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)

DNA polymerase alpha (DNA-P alpha) in the nuclei of hepatocytes was visualized by the immunoperoxidase method to study the number of liver cells which were at the stage of G1, S, and G2 stage in the cell cycle. Seven liver specimens from patients with acute hepatitis (AH), 17 with chronic persistent hepatitis (CPH), 32 with chronic active hepatitis (CAH), 6 with liver cirrhosis (LC), 4 with hepatocellular carcinoma (HCC) and 4 with hospital controls were studied. The number of DNA-P alpha-positive hepatocytes in 1000 hepatocytes were as follows: 19.1 +/- 18.0 in AH, 8.8 +/- 6.1 in CPH, 27.3 +/- 23.8 in CAH, 21.8 +/- 14.3 in LC, 545.3 +/- 184.0 in HCC and 1.1 +/- 1.1 in hospital controls. The number of DNA-P alpha-positive hepatocytes in HCC were significantly increased compared with other liver diseases. Likewise, those in CAH and LC were higher than those in CPH and hospital controls. The liver cell necrosis was thought to be one of the secondary stimulators for cell division of hepatocytes.
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PMID:[A cell kinetic study of liver cells in various liver diseases by the detection of DNA polymerase alpha]. 268 24

Twenty-one adult patients with chronic hepatitis B and active viral replication as indicated by the presence of hepatitis Be antigen (HBeAg), increased DNA polymerase (DNAp) and positive hepatitis B virus DNA (HBV-DNA) for more than 6 months, were entered into a prospective trial of recombinant human interferon therapy. Ten patients had chronic persistent or chronic lobular hepatitis, 8 chronic active hepatitis and 3 postnecrotic cirrhosis. All cases were treated with 5 x 10(6) units of recombinant interferon alfa-2B given subcutaneously every other day for 12 weeks. During treatment, 18 patients (86%) showed a significant reduction of DNAp levels, which reached normal values in 10 patients (48%). Viral replication was controlled over a 10-month follow-up period in 7 out of 21 patients (33%). Of these 7, five patients became HBeAg negative and HBeAb positive. HBsAg disappeared in one patient. The only serious adverse effect was thrombocytopenia in one patient in whom rapid recovery occurred when interferon was withdrawn. Treatment was also terminated in a second patient because of local reactions at the injection sites occurring after 10 weeks of therapy. Our data indicate that relatively small doses of recombinant alfa-2B interferon given during a 12-week period induce a significant reduction in viral replication and might approximately triple the spontaneous seroconversion rate observed in patients with chronic hepatitis B.
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PMID:Prospective trial of recombinant leucocyte interferon in chronic hepatitis B: a 10-month follow-up study. 268 91

In 21 patients from the out-patient clinic of the Internal Medicine Department of our hospital with chronic hepatitis (HC) due to B virus (HBV) and anti-HBC (IgG) serology but not HBsAg, a study was made of the possible correlation between viral replication levels (RV) --as expressed by DNA polymerase values (DNAp)-- and, respectively, histologic changes and serum enzyme movements (GPT, GOT). Our study parted from the diverse criteria cited in the literature concerning the role assigned to viral replication per se and/or immune response per se in the genesis of histologic damage (DH). All patients exhibited signs of moderate clinical and enzymatic activity. The levels of viral replication in the group studies were significant (compared to a control group), which supports the thesis that a certain degree of viral replication, although very attenuated, persists in these patients and is the basis of the continued histological damage that eventually leads to liver cirrhosis (CH) and its derivatives, often with little clinical translation. As regards histologic damage, the correlation with DNAp is reciprocal and of moderate significance, supporting the criterion that the multiform expression of histologic damage in liver cirrhosis due to HBV (HCB) (cellular necrosis, intracellular degenerative phenomena, inflammatory cellular infiltrate, fibrosis) is, at the very least, unproportional to the degree of viral replication and can even be reciprocal. Only the severity of the overall hepatic process remains a function of immune response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Viral replication, histologic damage and enzymatic activity in chronic hepatopathies caused by B virus. Analysis of 21 patients]. 276 33

