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)

In the introduction, a brief overview is given on the clinical aspects and classification of non-A, non-B hepatitis and on the discovery of hepatitis C virus. Using a recombinant hepatitis C virus antigen in an ELISA test system, for the demonstration of the antibody to hepatitis C virus, a new possibility became available in the serological diagnosis of non-A, non-B hepatitis. According to the previous hepatitis C virus antibody studies performed in Western Europe and in Hungary, the results of the present multicentre study also show that hepatitis C virus infection is frequent mainly in the post-transfusion chronic non-A, non-B hepatitis (87%) and in haemophiliacs (86%). In addition, antibody to hepatitis C virus occurs in open-heart surgery (27%) as well as in haemodialysed patients (20%), furthermore, it can be found in other forms of liver disease of various aetiology, e. g. in chronic HBsAg-positive hepatitis (33%), autoimmune liver diseases (20%) and chronic alcoholic hepatitis (14%) as well. The parenterally transmitted non-A, non-B hepatitis, practically the hepatitis C virus-related liver disease often leads to cirrhosis or even carcinoma. As its treatment is unsolved question yet, the prevention seems to be of great importance, the preventive measures of post-transfusion hepatitis C virus infection is listed.
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PMID:[Advances in the research on non-A, non-B hepatitis: hepatitis C virus. Multicenter anti-HCV studies]. 217 88

Beta 2-Microglobulin expression on hepatocyte membrane was studied in 117 liver biopsies from patients with acute and chronic hepatitis B and in 11 subjects with normal liver function, using immunohistochemical PAP method. In normal liver beta 2-microglobulin could not be detected on hepatocyte membrane, compared with that in subjects with normal liver, in asymptomatic HBsAg carrier and in patients with chronic persistent hepatitis, there is significant enhancement of beta 2-microglobulin expression in patients with acute mild hepatitis and chronic mild active hepatitis. Beta 2-Microglobulin expression in patients with chronic active hepatitis with moderate to severe activity and cirrhosis has a significant enhancement, when compared with acute mild hepatitis and chronic mild active hepatitis. Moreover, location of beta 2-microglobulin expression on hepatocyte membrane was associated with lesion of hepatocytes. Enhanced expression of beta 2-microglobulin on hepatocyte membrane in acute and chronic hepatitis B probably reflects enhanced display of HLA-ABC antigens and may influence the course of hepatitis B virus infection by increasing susceptibility of T cell-mediated hepatocytelysis.
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PMID:[A study of the relation of the expression of beta-microglobulin and hepatocytic lesions in hepatitis B]. 220 29

Cases of acute exacerbation in chronic liver disease ("acute-on-chronic") in Japan were surveyed by questionnaire method since 1986 and 220 cases were collected. 73 pathological specimens of 102 cases which were autopsied were subjected to morphological analysis. The cases were divided according to causes of acute exacerbations: namely super-imposed viral infection or drugs (Group I), unknown causes or post immunosuppressant therapy (Group II), alcohol abuse (Group III), operation, digestive tract hemorrhage or post TAE etc, (Group IV). Area of hepatic necrosis was large and regeneration of hepatocytes were significantly strong in Group I and II compared with cases of Group IV. Regeneration was also inhibited in liver of habitual alcohol drinker. Significant difference was shown in cases of Group IV. Pathologically liver of 10 cases of Group III divided to florried cirrhosis (3 cases), alcoholic liver cirrhosis (4 cases) and alcoholic hepatitis combined with post hepatitic liver cirrhosis (3 cases, all HBV carriers).
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PMID:[Histopathological analysis of 73 autopsy cases of "acute-on-chronic" in Japan--influence of alcohol abuse on exacerbation of chronic liver disease]. 221 72

