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)

Since 1989, some schemes of treatment for Chronic hepatitis C (CHC) have been investigated, including alpha and beta interferon (IFN), ribavirin, and amantadine either alone or in combination. These studies have been performed in other countries. In our study, we investigated the outcome of Mexican patients with CHC treated with IFN. Twenty-six patients with five years follow-up treated with IFN in monotherapy were studied. We evaluated three kinds of response: sustained response (SR); non response (NR), and partial response (PR). Patients were evaluated biochemically and histologically by means of aminotransferase levels (pretreatment and serial) and hepatic biopsy (pretreatment and control). The data were obtained from clinical records. Aminotransferase levels at the end of treatment and six months later as well as histologic damage score showed the following results: 16 patients were cataloged as NR (61.5%), four as PR (15.3%), and six as SR (23.1%). Ten patients developed cirrhosis during follow-up, eight from NR group, one from PR group, and one from SR group. CHC patients treated with IFN alone obtained SR in 19% of cases; the patient who developed cirrhosis was not included. A study for longer time, prospective and protocolized to evaluate standardized IFN dose as well as evaluate combined treatment, is necessary.
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PMID:[Biochemical and histologic changes in patients with chronic hepatitis C under treatment with interferon. a 5-year cohort study]. 1294 94

Heavy iron overload, in both primary and secondary hemochromatosis, may cause fibrosis of parenchymal organs, especially the liver. The toxicity of iron is believed to involve increased oxidative stress, with iron-catalyzed production of reactive oxygen species causing oxidative damage to lipids, proteins, and nucleic acids. Lesser degrees of hepatic iron deposition are also associated with, and seem to be risk factors for, certain nonhemochromatotic liver diseases. Porphyria cutanea tarda is associated with hepatic iron overload and responds to iron-reduction therapy. Results of recent studies have demonstrated high prevalences (about 60%-80%) of HFE gene mutations in patients with porphyria cutanea tarda. Chronic hepatitis C is another risk factor for porphyria cutanea tarda. Other recent evidence indicates that the prevalence of HFE gene mutations is increased in chronic viral hepatitis and that patients with chronic hepatitis C harboring especially the C282Y mutation are more likely to suffer from advanced hepatic fibrosis or cirrhosis and to do so at younger ages. A role for modest iron overload in increasing severity of alcohol-induced liver disease has been well established from results of experimental studies. However, it is currently unresolved whether mild-to-moderate hepatic iron deposition or heterozygosity for the C282Y mutation plays a role in human alcoholic liver disease or in nonalcoholic fatty liver disease or nonalcoholic steatohepatitis. There is persuasive evidence that iron reduction decreases insulin resistance, and it likely also decreases oxidative stress, two key pathogenic features of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. Iron loading has also been described after portosystemic shunts and in end-stage liver disease.
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PMID:Iron as a co-morbid factor in nonhemochromatotic liver disease. 1295 98

Chronic hepatitis C entails a life-long risk of developing cirrhosis and hepatocellular carcinoma and eradication of the hepatitis C virus (HCV) is the only realistic approach for lowering the risk of disease progression. Treatment is indicated for patients with high transaminases and histologic signs of chronic hepatitis: 6-12 month therapy with 3-6MU interferon alfa thrice weekly combined with 1-1.2 grams ribavirin yielded up to 30% sustained virological responses (SVR). SVR raised up to 50% with pegylated interferons combined with ribavirin. Favourable predictors of response to the former treatment are genotype 2 or 3, less than 2 million copies of HCV, no or portal fibrosis at biopsy, age less than 40 yr and female gender. The same was true for the latter treatment, however, with body weight less than 82 kg replacing female gender. Six month treatment is enough for treating genotype 2 or 3 patients whereas 12-month therapy is indicated for the more resistant patients with genotype 1 or 4.98% cure of community-acquired acute hepatitis C was achieved with early treatment with daily doses of 5MU interferon, compared to a calculated 30% virus clearance occurring in untreated patients. Cost-effective stopping rules based upon early clearance of serum HCV-RNA, are under investigation. A cut-off equal or more than 2 log decrease in serum HCV-RNA at week 12, has 97% negative predictive value and 60% positive predictive value. Treatment could be optimized also by retreatment with combination therapy of relapsers and non-responders to monotherapy, with SVR rates of 50% and 25%, respectively. Difficult-to-treat patients include patients who have high genotype 1 and 4 viremia or coinfection with HIV or hepatitis B virus as well as patients who carry an organ graft. Extended treatment of virological non responders with pegylated interferons might slow down progression of hepatic fibrosis and prevent hepatocellular carcinoma.
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PMID:Treatment of chronic hepatitis C. 1451 11

