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)

Two distinct serologic types of chronic hepatitis B have been identified, namely the "classical" HBeAg positive form and the "atypical" HBeAg negative, anti-HBe positive variant which is due to infection by a mutant HBV having a pre-core stop codon that makes the virus unable to produce HBeAg. The anti-HBe positive form is currently the prevalent type of chronic hepatitis B in the Mediterranean area, being associated with a more severe clinical course compared to HBeAg positive cases. The response to interferon therapy in patients with anti-HBe positive chronic hepatitis B has been recently investigated in control trials. These studies have shown that normalization of ALT with efficient suppression of virus activity can be achieved in 50-80% of patients while treated with interferon alpha indicating that also the pre-core mutant of HBV is sensitive to the antiviral effect of interferon. However, reactivation of hepatitis occurs in a variable percentage of initial responders when interferon is stopped. The probability of reactivation increases when the disease is of long duration, when cirrhosis is present and particularly if the pre-core mutant of HBV has become the predominant type of circulating virus, indicating that this HBV variant is more resistant to immunoclearance compared to wild type HBV.
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PMID:Interferon therapy for the anti-HBe positive form of chronic hepatitis B. 752 89

Immunoglobulin A class antibody to hepatitis C virus core antigen (IgA anti-HCc) was measured in the serum of 128 patients with type C chronic liver disease. Fifty-eight patients (45.3%) were seropositive. IgA anti-HCc was detected in only one of 20 patients with chronic persistent hepatitis; however, 52.3% (46/88) of patients with chronic active hepatitis and 55% (11/20) of patients with liver cirrhosis were seropositive. Histological examination revealed that 22 (71.0%) of 31 patients with severe disease activity were seropositive compared to 35 (44.9%) of 78 patients with moderate (P < 0.05) and one (5.3%) of 19 patients with mild (P < 0.01) histological changes. IgA anti-HCc was measured sequentially in 65 patients who underwent interferon therapy. There was a significant difference between responders and other patients in the mean ratio of IgA anti-HCc titers one month after therapy. Three months after therapy, IgA anti-HCc was detectable in only two of 15 responders who were IgA anti-HCc seropositive at the start of therapy. In contrast, IgA anti-HCc reappeared three months after therapy despite a temporary decrease to undetectable levels in all nonresponders. We conclude that IgA anti-HCc is a useful marker to identify the presence of active type C liver disease and that the disappearance of IgA anti-HCc three months after interferon therapy predicts a good response in treated patients.
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PMID:Clinical study of IgA antibody against hepatitis C virus core antigen in patients with type C chronic liver disease. 753 36

Hepatitis C virus (HCV) is the major cause of non-A, non-B hepatitis worldwide. Since the HCV viral genome was molecularly cloned and antibody detection systems were established, a considerable amount of information on HCV has been accumulated. In the present study, I have examined the sera and liver tissues of the patients of type C chronic liver disease using molecular biological methods and tried to correlate the data obtained with the clinical, pathological and therapeutic outcomes. A reverse transcription-polymerase chain reaction (RT-PCR) method using radiolabeled nucleotides provided constant results in genome amplification, and could be shown to be a reliable method for quantifying the levels of HCV genome. The amount of HCV RNA in the serum tended to increase as a function of the duration of the disease and the progression of histopathologic changes of the liver. In addition, the serum HCV RNA titers correlated well with those of liver tissues, which showed that the amount of circulating HCV genome reflected the intrahepatic amount of HCV. HCV, a positive-stranded RNA virus, is likely to make a negative strand during viral replication. In studies to detect the positive and negative strands of HCV RNA separately using strand specific primers, the existence of both strands in the liver was demonstrated, confirming viral replication in the liver. The ratio of negative to positive strands ranged from 0.03% to 30%, being 3.7% in chronic persistent hepatitis, 4.8-6.0% in chronic aggressive hepatitis and 6.7% in liver cirrhosis. The viral factors influencing the interferon (IFN) response were also examined. Individuals who had low titers of HCV genome tended to respond well to IFN. Moreover, IFN was more effective for patients with HCV type III than for those with HCV type II. Thus, IFN response was shown to depend both on virus titers and genotypes. However, mean levels of HCV RNA were almost the same between the patients with HCV type II and those with HCV type III before the treatment, there were significant differences in the disappearance of HCV and the effects of IFN therapy. It is suggested that the susceptibility to IFN is different for each genotype. Hokkaido J Med Sci 69 (6), 1382-1398, 1994.
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PMID:[Clinical studies on the detection of hepatitis C virus genome in the serum and the liver]. 753 30

