Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic hepatitis C (non-A, non-B hepatitis) is a common and often progressive viral liver disease. To assess the efficacy of therapy with the antiviral agent interferon alfa, we randomly assigned 166 patients with chronic hepatitis C to treatment with either 3 million or 1 million units of recombinant interferon alfa three times weekly for 24 weeks, or to no treatment. The probability of normalization or near normalization of the serum alanine aminotransferase levels after six months of interferon therapy was 46 percent in patients treated with 3 million units of interferon (P less than 0.001) and 28 percent in those treated with 1 million units (P less than 0.02), but only 8 percent in untreated patients. The serum alanine aminotransferase level became completely normal in 22 of the 26 patients (85 percent) who responded to treatment with 3 million units of interferon and 9 of the 16 patients (56 percent) who responded to treatment with 1 million units. The patients who received 3 million units of interferon had histologic improvement because of the regression of lobular and periportal inflammation. Relapse within six months after the completion of treatment occurred in 51 percent of the patients treated with 3 million units of interferon and 44 percent of those treated with 1 million units. We conclude that a 24-week course of interferon therapy is effective in controlling disease activity in many patients with hepatitis C, although relapse after the cessation of treatment is common.
 ...
PMID:Treatment of chronic hepatitis C with recombinant interferon alfa. A multicenter randomized, controlled trial. 250 16

Chronic hepatitis C is common in Saudi Arabia and most often presents in an advanced stage. To assess the response of patients to interferon, a randomized placebo-controlled double-blind study was undertaken. All but 1 patient had cirrhosis or fibrosis before interferon. After a 24-week observation period patients received alpha 2a interferon, 3 mega units sc tiw or placebo for 24 weeks, then the opposite treatment for another 24 weeks followed by 24 weeks of observation. Liver biopsies were performed before and after each of the treatment phases. Twenty-two out of 24 patients completed the study. The mean alanine aminotransferase (ALT) levels fell from 150.7 +/- 118.7 units/l to 91.0 +/- 42.6 units/l after 6 months interferon treatment (P = 0.03) but only 3 patients (14%) had complete normalization of mean ALT levels and 4 (18%) had > 50% reduction. The mean hepatitis activity index fell from 12.2 +/- 2.6 immediately before to 11.6 +/- 2.5 just after interferon (P = 0.4). After interferon there was an insignificant raise in 6-month mean ALT. Hepatitis C virus-RNA was positive in all 17 patients tested and remained so after treatment. Side-effects were mild and well tolerated. Alpha interferon 3 mega units tiw for 24 weeks is not an effective treatment of histologically advanced chronic hepatitis C.
 ...
PMID:Histologically advanced chronic hepatitis C treated with recombinant alpha-interferon: a randomized placebo-controlled double-blind cross-over study. 751 10

Hepatitis C virus (HCV) has been associated with acute and chronic posttransfusion and with sporadic non-A non-B (NANB) hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). Cloning of the sequence encoding an antigenic component of HCV in 1989 led to the development of tests to detect antibody to HCV in serum. Viral HCV RNA can be detected and estimated with polymerase chain reaction (PCR) and branched-chain DNA (bDNA) signal amplification tests. The entire viral genome has been sequenced. The HCV envelope region varies considerably, and infections with mutant HCV have been described. Approximately 0.5-1.5% of healthy blood donors test positive, and HCV infection can be acquired by blood transfusion or i.v. drug abuse. Vertical and sexual transmission of the virus is rare, and the transmission mode remains obscure in a large group of patients. Acute hepatitis C is mild and often asymptomatic. Chronic hepatitis C has an indolent course but may progress to cirrhosis and HCC. Recombinant alpha interferon (IF) is used to treat chronic HCV disease, but no consensus has been reached on patient selection, dose, and duration of treatment. Approximately 50% of treated patients respond, but 50-80% of responders relapse over time. Liver transplantation in patients with end-stage, HCV-related liver disease is often followed by allograft infection. Short-term survival with reinfection is good, but the long-term consequences remain to be defined.
 ...
PMID:Hepatitis C: an overview. 759 67

