decompensated liver cirrhosis. Before OLT, GBV-C sequences were found by reverse transcription nested polymerase chain reaction with primers derived from the helicase-like region in six (10%) of the HBV- and in six (8%) of the HCV-infected patients. Specificity of the polymerase chain reaction products was confirmed in eight of them by direct sequencing. Pretransplant GBV-6 viremia was associated with posttransplant viremia in 75% of patients. The comparison of GBV-C nucleotide and amino acid sequences within the helicase-like region revealed that pre- and posttransplant sequences differed only in 0-7 nucleotide exchanges, and with the exception of one, all of them were silent mutations. After OLT, 29% of the HBV- infected and 12% of the HCV-infected patients became GBV-C positive,indicating a high rate of "de novo" GBV-C infection. By correlating the GBV-C status with the frequency of the occurrence of graft hepatitis in both groups of patients, it became evident that posttransplant GBV-C viremia did not increase the risk for this clinical condition. However, we found a significantly higher percentage of hepatocellular carcinoma in patients with pre-OLT GBV-C/HCV coinfection compared with patients with HCV infection alone (5/6 vs. 16/68;P<0.01).
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PMID:GB virus C infection in patients with chronic hepatitis B and C before and after liver transplantation. 882 65

To investigate the influence of human immunodeficiency virus (HIV) coinfection on preexisting long-term chronic C hepatitis (HCV) 68 liver biopsies from 22 HIV/HCV-coinfected, 13 HIV- and 33 HCV-monoinfected patients and 71 livers obtained at autopsy from 26 HIV/HCV-coinfected and 45 HIV-monoinfected patients were studied by histo- and immunohistochemistry. All HIV patients had reached the advanced stage of immunodeficiency (stage III CDC), except for 3 haemophilias (stage II CDC). HCV infection was associated with a higher degree of portal, periportal and lobular inflammation-regardless of whether there was concurrent HIV infection. HIV/HCV coinfection was associated with a significantly higher rate of granulocytic cholangiolitis than HCV and HIV monoinfection (P < 0.05), a histological feature uncommon in C hepatitis. In HIV/HCV coinfection cholestasis was a predominant histological feature. HCV monoinfection and HCV/HIV coinfection were associated with the highest fibrosis index. In HIV/HCV coinfection centrilobular fibrosis was significantly more marked than in HCV monoinfection (P < 0.05), suggesting an HIV-associated fibrogenic effect. Patients with chronic C hepatitis showed a significantly increased rate of posthepatitic cirrhosis compared with the patients without HCV infection (P < 0.05). At autopsy, 10 of the 20 HIV/HCV-coinfected haemophiliacs had developed cirrhosis because of chronic C hepatitis, whereas cirrhosis was found in only 2 of 6 HIV/HCV-coinfected non-haemophiliacs (1 case of chronic B and C hepatitis, and 1 case of chronic alcohol abuse). No cirrhosis was observed in the 45 autopsy patients with HIV monoinfection. The findings suggest that HIV coinfection aggravates the course of preceding long-term chronic C hepatitis by a more marked (centrilobular) fibrosis. HIV/HCV-coinfected patients are threatened by a higher rate of posthepatitic cirrhosis-particularly in multitransfused haemophiliacs-and cholestatic hepatopathy.
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PMID:Liver histopathology in patients with concurrent chronic hepatitis C and HIV infection. 913 37

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

Concurrent infections with HGV and/or HCV (HGV/HCV) were investigated in 196 patients with HBV-related chronic liver disease (115 chronic hepatitis, 31 liver cirrhosis, 50 hepatocellular carcinoma), and in 100 HBsAg carriers. Coinfections were detected in 18 (9.2%) patients with HGV (10) or HCV (5) or both agents (3), but in none of the HBsAg carriers. Patients with coinfection were more frequently exposed to blood transfusions (55.6% vs 5.6%) and also were more commonly anti-HBe positive. Serum levels of HBV-DNA were lower in patients with HCV coinfection than in those coinfected with HGV. Interferon was administered to 39 patients with chronic active hepatitis including 7 patients with HGV/HCV coinfection. Sustained clearance of HBV-DNA was observed in 10 (25.6%) patients who were solely infected with HBV. These patients were significantly younger and had much lower histological scores than non-responders. Patients with HCV coinfection had significantly higher pre-treatment histological scores than those without HCV. After interferon treatment, a significant reduction in histological scores was observed in all patients except those coinfected with HGV/HCV. None of the 7 patients with coinfection had sustained clearance of HBV-DNA or HCV-RNA, and only one had cleared HGV-RNA. These results suggest that parenteral exposure is a risk factor for HGV/HCV coinfection in chronic HBV infection. HGV infection shows no significant impact on chronic HBV infection. HCV coinfection appears to inhibit HBV replication, but causes more severe chronic hepatitis and increases resistance to interferon therapy.
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PMID:Coinfections with hepatitis g and/or c virus in hepatitis B-related chronic liver disease. 1092 69