Hepatitis C virus (HCV) populations in vivo exist as a mixture of heterogeneous viruses called quasispecies, which have variations in the hypervariable region (HRV). However, the relationship between the diversity of HVR quasispecies, the disease stage, or the interferon (IFN) responsiveness remains to be elucidated. To study these, serum samples were obtained from 42 patients with chronic hepatitis C virus infection; 24 with chronic active hepatitis (CAH) treated with IFN, 9 with cirrhosis, 9 with hepatocellular carcinoma (HCC). HCV quasispecies populations were separated by the single-strand conformation polymorphism (SSCP) method targeted to the HVR. The patients were classified into two groups; a single-band group (n = 12) in which HVR quasispecies was homogeneous and a multiple-band group (n = 30) in which HVR quasispecies was heterogeneous. Patients with multiple bands had significantly more advanced liver disease than those with a single-band group (P = .0082). The percentage of patients with single band were 41% in CAH, 22% in cirrhosis, and 0% in HCC. Multivariate analyses showed that viral diversity was independently related to the progression of liver disease and was not correlated with the duration of infection. We also found that in CAH, the patients who had multiple bands (n = 14) were more resistant to IFN therapy than those who had a single band (n = 10) (P = .002). These results indicate that the diversity of HCV quasispecies becomes more complex as the disease stage progresses and that CAH with more complex diversity shows less IFN effectiveness.
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PMID:Diversity of quasispecies in various disease stages of chronic hepatitis C virus infection and its significance in interferon treatment. 754 87

The behavior of hepatitis C virus (HCV) infection with regards to type and number of HCV genotypes (tested with genotype-specific nested polymerase chain reaction) was evaluated in 60 patients with anti-HCV-positive chronic active hepatitis without cirrhosis [17 untreated and 43 subjects undergoing single or repeat courses of interferon (IFN) therapy] during a mean follow-up period of 76 +/- 18 months. In untreated patients (2 genotype I, 6 genotype II, 9 mixed infections) 4 out of 9 mixed infections selected for genotype II at the end of follow-up. Of the 43 treated patients 10 were long-term responders with histological remission, 6 were short-term responders, and 22 did not respond. Fifteen of the latter patients received another course of IFN therapy, and only 3 patients responded. Eight of the 10 responders had infection with a single genotype (4 gt I, 3 gt II, 3 gt III). After IFN therapy, all but 2 patients cleared the HCV infection. The responders to the second IFN course (1 gt I, 1 gt II, 1 gt III) remained viremic. Of the short-term responders, 2/6 patients had genotype II and 4 had a mixed infection (3 gt II +/- I and 1 gt II +/- III); gt III became prevalent in the latter in all but one patient. Of the nonresponders 18/24 had more than one genotype, 5 were genotype II at baseline and one had genotype I. At the end of the follow-up period 15/18 with mixed infection had selected for gt II (P < 0.01 vs. untreated patient).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Selection of more pathogenic hepatitis C virus genotype II during long-term follow-up of interferon-treated patients. 754 26

The prevalence of HBV recurrence after liver transplantation is higher in patients with viral B cirrhosis than in patients with viral B-D cirrhosis or fulminant hepatitis B and is related to the presence of HBV replication prior to transplantation. Long-term passive anti-HBs immunoprophylaxis is the best current way for prevention of HBV reinfection and improved long-term survival. The rate of recurrence of HCV infection is high, reaching 85%, and the rate of HCV hepatitis in the graft is approximately 75%. In most cases, HCV hepatitis leads to chronic hepatitis. The severity of graft hepatitis is related to the level of viremia at the time of the hepatitis and to the genotype 1b. The methods of prevention of HCV infection after liver transplantation are yet to be found. The treatment of graft HCV infection with interferon should be well evaluated and given cautiously. Other antiviral treatments without an immunostimulating effect are needed. Finally, patients transplanted for hepatitis B without HBV replication, receiving posttransplant long-term anti-HBs immunoprophylaxis, and those transplanted for HCV cirrhosis have a 5-year survival similar to other groups of transplanted patients. Patients belonging to these groups can be considered as candidates for transplantation. Patients with active HBV replication should be included in specific trials for prevention of HBV reinfection.
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PMID:Liver transplantation for viral hepatitis: the experience of the hepatobiliary center at Hospital Paul Brousse. 754 34