Post-transfusion hepatitis was studied prospectively in 1,476 patients undergoing open-heart surgery between 1985 and 1988. Thirty-three (2.2%) patients suffered from post-transfusion hepatitis. Acute post-transfusion hepatitis was attributed to hepatitis B in one case and to hepatitis C in ten patients (0.7%). Four additional patients had preexisting serologic markers of hepatitis C. In 22 (1.5%) patients, hepatitis B or C was excluded as a cause of liver disease. Seroconversion for hepatitis C virus occurred from 3 weeks to more than 6 months after infection. Chronic hepatitis C developed in four patients. In addition, seroconversion to anti-HCV was observed in four patients with moderately elevated aminotransferases. In the control patients anti-HCV antibodies were found in 0.5%. The characteristics of acute hepatitis C after blood transfusion are shown and compared to 22 patients with acute hepatitis non-A, non-B, non-C. The etiology of these 22 cases is discussed.
 ...
PMID:Frequency of hepatitis C in acute post-transfusion hepatitis after open-heart surgery: a prospective study in 1,476 patients. 768 11

Recently antibodies to hepatitis C virus were detected in sera of chronic active hepatitis patients, with anti-smooth muscle autoantibodies or with anti-liver/kidney microsomal type 1 autoantibodies. As the latter were used to differentiate autoimmune chronic active hepatitis from chronic non-A, non-B virus hepatitis, it was mainly important to discover if autoantibodies were associated with chronic hepatitis C virus infection. The sera of 272 chronic hepatitis C patients were screened by indirect immunofluorescence for non-organ specific autoantibodies. Antinuclear antibodies and anti-smooth muscle autoantibodies were more frequent in chronic hepatitis C patients than in blood donors (n = 100). Anti-liver/kidney microsomal type 1 autoantibodies were not detected in the sera of the blood donors, in the 74 hepatitis B patients or in the 30 alcoholic hepatitis or cirrhotic patients' sera tested as controls. They were detected in 14 chronic hepatitis C patients. These antibodies were compared in immunodiffusion to anti-liver/kidney microsomal type 1 autoantibodies sera obtained from type-2 autoimmune chronic active hepatitis patients and an identity reaction was observed. Chronic hepatitis C patients without or with anti-liver/kidney microsomal type 1 autoantibodies, did not differ in age, sex ratio, transaminases and gammaglobulin level, risk factors for hepatitis C virus infection, association with other autoimmune diseases. These patients differed significantly from type-2 autoimmune chronic active hepatitis patients. We conclude that: (i) in some chronic hepatitis C patients the pattern and the titer of autoantibodies may create confusion with an autoimmune chronic active hepatitis; (ii) There is no serological evidence for a hepatitis C virus infection in true type-2 autoimmune chronic active hepatitis.
 ...
PMID:Non-organ specific autoantibodies associated with chronic C virus hepatitis. 822 18