To clarify the significance of the X gene of hepatitis B virus, we have tested for anti-HBx in the serum and HBxAg in the liver at different stages of the natural history of hepatitis B virus infection. Sera were screened by enzyme-linked immunosorbent assay and positive results confirmed by immunoblot. Purified recombinant MS2 Pol-HBx fusion protein was used as target for both assays. Among serial sera of patients with nonfulminant acute hepatitis, 24 of 64 patients (37.5%) were positive for anti-HBx. In fulminant cases, 15 of 36 patients (42%) had anti-HBx. In chronic hepatitis patients with high rates of hepatitis B virus replication, we found a significantly (p less than 0.01) higher prevalence of anti-HBx, 14 of 25 patients (56%), than in those with low replication, 14 of 66 patients (21%), or among asymptomatic HBsAg carrier blood donors (20 of 126 = 16%) without detectable hepatitis B virus replication (p less than 0.0001). The highest prevalence of anti-HBx was found in HBsAg carriers with cirrhosis (41 of 54 patients = 76%) and/or with hepatocellular carcinoma (18 of 33 patients = 54%). The findings suggest that anti-HBx appears as a common and early marker of hepatitis B virus infection, transient in self-limited hepatitis but persisting with progression to chronicity. In chronic hepatitis, the prevalence of anti-HBx correlated with the intensity and duration of hepatitis B virus replication but neither with the severity of the liver disease nor with malignant transformation per se.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early and frequent detection of HBxAg and/or anti-HBx in hepatitis B virus infection. 225 44

Common features of chronic alcoholic liver disease are progressive hypoalbuminemia and a spectrum of liver fibrosis. The molecular mechanisms that account for these effects are still the subject of controversy. Therefore, in the present study we evaluated albumin and collagen gene expression in livers of alcohol abusers and patients with virus-induced liver disease. Albumin and pro alpha 1(I) collagen messenger RNA levels were determined in 30 patients who underwent diagnostic liver biopsy. Of 14 alcoholics, 7 had alcoholic hepatitis alone and the other 7 had cirrhosis plus alcoholic hepatitis. Of 16 nonalcoholic patients with chronic viral infection, 6 had chronic active hepatitis and 10 had cirrhosis plus chronic active hepatitis. Total RNA was extracted from a portion of each biopsy specimen, hybridized with a human albumin or collagen complementary DNA clone, and compared with 2 normal surgical specimens, which served as controls. The Northern hybridization studies showed that (a) despite the presence of inflammation and fibrosis, the albumin messenger RNA levels of alcoholics were similar to those of the controls; (b) these alcoholics had significantly higher levels of albumin messenger RNA than did patients with similar histological levels of disease due to viral infection; and (c) all the categories of patients had markedly increased procollagen messenger RNA levels compared with controls. Given these results it is tempting to speculate that alcohol may actually increase albumin messenger RNA content in humans as it does in animals. Furthermore, the increased procollagen messenger RNA levels in fibrotic livers suggest that an increase in collagen syntheses may be a significant factor in the pathogenesis of hepatic fibrosis.
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PMID:Albumin and collagen gene regulation in alcohol- and virus-induced human liver disease. 229 78

The aim of this study was to evaluate the long-term outcome of chronic hepatitis B in 27 children who had increased alanine aminotransferase activity and antibody to hepatitis B e antigen in serum from the time of their first clinical observation. Initial histologic changes were consistent with chronic active hepatitis in 13 cases (three with associated cirrhosis) and with persistent or lobular hepatitis in the remaining cases. On the basis of virologic testing, three groups of patients were identified: (1) two children had hepatitis delta antigen in the liver and anti-delta antibody in serum, and both had severe hepatitis; (2) 10 children had hepatitis B virus DNA in serum, and 60% of them had active hepatitis; (3) 15 patients had no hepatitis B virus DNA, and 33% of them had active hepatitis. During a follow-up period of 12 months to 12 years (mean +/- SD: 6.1 +/- 2.4 years), the disease remained active in both children with anti-delta antibody, but they had no major complaints. In all eight patients who could be followed in group 2, test results became negative for hepatitis B virus DNA and alanine aminotransferase activity normalized within 4 years; biochemical remission was delayed in three patients with higher hepatitis B virus DNA levels on entry, and one of these patients had a severe exacerbation of disease activity before remission. In group 3, a total of 10 patients (71%) achieved biochemical remission within 1 year, and two within 26 months; only two patients, who were transfused at birth, had long-lasting liver damage. These results indicate a trend to early remission of liver disease in children with chronic hepatitis B with antibody to hepatitis B e antigen without delta virus infection. Antiviral therapy aimed at accelerating the termination of hepatitis B virus replication may be indicated only in those with higher levels of hepatitis B virus DNA.
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PMID:Long-term evolution of chronic hepatitis B in children with antibody to hepatitis B e antigen. 231 1

