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 may be caused by hepatitis A virus, hepatitis B virus, hepatitis C virus (classic non-A non-B viral hepatitis), hepatitis D virus (delta agent), and hepatitis E virus (epidemic non-A non-B viral hepatitis). Cytomegalovirus, Epstein-Barr virus, and herpes simplex virus may also occasionally cause hepatitis. Some forms of hepatitis carry the risks of chronic infection, cirrhosis, or hepatocellular carcinoma. Treatment options for viral hepatitis are limited and, in many cases, still under investigation. Prophylaxis is available for many forms of hepatitis and should be offered to those at risk.
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PMID:Viral hepatitis. The new ABC's. 212 Jun 86

To clarify the correlation of hepatitis D virus (HDV) infection and viral replication in liver diseases, the authors detected HDV RNA and serological HDV markers in serum from 285 patients with hepatitis B and 45 asymptomatic carriers of HBsAg. With dot blot hybridization, serum HDV RNA was detected in 8.8% (29/330) of the patients with HBV infection. The positive rate of HDV RNA in fulminant hepatitis was higher than that in benign hepatitis (15/74 vs 3/47, P less than 0.05). 10 of the 139 patients with chronic active hepatitis and 1 of the 6 cases with cirrhosis were positive for HDV RNA. However, all of the 19 cases with chronic persistent hepatitis and 45 asymptomatic carriers of HBsAg were negative fo, HDV RNA. Serological HDV markers, HDAgr anti-HD and IgM-anti-HD, were determined with ELISA. HDV RNA was detected in all of the serum samples with positive HDAg and/or IgM-anti-HD, in 15 of the 26 cases with positive-anti-HD and in 8 cases without HDV markers. Our results showed that 40 of the 330 patients with HBsAg were infected by HDV. This investigation suggests that HDV is one of the etiological factors for fulminant hepatitis and chronic active hepatitis.
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PMID:[Hepatitis D virus RNA in serum from patients with hepatitis B]. 226 30

To establish the impact of cyclosporine on the development of chronic hepatitis in hepatitis B surface antigen (HBsAg)-positive renal allograft recipients, the incidence and outcome of chronic hepatitis in 20 cyclosporine-treated patients (CsA group) were compared with 13 azathioprine-treated patients (AZA group). All 33 patients had a functioning graft for 2 years or longer. Twenty-nine of the 33 patients were HBsAg-positive prior to the initiation of hemodialysis. The difference in the incidence of chronic hepatitis between these 2 groups was not statistically significant (78.6% in the AZA group vs. 52.4% in the CsA group, P = 0.12). In the CsA group, 3 patients (15%) developed liver cirrhosis, and there was a 5% mortality. The AZA group had a 7.7% mortality, and 4 patients (30.8%) developed liver cirrhosis. Serial serum samples obtained from these 33 HBsAg-positive renal allograft recipients were analyzed for antibody to hepatitis D virus (anti-HD). Anti-HD was found in 3 patients. Two of them developed anti-HD seroconversion after renal transplantation during a mean follow-up of 4 years. All 3 patients developed chronic hepatitis and 2 of them have subsequently developed liver cirrhosis. There was a mortality of 6.1% in 33 HBsAg-positive patients compared with a 5.3% mortality in 57 HBsAg-negative renal allograft recipients. The difference was not statistically significant. We conclude from this study that (1) CsA-treated HBsAg-positive renal allograft recipients have a tendency to develop chronic hepatitis like AZA-treated patients; (2) HBsAg-positive patients have an increased risk of HDV superinfection after renal transplantation, and this may result in rapid progression to liver cirrhosis; (3) HBsAg-positive patients who acquire HBsAg prior to renal transplantation have a low overall mortality, including death due to liver disease, for a mean follow-up of 4 years.
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PMID:Hepatitis B liver disease in cyclosporine-treated renal allograft recipients. 231 16

We have investigated the usefulness of serum hepatitis delta virus (HDV) RNA detection using a slot hybridization analysis of serum samples from ten patients with acute hepatitis and delta markers (group I), from 28 patients with chronic delta hepatitis (group II) and from seven liver graft recipients with hepatitis B virus (HBV) and HDV related cirrhosis or fulminant hepatitis (group III). The slot-blots were hybridized with both HDV-complementary DNA and single-stranded RNA probes. With the single-stranded RNA probe, HDV RNA was detected in the first serum sample available in 9/10 of the patients with acute hepatitis (group I). In addition, HDV RNA was detected in 8/9 and 7/8 of the samples obtained within and after 1 month of the onset of hepatitis. Five of the ten patients scored positive for HDV RNA and negative for hepatitis delta antigen (HDAg) while one was negative for HDV RNA and positive for HDAg. The same RNA probe enabled the detection of serum HDV RNA in 21/28 chronic hepatitis patients (liver HDAg and/or IgM anti-HD positive) (group II). Among the liver graft recipients (group III), 7/7 had a recurrent delta infection. Serum HDAg, liver HDAg and anti-HD IgM were identified in 3/7, 6/7 and 5/7 of the patients, respectively. HDV RNA was detected in the seven patients with either persistent (4/7) or transient (3/7) positivity. In addition, HBsAg and HBV RNA were persistently shown in 4/7 patients with continuous HDV replication. In the remaining three patients, HDV RNA was detectable despite the absence of HBsAg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum hepatitis delta virus RNA in patients with delta hepatitis and in liver graft recipients. 239 61