Autoimmune hepatitis is an inflammatory disease of the liver of unknown etiology that progresses toward cirrhosis and liver failure and is generally responsive to immunosuppressive treatment. The presence of anti-smooth muscle antibodies with anti-actin specificity and of anti-liver kidney microsomal antibodies defines two distinct subgroups of the disease. An autoantibody against liver cytosolic antigens has recently been described. Management of autoimmune hepatitis relies on immunosuppressive therapy with steroids alone or combined with azathioprine. When the disease is poorly controlled, despite good patient compliance to therapy, cyclosporin should be recommended. Progressive liver disease in chronic hepatitis B in adults has been associated with the presence of precore mutants of hepatitis B virus. In children, the presence of precore mutants seems not to affect the rate of seroconversion to anti-hepatitis B e antigen. However, high viremic levels of precore mutants are associated with persistent viral replication and liver disease. Interferon alfa seems to be less effective in children than in adults in the treatment of chronic hepatitis B; however, it hastens the seroconversion rate to anti-hepatitis B e antigen, accelerating the spontaneous clearance of the virus in children with already low levels of viral replication. Blood transfusions, especially those received in the perinatal period, are the single most important source of infection with hepatitis C in childhood. HIV coinfection is a major risk factor for vertical transmission of hepatitis C virus in pregnant women. Chronic hepatitis C in children is usually an asymptomatic disease associated with mild to moderate fluctuation of aminotransferase activities and histologic features of mildly active hepatitis. Severe active hepatitis and cirrhosis are infrequent during childhood and adolescence. Interferon may have a place in the treatment of chronic hepatitis C in children.
 ...
PMID:Chronic hepatitis in children. 854 54

Chronic inflammatory liver diseases can be induced by virus infections, toxic-metabolic factors and/or autoimmune mechanisms. This overview deals with the immunopathogenesis of chronic hepatitis B and C and autoimmune hepatitis (AIH). 1. Chronic hepatitis B: The immune response to HBV-antigens is responsible both for viral clearance and disease pathogenesis during HBV-infection. The humoral immune response to HBsAg contributes to the clearance of circulating virus particles, the cell mediated immune response to HBsAg, HBcAg and polymerase antigen eliminates infected cells. The class I- and class II restricted T-cell-responses to HBV is strong, polyclonal and multispecific in acute HB with successful clearance of the virus, but weak or incomplete in chronic HB with viral persistence. In addition to ineffective immune response host and viral factors as well as abnormalities in virus-host interactions may be the main reasons for the maintenance of HBV-carrier status. 2. Chronic hepatitis C develop in more than 60% of infected patients. There is increasing evidence that the immune response to HCV-epitopes plays an important role in the course and the pathogenesis of the disease. It has been shown that CD4+ and CD8+ T-cells recognize viral peptides in the presence of class I and II molecules. The fine specificity and functional significance of liver infiltrating and peripheral blood T-cells demonstrate HCV specific immunodominant epitopes targeted by class Ii restricted CD4+ cells in patients with chronic HCV infection. The T-cell response correlates with disease activity. The cytokine release of T-cells resemble a TH1-like profile. Studies of the humoral immune response to HCV show a correlation between IgM-anti-HCV and disease activity. In vitro and in vivo anti-HCV secretion by PBMC is due to persistent antigenic stimulation of B-cells by ongoing production of viral antigens and reflects HCV replication in PBMC. Of special interest are several immune mediated disease and immune abnormalities in chronic hepatitis C. 3. Autoimmune hepatitis (AIH) is a distinct group of acute and chronic necro-inflammatory disorders of unknown etiology characterized by immunological and autoimmunological features including the presence of autoantibodies but without an antecedent of viral infections. Marker autoantibodies define 3 subtypes: Type I (ANA/SMA), Type II (LKM1-AB), Type II (SLA-AB). AIH is associated with a distinct genetic background (HLA A1, B8, DR3 or DR4). Several studies clearly demonstrate that liver cell damage in AIH is mediated by autoimmune reactions against normal constituents of hepatocytes. Although the precise mechanisms are not yet fully understood, there is now considerable evidence that autoantigens of the hepatocellular membrane in particular the ASGPR are important targets of liver damaging autoreactions in AIH. Cellular and humoral immune reactions against the human ASGPR correlate with disease activity and usually disappear under immunosuppressive therapy.
 ...
PMID:[Immunopathology of chronic liver diseases]. 860 Jun 84

