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)

Hepatitis B virus (HBV) is one of the most important causes of chronic liver disease. HBV is a DNA virus with an external glycoprotein surface and an internal nucleocapsid which contains the viral genome. HBV infection is revealed by the appearance of specific markers. Some of these markers are well known and their presence in serum is important to understand the behaviour of the disease. Among them HBsAg, HBeAg, anti-HBs and anti-HBe are found in serum, so as anti-Core; the HBcAg may be found in hepatic tissue and marks infectivity and virus replication. In the few last years some new antigens and antibodies have been studied and their importance in diagnosis and follow-up of hepatitis has been recognized. HBxAg, Pre-S and DNA-Polymerase (Pol) seem to be specific and early signals of viral replication. More studies showed the trans-activating properties of HBxAg; actually the X protein seems to be involved in replicative cycle of HBV. Many Authors also demonstrated a relationship between the presence of X in serum and/or liver and the progression of disease to cirrhosis and hepatocellular carcinoma. The Pol antigen and its antibody seem to be very common markers of HBV infection in serum of patients with hepatitis. Moreover their presence is the only signal of viral infection in some patients which have no other marker of HBV. More studies are of course needed to exactly establish the significance of these new markers and their importance for diagnosis and prognosis of HBV infection.
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PMID:[Hepatitis B virus: new markers and their immunology]. 848 26

Polymerase chain reaction (PCR) has been used to study liver biopsy tissue in patients with known or suspected hepatitis C virus (HCV). Recent studies of cryptogenic cirrhosis using PCR have been based on study of sera, and HCV has not been shown. The failure to show HCV in patients so studied has left unanswered the question of whether or not patients with cryptogenic cirrhosis could still harbor the virus in the liver. The authors studied liver tissue, obtained at the time of orthopic liver transplantation from 10 patients clinically diagnosed as having end-stage liver disease without demonstrable origin, so-called cryptogenic cirrhosis, using reverse transcription (RT)-PCR to try to recover HCV-RNA. Formalin-fixed, paraffin-embedded tissue was used. For comparison, the authors also studied similarly obtained samples from 10 patients with typical hepatitis C-associated cirrhosis and 10 patients with end-stage liver disease resulting from autoimmune hepatitis. The authors recovered HCV-RNA from 9 of 10 livers from patients with cirrhosis resulting from HCV, and 3 of 10 livers from patients with autoimmune hepatitis. HCV-RNA was not recovered from any of the livers of the 10 patients designated as having cryptogenic cirrhosis.
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PMID:Hepatitis C virus is not recoverable from liver tissue in cryptogenic cirrhosis: failure to identify hepatitis C virus-RNA using reverse transcription-mediated polymerase chain reaction. 891 25

Recurrence of hepatitis C virus (HCV) after orthotopic liver transplant (OLT) may be mild or may lead to progressive liver disease requiring retransplantation (re-OLT). Results of re-OLT for hepatitis C are not well known. We analyzed outcomes in 14 patients retransplanted for recurrent hepatitis C. All had evidence of recurrent hepatitis on multiple biopsies. Polymerase chain reaction (PCR) was performed in blood or tissue samples from 12 patients when recurrence was suspected; all 12 were positive for HCV-RNA. Explants showed chronic hepatitis with bridging necrosis in 3 patients, hepatitis with transition to cirrhosis in 2, hepatitis and cirrhosis in 3, and cirrhosis alone in 2. In 2 patients, in whom immunosuppression had been withheld for 4 to 6 weeks, there was also evidence of chronic rejection. Four died of sepsis perioperatively (median, 32.5 days; range, 9-59); pre-OLT, 3 of 4 had renal failure, and 1 had fever with no obvious source of infection. Ten patients did well early after OLT and were discharged. One patient was readmitted 6 weeks after discharge and died of cytomegalovirus (CMV) infection 127 days after re-OLT. One patient with concomitant vanishing bile duct syndrome, probably due to chronic rejection, developed recurrent hepatitis and died of progressive liver failure 161 days after re-OLT. Eight patients are well at a median of 926 days (range, 315-1930) after re-OLT. Three have evidence of mild recurrent hepatitis on liver biopsy, one is overweight with severe steatosis on biopsy, and four have no evidence of recurrent hepatitis. Retransplantation for hepatitis C should be considered a viable option for patients who develop end-stage hepatic dysfunction secondary to recurrent disease and should be performed before development of infectious complications and renal insufficiency.
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PMID:Retransplantation for recurrent hepatitis C. 934 26

