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)

Sera from patients with hepatoma, metastatic liver disease, cirrhosis of the liver, and benign diseases of the digestive tract have been tested for a virus-inhibiting factor. Serum samples exerting complete inhibition of virus CPE in a dilution of at least 1:10 per 0.2 ml are considered positive, and those exerting 50% inhibition of CPE are regarded as weakly positive. An apparently positive antiviral activity was noted in the sera of patients with hepatoma (53.3%) and metastatic liver disease (46.6%). Patients with cirrhosis of the liver showed positivity in one of ten sera; no positive antiviral activity could be found in the sera of patients with benign diseases of the digestive tract. The percentage of weakly positive response was 33.3% and 13.3% for hepatoma and metastatic liver disease, respectively, and 10.0% for the benign diseases and 20.0% for the cirrhotic sera. The antiviral activity was more prominent in the embryonic foreskin fibroblasts and to a lesser degree in the bovine epithelial cells NBL-1.
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PMID:Virus-inhibiting factor in primary and metastatic carcinoma of the liver. 301 59

The attempt to divide the large group of chronic HBsAg carriers into "healthy" vs. those with chronic hepatitis of various intensities is sometimes difficult. The major problems are overlap in clinical manifestations, hepatic test results and histologic as well as virologic features. Nevertheless, this separation is not only conceptually important, but may also be useful in patient management, particularly because of the risk of transition to cirrhosis and HCC. Although at least 75% of patients with HCC associated with HBV have cirrhosis, the time point at which the cirrhosis developed is not established, particularly since the vast majority of chronic HBsAg carriers fall into the "healthy" category. Important unanswered questions are, therefore: how often do "healthy" carriers develop cirrhosis and/or HCC, including the time relations between the two? Does the transformation to HCC result from one or several identifiable acute events in the "healthy" carrier (or in mild CPH) or is it a gradual process of progressing chronic hepatitis B in which intercurrent exacerbations may still play a role? Do the quantitative observations as to the relation between persistent HBV infections and HCC in the East apply to Western countries? Our hypothesis concerning pathogenesis is based on pathologic, molecular, clinical and epidemiologic observations and concepts, and is supported by studies of hepadna virus-infected animals. This thesis proposes that integration of HBV DNA into host chromosomes in acute or chronic hepatitis or during the "healthy" carrier state corresponds to an initiation event similar to that described in chemical carcinogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relation of the hepatitis B virus carrier state to hepatocellular carcinoma. 303 25

A study was made of the indices of lipid peroxidation (LPO)--conjugated dienes (CD) and diene ketones (D), cyclic nucleotides (CN)--cAMP and cGMP, prostaglandins (PG) E and F2 alpha in biopsy tissue of the liver in 55 patients with chronic hepatitis (CH) and liver cirrhosis (LC). LPO was determined by spectrophotometry, CH and LC--by a radioimmunoassay. In patients with CPH and CAH the indices of LPO and cGMP were normal, cAMP, PG and PGE/PGF2 alpha were raised. In a severe fast progressive liver lesion disorder of coordination activity of the cell membranous systems was characterized by a high LPO activity, a decrease in cAMP and relative deficit of liver PG.
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PMID:[Lipid peroxidation and the mechanisms of hepatocyte damage and protection in chronic hepatitis and cirrhosis]. 336 64

One hundred and twenty HBsAg positive patients with chronic liver disease, 94 with CAH and 26 with CPH, were studied in order to characterize chronic HBsAg positive hepatitis virologically. All patients came from a geographical area (Campania, Italy) with a high prevalence of HBV and HDV infection. Each patient was tested for the presence of HBsAg, HBeAg, anti-HBe and anti-delta in serum (by RIA techniques), and of HDV (by direct immunofluorescence) and HBcAg (by indirect immunofluorescence and PAP-immunoperoxidase) in liver biopsy specimens. Anti-delta serum positivity was remarkably more frequent in patients with CAH (40%) than in those with CPH (19%). Delta-Ag was found in 94.7% of the anti-delta positive patients with CAH, but in none of the five anti-delta positive patients with CPH. In contrast, the frequency of HBcAg tissue positivity was similar in CAH and CPH. Positivity for HBcAg was less frequent in CAH with cirrhosis than in CAH without cirrhosis, while there was no difference in the prevalence of delta-Ag.
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PMID:Prevalence of HBcAg and delta-Ag in liver tissue of patients with HBsAg positive chronic hepatitis. 341 90