Hepatitis C is a disease with varying rates of progression. The role of hepatitis B virus (HBV) as a cofactor in the development of hepatitis C virus (HCV)-related cirrhosis and hepatocellular carcinoma (HCC) has been suggested and the use of HBV vaccine in all HCV-infected patients has been advocated. This review presents the implications of HBV and HCV coinfection and addresses the issues of HBV vaccine immunogenicity and safety in patients with chronic HCV infection.
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PMID:Hepatitis B virus vaccine for patients with hepatitis C virus infection. 1113 51

Hepatitis C virus (HCV)/HIV coinfection is a burgeoning epidemic that received considerable attention at the 12th World AIDS Conference. Risk factors, transmission, coinfection and disease progression, treatment options, and the side effects of hepatitis B virus (HBV)/HCV coinfection are discussed. Among the findings are that HCV appears to help HIV progress faster, that highly active antiretroviral therapy (HAART) may even contribute to more rapid HCV infection of coinfected patients, and that an undetectable viral load does not influence HCV replication in HCV/HIV coinfection. Further, HAART appears to not have long-term beneficial effects on HCV viremia. Chronic active hepatitis and cirrhosis are the most relevant complications of long-term HIV survivors with HCV/HIV coinfection, a condition that will be more prevalent as patients survive longer.
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PMID:Hepatitis C virus (HCV) and HIV coinfection. 1136 99

Hepatocellular carcinoma (HCC) is a common cancer. Its incidence is higher in countries where hepatitis B is endemic. HCC is substantially a complication of liver cirrhosis. Hepatitis B virus (HBV) and hepatitis C virus (HCV) are the predominant causes of cirrhosis, and as such, HCC. The link between HCC and alcoholic cirrhosis is less strong. Other less common forms of chronic liver disease can also lead to HCC. HBV is the HCC-determining disease worldwide. In endemic regions, it tends to be acquired early in life. The largest strides in prevention of HCC have been made with the HBV vaccine. HCV has a lower global prevalence than HBV, but HCV causes the most HCC in economically developed regions. In these areas, where the incidence of HCC is low, HCV now accounts for more than 50% of HCCs. There is no vaccine for HCV, so prevention of HCV-associated HCC will focus on prevention of initial infection and elimination of infection through antiviral therapies. HBV-HCV coinfection, and the combination of either with alcohol abuse or aflatoxin exposure seems to raise the risk of HCC development further. Liver transplantation and other adjuvant therapies may offer better options for secondary prevention of HCC than resection alone.
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PMID:The epidemiology and prevention of hepatocellular carcinoma. 1168 37

Liver transplantation in patients with hepatitis B has been under discussion for 20 years because of inferior results without reinfection prophylaxis; therefore, we analyzed our overall experience with liver transplantation in hepatitis B patients with immunoprophylaxis, particularly the influence of the available antiviral treatment in different periods. From 1988 to 2000, 228 liver transplants in 206 hepatitis B patients were performed. Indications were acute liver failure (10%), hepatitis B virus (HBV) cirrhosis alone (67%) or with hepatitis D virus (HDV) (13%), or hepatitis C virus (HCV) coinfection (7%). All patients received long-term immunoprophylaxis (anti-HBs > 100 U/L). HBV DNA-positive patients were treated before and after surgery with famciclovir or lamivudine since 1993 and 1996, respectively. Since 1993, antivirals also were used for HBV reinfection. The 1-, 5-, and 10-year patient survival rates were 91%, 81%, and 73%. In patients with hepatocellular carcinoma (HCC) (60% 5-year survival, P <.01) or HBV reinfection (69% 5-year survival, P <.01) survival was significantly impaired. Those with HDV or HCV coinfection had a slightly better survival than with HBV monoinfection (P >.05, not significant). Preoperative positive HBV DNA (hybridization-assay) test results were associated with a slightly impaired patient survival (78% 5-year survival, P >.05, not significant versus DNA-negative). Preoperative positive hepatitis B e antigen (HBeAg) predicted significantly worse survival (P <.05 versus negative HBeAg). Graft loss caused by reinfection was most frequent before the availability of antiviral drugs. Two-year patient survival increased from 85% in era I (1988-1993) to 94% in era III (1997-2000, P <.05). The 2-year recurrence rates in these 2 periods were 42% and 8% (P <.05). In conclusion, excellent long-term results can be achieved in hepatitis B patients after liver transplantation with modern strategies, and survival rates are similar to other indications. Based on our experience, hepatitis B patients, including those with active viral replication, should not be excluded from liver transplantation.
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PMID:Increasing applicability of liver transplantation for patients with hepatitis B-related liver disease. 1202 40

HIV/HCV coinfection is characterized by a progredient course of hepatitis C. A more rapid development to cirrhosis, and especially in the presence of progredient immunodeficiency, an increased mortality due to liver failure has been described in coinfected patients. In addition hepatitis C has an unfavorable impact on the progression of HIV. The worse course of hepatitis C in HIV-coinfected patients as well as the faster progression of HIV underline the need for development of treatment options for hepatitis C in HIV-coinfected patients. First results from trials looking at the effect of pegylated interferon and ribavirin for treatment of hepatitis C in HIV-coinfected patients found primary response rates of around 50% which were clearly better than the response rates observed under non-modified interferon/ribavirin therapy in HIV/HCV-coinfected patients so far.
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PMID:[Hepatitis C and HIV coinfection. Current aspects of therapy]. 1204 70


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