In a previous study a partial inhibition of viral replication was observed in HBeAg-positive patients after acyclovir (ACV) treatment. To assess those results and to evaluate different treatment regimens, a randomized controlled trial with ACV given at 45 mg/kg/day by continuous infusion (in 5 patients) or by intermittent 8-hourly infusion (in 6 patients) for 28 days versus placebo has been performed in 20 patients affected by chronic hepatitis positive for both HBsAg and HBeAg for at least 6 months. Patients were stratified for sex, presence of cirrhosis and homosexual activity. Modest inhibition of serum DNA polymerase activity was observed after intermittent ACV treatment but not with the continuous infusion. After a 8-12 months follow-up, 2 of 10 of the ACV-treated patients and 3 of the controls had become HBeAg-negative, with 1 and 2 seroconversions to anti-HBe in the treated and placebo group respectively. No adverse effects were observed in ACV-treated patients after continuous infusion, but 2 of 6 patients who received intermittent therapy had to stop treatment, because of abdominal colics and elevation of the serum creatinine. Our data confirm that ACV partially inhibits viral replication in HBeAg-positive patients but without significantly affecting the rate of seroconversion to anti-HBe.
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PMID:Treatment of chronic HBeAg-positive hepatitis with acyclovir. A controlled trial. 329 5

The detection of HBe antigen (HBeAg) in the sera of chronic HBV carriers is classically used as a marker of viral replication and therefore of development and infectivity of the disease. On this basis, it was used for the selection of patients for antiviral treatment. However, discrepancies between the presence of HBeAg and signs attesting to viral replication, namely HBV DNA and DNA polymerase, have been reported. We attempted to determine the prevalence of markers of viral replication in a group of patients with chronic active hepatitis associated or not with cirrhosis. All 41 patients were HBs Ag carriers; HBe Ag was present in 36 (88 p. 100), and HBV DNA in 28 (68 p. 100). A statistically positive correlation was found between the presence of cirrhosis and the absence of viral replication. In spite of the detection of HBe Ag, no direct signs of viral replication were observed in 30 p. 100 of patients, mainly those with cirrhosis. Therefore it is clear that the detection of HBe Ag alone cannot be considered as a sign of viral replication. Direct signs of viral replication should help to select patients for antiviral therapy, which should be started before the occurrence of cirrhosis.
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PMID:[HBe antigen and B virus DNA in patients with chronic active hepatitis]. 380 9

We conducted a clinical trial to study the effects of a 10-week course of prednisone therapy and its withdrawal on serum aminotransferase levels and on hepatitis B virus (HBV) markers in patients with hepatitis B surface antigen (HBsAg) positive chronic active hepatitis (CAH-B). Eighteen patients with CAH-B were treated with prednisone, while another 18 patients matched for age, sex, race and sexual preference were followed simultaneously without treatment for the same duration. Nine of 18 prednisone-treated patients became transiently DNA polymerase positive. All nine patients developed a transient rise in serum alanine aminotransferase (ALT) levels of greater than 300 U/L above baseline values, which was associated with a drop in HBsAg levels from a mean of 186 micrograms/ml prior to therapy to 92 micrograms/ml at 6 months following treatment. Six of these patients developed fatigue, anorexia and dark urine, and four also developed either ascites or hemorrhage from esophageal varices, which was accompanied by hepatic encephalopathy. All six of these patients had histologic evidence of CAH with cirrhosis. In comparison, none of the control, untreated patients with CAH-B had any change in either HBV markers or serum ALT levels. Therefore, even a short course of prednisone in patients with CAH-B with cirrhosis is detrimental and its use should be discouraged.
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PMID:Effects of short-term, high-dose prednisone treatment of patients with HBsAg-positive chronic active hepatitis. 388 51

We measured serum markers of hepatitis B virus replication in two HBsAg-, HBeAg-positive hepatitis B carriers with chronic active hepatitis and cirrhosis. The first of these patients was HBsAg-, HBeAg-, HBV DNA- and HBV DNA polymerase-positive initially and spontaneously lost HBV DNA polymerase and HBV DNA. During the HBeAg-positive, DNA polymerase-negative "window phase", an increase in viral replication, characterized by the reappearance of HBV DNA and HBV DNA polymerase occurred, together with an aggravation of the underlying chronic hepatitis. In the second HBsAg-, HBeAg-positive carrier, spontaneous fluctuations in HBV replication were associated with clinical deterioration. Delta agent and hepatitis A virus superinfection were excluded. These observations suggest that spontaneous low-grade fluctuations of HBV replication accompanied by an increase in the biochemical activity of the underlying chronic hepatitis can be observed in certain HBV carriers.
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PMID:Clinical and serological events accompanying changes in hepatitis B viral replication: case reports. 399 35