Orthotopic liver transplantation was performed in a 29-year-old woman because of increasing decompensation of HBs-antigen positive post-hepatitic cirrhosis. Postoperatively she developed a mild rejection reaction and diabetes mellitus. Thirteen months after the transplant she conceived twins. This high risk pregnancy was complicated by a febrile viral infection with purulent tracheobronchitis at 9 weeks and a threatened abortion at 11 weeks. At 33 weeks there was a sudden drop in haemoglobin due to a minor uterine rupture which necessitated cesarean section. The female infants--of development in keeping with the dates--showed no clinical or ultrasound evidence of any malformations. Apart from initial difficulties--asphyxia (second twin), fluctuating glucose and calcium levels, an episode of neonatal jaundice which required phototherapy, reluctance to suck and hypotonia--the further development of both twins proceeded normally. The maternal diabetes disappeared after delivery, HBs-antigen remained negative and the HBs-antibody titre rose. The patient has remained in good condition, both mentally and physically.
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PMID:[Twin pregnancy after liver transplantation]. 235 62

It is probable that two or more different viruses account for non-A, non-B hepatitis throughout the world, with a third agent causing epidemic hepatitis in India and neighboring countries. NANB virus(es) is the major cause of transfusion-associated hepatitis, and is responsible for roughly 20% of sporadic hepatitis cases. NANB postransfusion hepatitis progresses to chronic hepatitis in half or more of cases. This form of chronic hepatitis, while usually minimally symptomatic, causes progressive liver destruction and eventual cirrhosis in a significant proportion of cases. To date, the NANB virus(es) has not been specifically identified, either serologically or by electron microscopy. When developed, serologic assays will find their most immediate application in the identification of NANB virus carriers among blood donors, thereby being applied to the prevention of post-transfusion hepatitis. No specific therapy is available for NANB virus infection. Gamma globulin is of uncertain prophylactic efficacy.
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PMID:The current status of non-A, non-B viral hepatitis. 240 71

The so-called novel inclusion body (NIB) is an intrahepatocytic structure which is frequently observed in human cirrhotic liver. It resembles very much to, but definitely differs from Hepatitis B surface antigen (HBsAg) morphologically. The age distribution of liver cirrhosis cases positive for NIB is similar to that positive for HBsAg, except for an existence of a time lag in mean age. One of the best staining methods to demonstrate NIB, for example, is to exhibit it as a reddish body stained by Luna, with a contrast of HBsAg counterstained purple in color by aldehyde fuchsin after thiosulfation. Electron microscopy of the liver obtained from a patient, negative for both HBsAg and Hepatitis B e antigen (HBeAg) but positive for Hepatitis B core antibody (HBcAb) and Hepatitis B surface antigen antibody (HBsAb) clinically, revealed some unfamiliar, tubular and cisternal arrays showing a network pattern and ring-shaped structure at the site exactly corresponding to NIB localization. These are considered to have been induced from the endoplasmic reticulum by an unknown agent, for which non A non B hepatitis virus (NANBV) is rationally postulated as one of the possibilities. A close relation between NIB and NANBV is highly suspected because of much similarities in histology, histochemistry, age distribution, and electron microscopy. The true nature of NANBV should be rescrutinized, especially in relation with Hepatitis B virus infection, since NIB is quite often observed also in cirrhotic liver positive for HBsAg.
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PMID:A study on so-called novel inclusion body in human hepatocyte. 241 47

We have used a death-record search to define the frequency of lethal outcomes of hepatitis B virus infection among a population of more than 15,000 overtly healthy blood donors found positive in routine HBsAg testing. We have compared the study population with a control group of some 18,000 donors selected on the basis of a negative test result. The index and control groups were observed for periods reflecting a total of 55 and 59 thousand person-years, respectively. Twenty percent of the 134 deaths identified among HBsAg positive donors were in some way liver related, including seven deaths due to hepatitis, seven to cirrhosis and six to hepatoma. In contrast, only one of the 95 deaths in the control population was liver related, and was due to fatty degeneration of the liver. The majority (four) of the hepatoma deaths occurred among blacks, three of whom were less than 35 at the time of death. In contrast, deaths from cirrhosis were all among whites. We conclude that there is significant mortality associated with the HBsAg positive state, even though the affected individuals may be asymptomatic and well enough to give blood at some stage. We estimate the standardised mortality ratio for hepatoma among HBsAg-positive persons in the United States is at least 27, confirming the association observed in other populations. The risk for hepatoma among young, HBsAg positive black males appears to approach that reported for HBsAg positive males in Taiwan. Data on the feasibility of AFP testing for early detection of hepatoma are included and discussed.
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PMID:Increased risk for lethal forms of liver disease among HBsAg-positive blood donors in the United States. 244 15


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