Hepatitis B virus (HBV) and hepatitis C virus (HCV) are not only hepatotropic but possibly hematotropic. Recent studies showed the presence of HBV in lymphoma cells of extrahepatic origin. In the current study, we examined the presence of HBV DNA and HCV RNA in the tumor tissues of nine patients with primary hepatic lymphoma (PHL). Immunohistochemical study using polyclonal anti-HCV antibody was possible in four cases. The age of the patients ranged from 45 to 78 years (median, 58 yr), with a male-to-female ratio of 2:1. A history of chronic hepatitis was found in three patients and of cirrhosis in one. Histologically, all of the cases were non-Hodgkin's lymphoma of B-cell phenotype, with a diffuse large cell type being the most common. Polymerase chain reaction using both the S and X region primers failed to detect HBV DNA in the lymphoma tissues. The HCV genome was detected by in situ hybridization in the tumor cells but not in the surrounding hepatocytes in the one case of cirrhosis, which probably resulted from a blood transfusion more than 20 years previous; immunohistochemical analysis revealed positive staining for anti-HCV antibody in the cytoplasm of lymphoma cells in this case. In two cases, positive signals were found only in the hepatocytes surrounding the lymphoma. This is the first report showing the presence of the HCV genome in the lymphoma cells of PHL. HCV could be involved in development of PHL directly or via exogenic antigenic stimulus from HCV-infected hepatocytes.
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PMID:Hepatitis C viral genome in a subset of primary hepatic lymphomas. 961 1

The possible causative role of novel TT virus in liver diseases has been intensively studied in regarding its hepatotrophy, ability to cause persistent infection and worldwide prevalence. The aim of this study was to estimate the prevalence as well as the clinical importance of TTV in a normal healthy population group in the Czech Republic and in a group of liver transplant recipients diagnosed with cryptogenic cirrhosis. Polymerase chain reaction (PCR) detected the DNA of TT virus in 68% (13/19) of samples isolated from peripheral blood leukocytes and in 21% (4/19) of plasma samples in the liver transplant group. The viral DNA was detected only in 11.8% (4/34) of leukocytes and in no plasma sample from the healthy population control group. All patients included in this study had good liver function and had no complications during the postoperative period. The prevalence of TTV DNA detection in healthy control group in Czech republic is similar to the rates reported in European and North American countries. Significant difference was proved between the prevalences of TTV in the groups of healthy controls and liver transplant recipients with cryptogenic cirrhosis. However, no association of TTV infection with possible postoperative complications could be found.
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PMID:[TT virus infection in liver transplant recipients with cryptogennic cirrhosis]. 1196 76