A series of 120 patients with chronic delta hepatitis virus (HDV) were investigated using a newly developed assay for the detection of serum delta RNA and this marker was correlated with other markers of HDV infection. The assay was shown to be both specific and sensitive and provides a direct non-invasive measurement of HDV infectivity. Serum HDV RNA was detected in 51.2% of all patients and in about 64% of those who were liver HDV antigen positive. Its presence was particularly associated with the early stages of the disease where it was found in 83% of cases with chronic active hepatitis (CAH) and progressively less common in CAH associated with cirrhosis and in inactive cirrhosis. The presence of both HBeAg (and HBV DNA) and high levels of HDV RNA in the sera of 5 of the patients analysed, clearly demonstrates simultaneous replication of both HBV and HDV. The serum HDV RNA 'slot blot' assay described in this study should prove invaluable in elucidating further the natural history of delta hepatitis and in monitoring antiviral therapy.
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PMID:Detection of hepatitis delta virus RNA in chronic liver disease. 276 95

The prevalence of hepatitis D virus infection was studied in 954 sera samples collected in Spain between 1974 and 1986 from 838 patients in a variety of epidemiological categories with HBsAg-positive liver disease, and from 116 haemophiliacs and drug addicts with hepatitis B antibodies. Hepatitis D markers were detected in 64% of drug addicts and 33% of HBsAg-positive haemophiliacs but were absent in asymptomatic chronic carriers, homosexual males, mentally retarded patients and haemodialysis patients. Hepatitis D markers were found in 6% of patients with acute hepatitis, in 5.6% of those with chronic hepatitis B from general population, and in 65% of those with acute hepatitis B and 67% of those with chronic hepatitis B among drug addicts. During the 12-year study, no changes were observed in the frequency of Delta infection. The prevalence was less than 10% in chronic HBsAg-positive hepatitis. These findings indicate that in Spain Delta infection is restricted mainly to HBsAg-positive drug addicts and multitransfused haemophiliacs, while in the general population only 6.7% of those with chronic hepatitis B show D superinfection. Anti-HD sera detection is correlated with more severe forms of chronic hepatitis such as chronic active hepatitis and cirrhosis.
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PMID:Epidemiology of delta infection in Spain. 320 67

The frequency of delta virus infection, immunoserological parameters and degree of liver inflammation were studied in 190 HBsAg carriers in the Berlin area from 1976 to 1986. Delta infection was detected in one of 50 HBsAg carriers (2%) in the period from 1976 to 1980. In contrast 19 of 140 HBsAg carriers (14%) with delta infection were found in the period from 1981 to 1986. This group included 12 Germans, 5 Turks and 2 Italians. Only 6 of these subjects belonged to a so-called risk group: 3 drug addicts, 2 homosexuals and 1 hemophiliac. Eighteen of the 20 patients with HDV infection showed progressive liver disease in the follow-up period. Nine cases developed complete liver cirrhosis over five years. Variable transaminase levels and elevation of immunoglobulin G were recorded. Humoral autoimmune phenomena were rarely observed. The increasing frequency of HDV infection in the Berlin area is presumably related to tourism, national origin and membership in specific risk groups. The data in our study underline the importance of effective prophylaxis by active immunization with HBsAg vaccines.
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PMID:[Frequency and clinical relevance of delta virus infection in HBsAg carriers in the Berlin area]. 326 46