The livers of 33 captive woodchucks were examined histologically in 30 biopsy and 10 autopsy specimens and the findings were correlated with serum determinations for woodchuck hepatitis virus (WHV), surface antigen (WHsAg) and antibody (anti-WHs), and WHV DNA and DNA polymerase. The liver appeared normal in all 3 serum-negative animals, 7 of 16 with indeterminate WHV status, and 1 of 4 with anti-WHs, but not in 10 animals with WHsAg, WHV DNA, and DNA polymerase. Mild hepatic inflammation was found in 7 woodchucks with indeterminate status, 4 with anti-WHs, and 2 with each marker of WHV infection. Significant inflammation was found in 2 of indeterminate status and 4 with every marker, whereas more severe lesions (2 of chronic active type) occurred, almost always in autopsy specimens, in 8 animals with every marker. Eight of 10 animals with all markers had orcein-positive inclusions (Shikata's technique) and 6 had hepatocellular carcinoma associated with acute and chronic hepatic inflammation and, usually, neoplastic nodules in the noncarcinomatous parenchyma. Features distinguishing the woodchuck lesion from human hepatitis B disease were: association of carcinoma with acute hepatic inflammation (but not with cirrhosis) and DNA polymerase in the serum; transition to carcinoma from neoplastic nodules; conspicuous plasma-cellular reaction of hepatic inflammation, and hematopoietic cells in the tumor. Significant hepatic lesions in the woodchucks were regularly associated with serum WHsAg, WHV DNA, and DNA polymerase. In contrast to man, hepatocellular carcinoma in woodchucks was regularly associated with these markers of active viral replication. The nature of the orcein-positive inclusions requires elucidation, although they may assist in screening for similar viruses in other species. The woodchuck may help in the study of the relation between hepatocellular carcinoma and hepatitis B, including the possibility of cocarcinogenic factors.
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PMID:Woodchuck hepatitis and hepatocellular carcinoma: correlation of histologic with virologic observations. 626 81

A recently modified method using peroxidase labeled antibodies for light and electron microscopic demonstration of hepatitis B virus (HBV) was applied to the evaluation of hepatitis B surface antigen (HBsAg) on the surface of liver cells in biopsy specimens from 24HBsAg chronic carriers. Membranous distribution of HBsAg was demonstrated in diffuse or scattered hepatocytes in all 4 asymptomatic carriers and in 3 of the 20 patients with HBsAg-positive chronic active hepatitis or liver cirrhosis. In these patients with membranous expression of HBsAg, hepatitis B e antigen, Dane particles and DNA polymerase were often detected in sera, and large amounts of hepatitis B core antigen appeared in the liver. These results suggest that membrane-bound HBsAg may be expressed by the HBV genome. The ultrastructural study of liver cells showing membranous expression disclosed dense deposits of reaction product indicative of HBsAg on the cell membrane and/or on assembled particles within the extracellular space. In some hepatocytes showing both diffuse cytoplasmic and membranous expression of HBsAg, HBsAg-positive membrane of cisternae open to the intercellular space was connected with the liver cell membrane. These findings supported the conjecture that HBV associated antigens are integrated into the liver cell membrane.
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PMID:Immunoelectron microscopic observation of hepatitis B surface antigen on the surface of liver cells from patients with hepatitis B virus infection. 644 86

Survival data from 379 patients with chronic hepatitis B were analyzed to determine life expectancy for the patient from the time of first contact. One hundred twenty-one patients had chronic persistent hepatitis, 128 had chronic active hepatitis, and 130 had chronic active hepatitis with cirrhosis. The frequency of symptoms (p less than 0.001), stigmata of chronic liver disease (p less than 0.001), and liver function test abnormalities (p less than 0.001) increased as the histologic features worsened, whereas the percentage of patients with circulating hepatitis B DNA polymerase declined (p less than 0.001). Women were uncommon in our series and had less severe disease than men (p less than 0.02). Fifty-one patients had died by the time of this analysis. The estimated 5-year survival rates were 97% for patients with chronic persistent hepatitis, 86% for those with chronic active hepatitis, and 55% for those with chronic active hepatitis with cirrhosis. The usual cause of death was liver failure and its sequelae. A multivariate analysis found age of 40 years or more, total bilirubin level of 1.5 mg/dL or more, ascites, and spider nevi to be factors that identified patients at a higher risk of death. The prognosis for patients with chronic hepatitis B is similar to that for patients with chronic hepatitis of other causes.
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PMID:Survival in chronic hepatitis B. An analysis of 379 patients. 648 92


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