Nitric oxide (NO), a recently discovered free radical, is overproduced in liver cirrhosis. Hepatitis C virus (HCV) might increase NO levels via increased inducible NO synthase (iNOS). This work was carried out to study the effect of HCV-induced liver cirrhosis on NO levels among Egyptian patients. The study included 46 patients with liver cirrhosis, and 30 healthy individuals of matched age and sex. NO levels determined as the stable endproduct nitrate, showed a statistically significant increase among patients compared to the control group (P < 0.001). Furthermore, NO levels increased proportionally with the severity of liver cirrhosis as assessed by Child's classification (P < 0.05). Moreover, schistosomial infection enhanced NO levels in cirrhotic patients with HCV infection compared to non-bilharzial patients (P < 0.001). Polymerase chain reaction (PCR) and branched DNA assays were used for detection of HCV RNA positivity, and measurement of the virus load, respectively. Both showed a positive correlation with the NO levels (P < 0.001). At a nitrate cutoff value of 70 micromol/L, the sensitivity and specificity were 83.0% and 73.0%, respectively. Chi square analysis showed a significant correlation between ALT levels and both HCV RNA positivity by polymerase chain reaction (PCR) (P < 0.02), and virus load (P<0.05). Interestingly enough, there was a significant positive correlation between HCV RNA and schistosomal antibody titer as measured by hemaglutination inhibition assay (HAI) (P < 0.05). The data presented in this report indicated an association between NO levels and the development and progression of liver cirrhosis. Furthermore, the findings obtained from this study demonstrated that schistomiasis is an important risk factor involved in enhancement of NO levels and virus replication. The latter may aggravate liver cell injury and hence the development of cirrhosis.
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PMID:Evaluation of nitric oxide (NO) levels in hepatitis C virus (HCV) infection: relationship to schistosomiasis and liver cirrhosis among Egyptian patients. 1251 9

Hepatitis C virus (HCV) exposure is due mainly to infected human blood. Most people with acute HCV infection are unable to clear the virus leading to chronic infection that may progress to cirrhosis and hepatocellular carcinoma. HCV genotyping is very useful to optimize the therapy because it helps to identify the patients that need a more aggressive management (e.g., type 1). The aim of this study was to detect the HCV genotype of 915 patients of Central Italy and to analyze the possible change in the prevalence of genotypes not common in Italy, such as type 4. We used a line-probe assay (INNO-LiPA HCV II, Innogenetics) based on reverse hybridization of HCV genome fragments previously amplified by a Polymerase Chain Reaction assay, COBAS System Amplicor HCV monitor version 2.0 (Roche Diagnostics Systems Inc.). HCV type 1 was detected in 448 cases (49.0%), type 2 in 318 cases (34.8%), type 3 in 109 cases (11.9%), type 4 in 33 cases (3.6%) and co-infections in 7 cases (0.7%). In particular, 339 cases (37.0%) showed subtype 1b, 302 cases (33.0%) 2a/2c, 108 cases (11.8%) 3a and 74 cases (8.1%) subtype 1a. The prevalence of type 4 was 3.3% from September 1999 to July 2002 and 4.5% from August 2002 to April 2003. We confirmed that HCV type 1 is prevalent in Central Italy, in particular subtype 1b, followed by type 2a/2c. We also described that the prevalence of type 4 seems to have increased whereas co-infection is a rare event.
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PMID:Prevalence of hepatitis C virus (HCV) genotypes in central Italy. 1498 78

We investigated glutathione S-transferase (GST) P1 Ile (105) Val, T1, and M1 polymorphisms in 45 patients with documented cryptogenic cirrhosis and 56 healthy control subjects. Polymerase chain reaction-based procedures were performed in the studied populations to confirm the genotypes of GSTT1, M1, and P1. Ile/Val and Val/Val GSTP1 genotypes were more frequent in the patients with cirrhosis (n=39, 87%) than in the control subjects (n=10; 18%) (odds ratio [OR] 34.04; 95% confidence interval [CI] 10.70 to 108.31, P<0.001). Among these patients with cirrhosis, 16 were heterozygous and 23 were homozygous, whereas only one person in the control group was homozygous. The GSTM1 null genotype was also more prevalent in cirrhotic patients than in healthy control subjects (OR 6.83, 95% CI 2.53 to 18.42, P<0.001). The rate of GSTT1 deletion did not show a significant difference between the two groups (OR 2.35, 95% CI 0.76 to 7.28, P=0.111). To our knowledge, this is the first evidence that GSTP1 and GSTM1 polymorphisms may be related to the development of cirrhosis by unknown mechanisms. The significant association of cryptogenic cirrhosis with Val/Val GSTP1 genotype encoding a low detoxification activity protein implicates this polymorphism as a risk factor for the occurrence of the disease.
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PMID:GSTP1, GSTM1, and GSTT1 genetic polymorphisms in patients with cryptogenic liver cirrhosis. 1512 Mar 66