Chronic hepatitis C is often asymptomatic, at least during the first decade following hematopoietic stem cell transplantation. Progression to advanced liver disease or cirrhosis in patients surviving more than 10 years is currently thought to be rare. Among 1078 patients who underwent an allogeneic transplantation between January 1973 and January 1995, 96 patients infected by hepatitis C virus (HCV) during the transplantation period were studied. Cumulative incidence and analysis of risk factors for cirrhosis were analyzed, and the rate and risk of cirrhosis in transplant recipients were compared with those of 158 HCV-infected controls who did not receive transplants. At a median follow-up of 15.7 years, 15 patients developed biopsy-proven cirrhosis, leading to a cumulative incidence of cirrhosis of 11% and 24% at 15 and 20 years, respectively. By multivariate analysis, extrahepatic HCV manifestations and HCV genotype 3 were associated with risk of cirrhosis. The median time to cirrhosis in transplant recipients was 18 years as compared with 40 years in the control population. The risk of cirrhosis in transplant recipients relative to controls was significantly higher by multivariate analysis (P =.0008). Roughly a quarter of long-term HCV-infected survivors with transplants progressed to cirrhosis that is much more rapid than in patients without transplants. Systematic detection of HCV infection, liver biopsy, and therapeutic intervention are therefore warranted in long-term marrow transplant recipients.
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PMID:Long-term outcome of hepatitis C infection after bone marrow transplantation. 1457 71

A 67 year-old female with a 10-year history of cirrhosis due to hepatitis C virus who developed a gastric carcinoid tumor of the corpus is described. Carcinoid tumor was identified during her last routine gastroscopic evaluation for portal hypertension. In the case, serum parietal cell antibodies, hypergastrinemia and atrophic gastritis were also found. Chronic hepatitis C virus infection is known to induce clinical and laboratory signs of autoimmunity. But the question of whether hepatitis C virus plays a pathogenic role in the development of gastric carcinoid tumor is unknown. As far as we know, this is the first report describing gastric carcinoid tumor in hepatitis C virus induced chronic liver disease. We suggest that the possibility of the development of autoimmune atrophic gastritis and carcinoid tumors should be considered in patients with chronic hepatitis C that coexists with autoimmune diseases and has positive parietal cell antibodies.
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PMID:Type 1 gastric carcinoid tumor: another extrahepatic manifestation of hepatitis C virus infection? 1465 65

Chronic hepatitis C virus (HCV) is the most common bloodborne infection in the United States. An estimated 2.7 million Americans are infected, with the greatest prevalence of infection in African Americans at 3.2%. African Americans account for 22% of Americans with HCV. Recent studies have shown that African Americans are less likely to have cirrhosis than similarly infected non-Hispanic white patients and are more likely to have genotype 1 infection and to develop hepatocellular carcinoma. Several studies have shown that the response rates of African Americans to interferon and ribavirin are significantly lower than those for non-Hispanic whites. Despite the relatively low percentage of African-American patients in these early studies, similar preliminary results are being found in larger prospective studies with the newer treatment regimens of pegylated interferon and ribavirin. Differences in immunologic status, viral kinetics, and iron studies have also been found in HCV-infected African-American patients. Less is known about Mexican Americans and other minority groups because they are poorly represented in clinical trials. Efforts at increasing racial diversity in clinical trials are ongoing.
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PMID:Chronic hepatitis C in African Americans and other minority groups. 1472 Apr 56