The natural history of hepatitis C is complex and still poorly known. Hepatitis C virus (HCV) replication can be detected very soon after exposure and, at least in the transfusional setting, it persists indefinitely in up to 90% of the cases. While liver damage during the acute phase of hepatitis is almost invariably mild (fulminant cases are exceptions), chronic sequelae of HCV infection may be severe in the long run. Chronic hepatitis C, in fact, is a long-lasting indolent process which leads to cirrhosis in approximately 20% of all infected patients. Hepatocellular carcinoma is a well-recognized complication of old infections, as are a number of extrahepatic manifestations, including type II cryoglobulinaemia. The determinants of the severity of the liver disease are still unclear. However, the risk of cirrhosis seems to be greater for patients with old infections, those infected with the genotype 1b and those with associated conditions. The latter are a heterogeneous and increasing group of 'problem' patients, including patients who are co-infected with the human immunodeficiency virus (HIV1), or who are being treated with cytotoxic or immunomodulating drugs. Data suggest that the natural history of hepatitis C is altered in patients with associated conditions, and this might have an impact on strategies of patient management and treatment.
 ...
PMID:The natural history of hepatitis C. 886 34

Hepatitis C virus (HCV) is a major cause of chronic hepatitis worldwide, which finally leads to development of hepatocellular carcinoma. Chronic hepatitis C is characterized by several histological features in the liver which discriminate it from other forms of hepatitis: bile duct damage, lymphoid follicles and steatosis (fatty change). Little is known, however, about the role of HCV or its viral proteins in the pathogenesis of hepatitis. Recently, the core protein of HCV has been suggested to have a transcriptional regulatory function, and thereby to be involved in inducing phenotypic changes in hepatocytes. To clarify whether or not the HCV core protein has an effect on pathological phenotypes in the liver, two independent transgenic mouse lines carrying the HCV core gene were established. These mice developed progressive hepatic steatosis, indicating that the HCV core protein plays a direct role in the development of hepatic steatosis, which characterizes hepatitis C. This transgenic mouse system would be a good animal model for the study of pathogenesis in human HCV infection.
 ...
PMID:Hepatitis C virus core protein induces hepatic steatosis in transgenic mice. 922 25

Chronic hepatitis C infection (CH-C) accounts for a significant number of patients undergoing orthotopic liver transplantation (OLT). Recently, hepatitis C virus (HCV) genotype-dependent differences in disease outcome and therapeutic responses have been suggested. The objectives of our study were to determine (1) the recurrence of HCV infection after OLT; (2) distribution of HCV genotypes in patients with CH-C who required liver transplantation compared with those who did not; and (3) the 1-year transplantation outcome in patients infected with different hepatitis C genotypes. RNA was extracted from sera of 20 patients who underwent OLT for end-stage liver disease secondary to CH-C (group I) and 52 patients with CH-C who did not require OLT (group II). For viral RNA detection, reverse transcriptase and polymerase chain reaction (RT/PCR) of 5'UT region was performed on all OLT patients both before and after OLT. For genotyping, RT-PCR of the NS 5 region was performed, followed by automated sequencing of the amplification products. Nineteen OLT patients had viral RNA detected by PCR both before and after OLT. One patient had no RNA detected before OLT but became viremic after OLT. The prevalence of HCV genotype 1b was significantly higher in group I patients compared with group II (53% v 23% respectively, P = .01). Examination of outcome at 1 year after OLT showed that 9 of 10 patients with HCV genotype 1b had histological evidence of hepatitis compared with 4 of 9 patients with other genotypes (non-1b) (P = .06). However, the number of patients who had one or more episodes of rejection, underwent retransplantation, or died at 1 year after OLT were similar. Recurrence of HCV infection after OLT was shown in all studied patients. Hepatitis C genotype 1b is more prevalent in our patients who underwent transplantation compared with a group with chronic hepatitis C who did not require transplantation (P = .01). Patients infected with HCV genotype 1b may have a higher risk of histological hepatitis after transplantation.
 ...
PMID:Hepatitis C genotypes in liver transplant recipients: distribution and 1-year follow-up. 934 11


1 2 3 4 5 6 7 Next >>