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

The interrelationship between hepatitis B virus (HBV) infection, hepatic injury and clinical activity in chronic HBV infection is incompletely understood. We have scored histologic activity, the expression of hepatitis B core (HBcAg) and hepatitis B surface antigen (HBsAg) and assessed HBV replication to correlate HBV antigen expression with histologic disease. Forty-seven formalin-fixed, percutaneous liver biopsies from HBeAg carriers were studied. Twenty-nine were Black, 16 Caucasian and two Oriental. Fifty-nine percent had chronic active, 35% chronic persistent hepatitis and 14% cirrhosis. None were positive for antibodies to Human Immunodeficiency Virus (HIV). HBsAg and HBcAg in tissue were detected by immunochemical staining. Diffuse HBsAg staining was observed in 10/15 patients with CPH, but there was no correlation between histologic score and HBsAg expression. Intracytoplasmic HBcAg was observed in patients seroconverting to anti-HBe, but was also detected in patients with minimal hepatitis. An inverse correlation between histologic score and HBcAg expression was observed. HBcAg expression was more widespread in patients with CPH (mean 37%) than in CAH (mean 18%). A positive correlation was observed between serum aminotransferase concentrations and histologic score. Although no consistent pattern can be discerned, HBcAg expression and hepatic injury are frequently dissociated in patients with chronic HBV infection; complex host responses may determine the variable degree of disease activity and hepatic injury.
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PMID:Hepatitis B core and surface antigen expression in HBeAg and HBV DNA positive chronic hepatitis B: correlation with clinical and histological parameters. 368 95

The authors have performed a longitudinal study of 118 children affected with B virus chronic hepatitis. Our first observation revealed 92 children with HBeAg positive (26 CPH, 66 CAH), 22 children with anti HBe positive (6CPH, 15 CAH, 1 cirrhosis), 4 children (CAH) with e/anti-e negative. A correlation between the severity of clinical forms and the behaviour of the e/anti-e system was not observed. Seroconversion was observed during the follow up period in 37 of 92 subjects in an average time of 59.83 +/- 32 months, time rather prolonged in patients under immunosuppressive therapy. To compare the clinical progress and the evolution of CPH and CAH respectively, always with regard to the e/anti-e system, statistically significant differences did not result. Only anti HBe positive recovered subjects, inclusive of seroconverted patients and those anti HBe from the first observation, showed significant results to the statistical analysis. Still, seroconversion corresponds frequently to a stable improvement of hepatitis. On the contrary evolution into cirrhosis was observed in 5 patients that had anti HBe antibodies.
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PMID:Correlation between e/anti e system and evolution of B virus chronic hepatitis in pediatric patients. 371 77

Sera of 190 HBsAg positive chronic hepatitis B patients were followed up for IgM class antibodies to hepatitis B virus core antigen (IgM-anti-HBc) by a commercial ELISA (Abbott) as well as a 19S(IgM) RIA until these antibodies were no longer detectable. IgM anti-HBc was detected only up to two of five years after onset of acute disease. The periods of detectable IgM anti-HBc in 34 chronic persistent and 36 chronic active hepatitis B (CPH, CAH) patients did not differ significantly on the basis of chi 2-test. 56% of the CPH and 47% of the CAH patients showed markers of infectivity in the sera recently cleared of IgM anti-HBc. Sera of both the IgM anti-HBc positive CPH and CAH patients had on the average fivefold elevated aminotransferase (SGPT) activity. In sera recently cleared of IgM anti-HBc, mean SGPT activity was detected twofold the normal value in CPH and threefold in CAH patients. Inflammatory activity in the liver biopsies was seen highly increased both in the IgM anti-HBc positive CPH and CAH patients. Fibrosis was most progressed and cirrhosis observed mainly in the liver biopsies of the IgM anti-HBc cleared CAH patients. In 3 IgM anti-HBc cleared chronic hepatitis B patients (CPH n = 1, CAH n = 2) converted to anti-HBe, IgM anti-HBc was detectable anew after a HBV superinfection with other HBsAg subtypes.
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PMID:Follow-up studies on IgM anti-HBc during chronic hepatitis B. 376 52

S9 fraction pools of liver biopsy samples, collected from 129 patients in two consecutive studies, were comparatively assayed for their ability to activate aflatoxin B1 (AFB1) and a tryptophan pyrolysate product (Trp-P-2) in a miniaturized Salmonella mutagenicity test system. Metabolic activation was not affected to a significant extent by most of the monitored variability factors, such as sex, alcohol, cigarette smoking and liver histology (minimal changes, chronic persistent (CPH) or active (CAH) hepatitis, CAH steatosis, or cirrhosis). Conversely, a significant enhancement of activation was observed for AFB1 in cases of mild CAH and especially for Trp-P-2 in hepatitis B virus carriers, irrespective of their histologic diagnosis.
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PMID:Metabolic activation of hepatocarcinogens in chronic hepatitis B. 393 46

Chronic hepatitis may develop after acute B-hepatitis or acute non A-non B-hepatitis, as well as after toxic liver damage. Microscopic examination after biopsy allows to differentiate between chronic persistent (CPH) and chronic active (CAH) hepatitis. CPH needs not to be treated, but just to be controlled. Immunosuppressive therapy with steroids, eventually combined with azathioprine, is recommended nowadays in HBsAg-negative CAH. It has been shown, that survival rates are higher in patients, when this therapy is applied during the early stage of the disease, than in patients without therapy; the development of cirrhosis of the liver however does not seem to be influenced by this therapy. Immunosuppressive treatment of HBsAg-positive CAH is still controversial. Antiviral therapy (anti-HBs-antibodies, interferon, adenine-arabinoside) or therapy using immunostimulation (transfer-factor, levamisole, BCG) are also still in an experimental state.
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PMID:[Therapy of chronic hepatitis (author's transl)]. 616 69


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