We investigated hepatitis B virus (HBV) DNA integration and expression of several proteins involved in the cell cycle and apoptosis, including cyclin A, retinoblastoma protein (pRB), Fas-associated death domain protein (FADD), tumor necrosis factor receptor-associated death domain protein (TRADD), and nuclear factor kappaB (NF-kappaB) in HBV-associated hepatocellular carcinoma (HCC) and liver cirrhosis (LC). Archival HCC and LC specimens were obtained from 35 patients each with HBV infection; 5 normal liver specimens used as controls were also obtained. Polymerase chain reaction and Southern blot hybridization were used to detect the integration of HBV DNA in the HCC and LC specimens. The protein levels were determined by Western blot assay. The difference in HBV DNA integration between HCC and LC and correlation between HBV-encoded X protein (Hbx) integration and protein expression were analyzed statistically. HBV DNA was detected in 33 (94%) of the HCC and LC specimens. HBx integration differed in the HCC [24 (69%)] and LC [14 (40%)] specimens (p=0.015). Sixty percent of the HCC specimens and 6% of the LC specimens had increased cyclin A expression. Also, 34, 37, 69, and 77% of the HCC specimens were positive for pRB, FADD, TRADD, and NF-kappaB expression, whereas 80, 60, 100, and 100% of the LC specimens were positive for pRB, FADD, TRADD, and NF-kappaB expression. Significant correlations between HBx integration and the level of expression of cyclin A (r=0.452; p=0.006), pRB (r=-0.419; p=0.012), and TRADD (r=0.470; p=0.004) were discovered. Therefore, integration of HBV DNA occurred frequently in HCC and LC cases with chronic HBV infection, whereas HBx integration occurred more often in HCC than in LC cases (p=0.015). HBx integration and altered expression of genes is a key to apoptosis and may play important roles in HBV-induced hepatocarcinogenesis.
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PMID:Integration of the hepatitis B virus X fragment in hepatocellular carcinoma and its effects on the expression of multiple molecules: a key to the cell cycle and apoptosis. 1564 32

The risk of hepatitis C virus (HCV) transmission to surgeons is related to the HCV prevalence in the surgical patient population. As HCV-related cirrhosis is the commonest indication for liver transplantation in Europe and North America, liver transplant surgeons are at particular risk. The prevalence of HCV infection in liver transplant surgeons is unknown. The aim of this study was to estimate the prevalence of HCV infection in liver transplant surgeons attending the 9th Congress of the International Liver Transplantation Society using unlinked anonymous testing for HCV. Surgeons attending the conference were invited to complete an anonymised questionnaire regarding their surgical and transplant practice and provide an unlinked anonymised blood spot sample by finger prick. Samples were screened for antibodies to HCV (enzyme-linked immunosorbent assay III, Ortho Diagnostics, Raritan, NJ). Polymerase chain reaction testing for HCV RNA was performed on reactive samples.A total of 117 liver transplant surgeons (79 European, 16 North American, 10 Asian, 9 South American, 3 Australasian) provided a blood spot sample. Two (1.7%) surgeons had antibodies to HCV, 1 (0.8%) had detectable HCV RNA (genotype 1a). Assuming that both infections were acquired during surgery, the estimated maximum rate of HCV transmission is 1 per 743 to 1,045 years of surgical (0.96 to 1.35 HCV transmissions per 1,000 years of general surgical practice) and 449 to 683 years of liver transplant practice (1.46 to 2.23 HCV transmissions per 1,000 years of liver transplantation practice). In conclusion, risk of HCV transmission to liver transplant surgeons appears to be low despite the particular risks associated with frequently operating on HCV infected patients.
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PMID:Anonymous pilot study of hepatitis C virus prevalence in liver transplant surgeons. 1679 57


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