Since the first classification of chronic hepatitis (CHH) more than 25 years have elapsed. Since then conditions for assessment of the etiology, pathogenesis and therapy of the disease have improved. These findings must be applied in the contemporary diagnosis of CHH. The first task is to assess the correct etiology of the disease because it is decisive for treatment, development and prognosis of the disease. The most important cause of CHH is viral hepatitis. Hepatitis B and C are frequently occurring diseases and may develop into CHH and cirrhosis of the liver. New therapeutic procedures, using interferons, can prevent this. Idiopathic autoimmune hepatitis is a serious form where interferon therapy is contraindicated, while the condition usually responds very well to treatment with corticoids and immunosuppressive substances. It is important to take into consideration also possible liver damage by drugs and the fact that the clinical picture is associated with a certain stage of metabolically conditioned changes, in particular Wilson's disease. It is important to examine carefully the histological finding and laboratory results, as it is possible to evaluate from them the severity of the disease. We should also attempt to evaluate these changes quantitatively.
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PMID:[Chronic hepatitis--diagnosis and differential diagnosis]. 755 46

To determine whether hepatic metabolic function affects the response to interferon treatment, we measured antipyrine clearance (APC) in 85 patients with chronic active hepatitis C and compared the results with treatment outcome. Among 55 patients who responded to interferon by normalization of alanine transaminase (ALT), median APC before treatment was 0.47 (range, 0.12 to 0.98; normal range, 0.34 to 1.02 mL/min/kg body wt), a value that was significantly greater than in 30 nonresponders (0.23; 0.08 to 0.67 mL/min/kg body wt, P < .001). APC was closely associated with response to interferon. The response rate among cases with values > 0.25 mL/min/kg body weight was 79%, the same as in cases without cirrhosis. Cases without cirrhosis and with APC of > 0.25 mL/min/kg body weight had an 85% chance of responding to interferon; this was unlikely a simple reflection of histological activity, because the correlation with Scheuer score was poor in this subgroup (r = -.31, P < .05). A second, independent group of 43 patients was used to test the predictive value of APC (using 0.25 mL/min/kg body wt as a cut-off) for response to interferon treatment. In this group, APC correctly predicted positive response to interferon in 75% of cases. APC was also used to measure the effects of treatment on hepatic metabolic function. Regardless of outcome, there was no change in APC at the end of a 6-month course of interferon treatment. Six months later, however, improvement in APC (14%; P < .05) was evident among responders but not in those who had failed to respond to interferon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antipyrine clearance and response to interferon treatment in patients with chronic active hepatitis C. 902 73

In acute hepatitis C, the efficacy of alpha interferon has not been definitively demonstrated. However, several small trials have suggested that interferon may decrease the chronicity rate of acute hepatitis C. In view of the high rate of chronic infection resulting from acute hepatitis C, it is warranted to treat patients during the acute phase of illness if they continue to have HCV RNA detectable in serum for 1 month after the onset of symptoms. The regimen of alpha interferon therapy should be 3 mu three times weekly for 24 weeks. In chronic hepatitis C, therapy with 3-5 mu of alpha interferon three times weekly for 24-48 weeks will induce a temporary remission in disease with loss of HCV RNA from serum, fall of aminotransferases into the normal range, and improvement in liver histology in 50% of patients, and a sustained remission persisting after therapy is stopped in 15% to 20% of patients. Younger patients with a short duration of disease, without cirrhosis, and with lower levels of HCV RNA in serum are the most likely to respond. Unfortunately, there are no completely reliable means of predicting which patients will derive long-term benefits from the use of interferon. Interferon remains the only approved therapy for chronic hepatitis C, although the low rate of sustained remissions and the incidence of side effects mandate a search for ways to improve the efficacy of interferon, as well as to find new, more potent agents for the treatment of this disease.
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PMID:Therapy of hepatitis C. 759 47

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.
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PMID:Hepatitis C: an overview. 759 67


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