Serum samples from 56 patients with biopsy-proven chronic B viral hepatitis without superimposed delta hepatitis were analyzed for the various markers of viral replication, including serum hepatitis B e Ag (HBeAg), hepatitis B virus deoxyribonucleic acid (HBV-DNA), and hepatitis B core antigen (HBcAg) in the liver tissues. Twenty-seven patients had persistent viral hepatitis (PH) and 29 patients had chronic active hepatitis (CAH) with or without cirrhosis. HBV-DNA was identified in the sera of 81% of patients with PH and 60% of patients with CAH. Significantly higher levels of HBV-DNA were found in patients with PH than in those with CAH. Both HBeAg in serum and HBcAg in liver correlated positively with serum HBV-DNA. Nine patients had serum HBV-DNA in the absence of HBeAg (four had anti-HBe), and seven of these nine patients had stainable HBcAg in the liver (two did not have staining). None of these patients had hepatic HBcAg in the absence of serum HBV-DNA. When these patients were stratified according to their epidemiologic background, serum HBV-DNA was present in a significantly higher number of male homosexuals than in any other groups. This was unrelated to their status of human immunodeficiency viral serology.
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PMID:Markers of viral replication in patients with chronic hepatitis B virus infection. 334 Dec 83

Ninety-four patients, who were admitted with symptoms of liver disease and found to be positive for hepatitis B surface antigen and antibody to hepatitis B e antigen (anti-HBe), were examined for hepatitis B virus (HBV) DNA in serum and immunoglobulin antibody to hepatitis B core antigen and liver biopsies were stained for hepatic hepatitis B core antigen. Of 94 patients, 34 (36%) had evidence of HBV replication and 35 (37%) evidence of hepatitis D virus (HDV) superinfection. Most of the latter two groups of patients (greater than 70%) had evidence of chronic active hepatitis or active cirrhosis in their liver biopsies. The majority of these patients (greater than 80%) also had high levels of serum alanine aminotransferase (greater than 200 U/L) during the acute stage of their illness, and suffered from prolonged hepatic inflammation (greater than 1 year). Many of the patients (59%) also experienced frequent (1-6 episodes) relapsing exacerbations during a two-year follow-up period. Thus, persistent replication or reactivation of HBV and HDV superinfection were the two major causes of clinical exacerbations in anti-HBe-positive chronic HBV carriers in Taiwan, and also played an important role in the progression of their liver diseases and unfavorable outcomes.
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PMID:Symptomatic anti-HBe positive chronic hepatitis B in Taiwan with special reference to persistent HBV replication and HDV superinfection. 339 22

Chronic evolution after acute hepatitis B virus infection. During a 13 months period 1977-1978 a total of 129 cases of acute viral hepatitis type B occurred among patients who were admitted with hepatitis to Roslagstull, Hospital, Stockholm, Sweden. Less than 1% progressed to chronicity. Prevalence of Delta superinfection was studied among 60 patients with chronic hepatitis B. Nineteen (32%) were anti-delta positive. The majority of the positive patients were either non-European immigrants or addicts, both 9/19 (47%). Infections with the delta agent was found to have occurred in Stockholm already in the early 1970s. Rate of HBeAg clearance during chronic HBV was studied among 36 HBeAg positive patients. Seroconversion to anti-HBe was noted in 17 patients (47%), whereas HBeAg persisted in 19 during a mean follow-up period of 53 months. The spontaneous annual HBeAg seroconversion rate was 11%. HBeAg clearance occurred as frequently among homosexual men as among patients in other categories. However, 12/14 homosexual men were HBeAg positive after 2 years follow-up, compared with 1/13 drug addicts. Thus, homosexual men seemed to require a longer time for HBeAg seroconversion than i.v. drug addicts. HBV-DNA in serum, a strong indicator of viral particles and infectivity was analysed among patients with HBeAg seroconversion, initial HBeAg negativity and/or delta superinfection. HBV-DNA was found in 75-80% of our HBeAg positive patients. A correlation between chronic liver disease and presence of HBV-DNA in serum was also found. Thus, HBV DNA was found in 63% of patients with CAH or CAH/CI as compared with only 39% of patients with CPH. Delta infected patients had HBV-DNA more often than those without hepatitis D infection. Seven delta infected, anti-HBe positive, patients were still HBV-DNA positive five to eight years later. Therefore delta infected anti-HBe positive patients can be infectious for prolonged periods. Histological outcome. 63% (12/19) anti-delta positive patients were classified as CAH with or without cirrhosis as against 39% (16/41) of the anti-delta negative patients. Eleven of 15 homosexual men (73%) had histological findings classified as CAH or CAH/CI. None of them were superinfected with HDV. Thus homosexual men developed severe hepatic lesions without being delta infected. In contrast 78% (7/9) i.v. drug addicts with CAH were delta infected. A numerical scoring system was applied and compared with conventional morphological classification of liver histology to assess the histological outcome of 42 patients with repetitive liver biopsies.
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PMID:Chronic hepatitis B. Impact of hepatitis D virus superinfection and the hepatitis B e-system on histological outcome, and correlation of the hepatitis B e-system to HBV-DNA in serum. 346 8


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