Recently attempts have been made to standardize terminology in the field of hepatic encephalopathy. We are now facing a new problem. Chronic hepatitis C-induced cirrhosis occurs in an older population; this may change the presentation pattern of hepatic encephalopathy in future. Ammonia has once again become prominent as the leading toxin likely to play a role in the pathogenesis of this syndrome. How ammonia interacts with other proposed mechanisms should be an area of active research. The treatment arena has seen some advances. Unfortunately, the economics of having newer treatments approved in the USA is formidable. Rifaximine, L-ornithine-L-aspartate, sodium benzoate and possibly flumazenil appear to be significant advances. More elective shunt suppression for selected patients will be seen. Liver transplantation remains the only option for truly intractable hepatic encephalopathy.
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PMID:Newer aspects of hepatic encephalopathy. 1502 47

Chronic hepatitis C virus (HCV) is a worldwide health problem. Approximately 4 million people in the United States are chronically infected with HCV. The incidence of infection peaked between 2 and 3 decades ago, and we are now beginning to see an increase in the complications of cirrhosis from HCV. This trend is expected to continue for another 2 to 3 decades. Survival is poor once complications of cirrhosis, such as liver failure or hepatocellular carcinoma, ensue, and liver transplantation is often the only option. Complications of chronic HCV are the most common indication for liver transplantation, accounting for more than 40% of transplants performed in the United States and Europe. HCV recurs in all patients and rapid development of hepatic fibrosis is very common. Several strategies have been proposed to reduce the risk of graft loss from recurrent HCV infection after transplantation, as the progression of the resulting liver disease is rapid. Although antiviral treatment is successful in some patients, it is extremely difficult to administer and requires dose reductions in the majority of cases. Retransplantation in the current era of the Model for End-Stage Liver Disease (MELD) system for prioritizing listing for transplant is associated with very low survival rates at a high cost. Furthermore, the system raises difficult ethical issues of utilization of limited resources and fairness to other transplant candidates.
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PMID:Chronic hepatitis C and liver transplantation. 1502 6

Chronic hepatitis C virus (HCV) and hepatitis B virus (HBV) infection is accompanied by inflammation and fibrosis eventually leading to cirrhosis. The chemokine CXCL12 is involved in chronic inflammatory conditions. The role of the CXCL12/CXCR4 pathway in HCV- and HBV-associated liver inflammation and fibrosis was therefore studied. The levels and tissue localization of CXCL12 in liver and plasma of HCV and HBV patients were tested using immunohistochemistry and ELISA. The expression and function of CXCR4 on liver-infiltrating lymphocytes (LIL) were tested by FACS and transwell migration assays. We found that CXCL12 is expressed by bile duct epithelial cells in normal liver tissue. Bile duct proliferation and liver fibrosis in chronic HCV and HBV infection result in the anatomical re-distribution of CXCL12 in the liver. Moreover, CXCL12 is up-regulated in the endothelium of neo-blood-vessels formed in active inflammatory foci and is significantly elevated, compared with controls, in the plasma of patients with advanced liver fibrosis. Complementing these observations were others indicating that over 50% of LIL express CXCR4 and, in response to CXCL12, migrated and adhered to fibronectin. These observations suggest an important role for the CXCL12/CXCR4 pathway in recruitment and retention of immune cells in the liver during chronic HCV and HBV infection.
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PMID:Involvement of the CXCL12/CXCR4 pathway in the advanced liver disease that is associated with hepatitis C virus or hepatitis B virus. 1504 28

Chronic hepatitis C leads to cirrhosis in 20 to 30%. Hepatocellular carcinoma can develop in 1 to 5%. This natural course is modified by several factors including age, sex and alcohol. This last one is an important risk factor for fibrosis, cirrhosis and hepatocellular carcinoma. Data about high alcohol consumption show an increased risk whereas the risk associated with light to moderate consumption of alcohol remains unclear. Treatment of chronic hepatitis C with pegylated interferon and ribavirine allows a viral response in 50 to 80%. Factors decreasing this response rate are high viremia, genotype 1 and 4, sex and alcohol. Again, at which limit alcohol consumption is becoming deleterious is not well known. According to epidemiological studies alcohol consumption higher than 40 to 50 g/day should be avoided and a 6 months abstinence period before antiviral therapy should be recommended. Is this enough? More studies are needed to answer these questions.
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PMID:[Hepatitis C and alcohol, which is the limit?]. 1508 56


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