Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the expression of Pre-S2 antigen (Ag) and antibody (Ab) in sera quantitatively using ELISA. Four patients with acute hepatitis B and 87 chronic HBV carriers were included in this study. We also investigated the expression of Pre-S2Ag in the liver tissues obtained from 26 chronic HBV carriers by direct fluorescent antibody method. There was a significant correlation between Pre-S2Ag titers and HBsAg titers in sera. Pre-S2Ag titers were higher in sera positive for HBeAg, HBV-related DNA polymerase or HBV-DNA than in sera negative for those markers. The ratio of Pre-S2Ag titers to HBsAg titers, however, was constant irrespective of virus replicative markers. Pre-S2Ag in the liver had almost same intracellular localization with HBsAg in the liver. It was suggested that Pre-S2Ag was expressed with an intimate relation to the expression of HBsAg and was not useful as a virus replicative marker. Pre-S2Ag titers/HBsAg titers tended to be high in patients with chronic active hepatitis and high serum GPT levels compared to patients with chronic inactive hepatitis. This may be explained by the release of Pre-S2Ag in the liver. In addition, all patients positive for Pre-S2Ag on the membrane of hepatocytes had chronic active hepatitis. The overproduction of Pre-S2-containing surface proteins in the liver may have some implication related to cell injury via the immune response to Pre-S2Ag etc. Pre-S2Ab was detected only in few cases of chronic HBV infected patients. The lack of immune response to Pre-S2 region may play a role in the persistence of HBV infection.
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PMID:[Expression of Pre-S2 antigen and antibody in patients with hepatitis B virus infection]. 268 90

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

We investigated the expression of Pre-S1 antigen and Pre-S1 antibody using a synthetic peptide and the monoclonal antibody against it. Four patients with acute hepatitis B and 87 chronic HBsAg carriers were included in this study. There was a significant correlation between Pre-S1 antigen titers and HBsAg titers. Pre-S1 antigen showed higher titers in patients with active viral replication, positive for HBeAg, HBV-DNA or HBV-related DNA polymerase. The ratio of Pre-S1 antigen titers to HBsAg titers, however, had no significant relationship with those replicative markers. It was suggested that Pre-S1 antigen was expressed with an intimate relation to the expression of HBsAg and was not so useful as a new replicative marker. Pre-S1Ag titers/HBsAg titers tended to be high in patients with chronic active hepatitis and high serum GPT levels. This may be due to the release of overproduced intracellular Pre-S1 antigen. Pre-S1 antibody was detected only in few cases of chronic HBsAg carriers. This result shows that the immune tolerance to Pre-S1 region may play a role in the persistence of HBV infection.
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PMID:[Expression of pre-S1 antigen and pre-S1 antibody in sera obtained from HBV infected patients]. 279 57

The presence and the level of hepatitis B surface antigen (HBsAg)/IgM complexes were determined in 54 chronic HBsAg carriers in relation to receptors for polymerized human serum albumin (pHSA-R) tested by specific radioimmunoassay, and to hepatitis B virus-DNA polymerase (HBV-DNAp). HBsAg/IgM complexes, correlated significantly with the HBsAg concentration but, at a similar HBsAg concentration, significant highest values of HBsAg/IgM complexes were found among HBeAg positive patients. In addition, a significant correlation was found between HBsAg/IgM complex levels, HBeAg titres and HBV-DNAp activity (r = 0.628, p less than 0.001 and r = 0.559, p less than 0.001, respectively). Moreover, a positive linear correlation was found when comparing HBsAg/IgM complexes and pHSA-R levels (r = 0.848, p less than 0.001). Patients who were positive for HBsAg/IgM complexes had a significantly higher glutamate-pyruvate transaminase (GPT) level than those who did not show any complexes. In conclusion, HBsAg/IgM complexes seemed to be indirectly related to HBV replication.
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PMID:Hepatitis B surface antigen/IgM complexes: relation to receptors for polymerized human serum albumin, hepatitis B virus (HBV) DNA polymerase activity and HBV markers. 288 20

We have investigated the efficacy of recombinant alpha-interferon treatment of chronic hepatitis B virus (HBV) infection in two therapeutic trials. Forty-four patients positive for HBsAg, HBeAg, DNA polymerase and HBV-DNA were studied. Fourteen carriers were treated in the first trial with doses ranging from 18 to 50 million units (mu)/m2 3 times per week. Six of 14 treated carriers (43%) have a sustained loss of HBeAg, HBV-DNA and DNA polymerase. Four lost HBsAg (29%). Two of 11 (18%) untreated carriers lost HBeAg, but none lost HBsAg (P = 0.05). Nineteen patients were entered in a second trial to assess dose response. Fourteen were treated with doses ranging from 2.5 to 10 mu/m2. Five patients were untreated. Two treated patients seroconverted to anti-HBe, and a third cleared HBsAg and seroconverted to anti-HBs. None of the controls was anti-HBe-positive. Thus 9/28 (32%) carriers have lost replicating HBV versus 2/16 (13%) of untreated patients. Elevated pretreatment serum ALT concentrations and severe chronic active hepatitis were associated with inhibition of viral replication in treated patients suggesting that seroconversion may require an appropriate host response. The efficacy of recombinant interferon is restricted, but it may be of benefit in a proportion of carriers.
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PMID:Recombinant leucocyte interferon treatment of chronic hepatitis B. An analysis of two therapeutic trials. 329 8

A randomized controlled study of one course of vidarabin was carried out in 30 patients with HBs Ag, HBe Ag, DNAp, positive chronic active hepatitis: 15 patients were treated with vidarabin given intravenously (15 mg/kg/day for 7 days then 7.5 mg/kg/day for 14 days); the other 15 patients received a placebo for 21 days. During treatment, DNA polymerase activity fell dramatically in 13 treated patients and in no controls (p less than 0.001). Six months after inclusion, ALT normalization was observed in 40 p. 100 of the treated patients and 6 p. 100 of the controls (p less than 0.05), a decrease in inflammatory activity on liver biopsies was observed in 70 p. 100 of the treated patients and 20 p. 100 of the controls (p less than 0.05), a permanent lost of DNA polymerase and of HBe Ag occurred in 33 p. 100 and 13 p. 100 of the treated patients and 20 p. 100 and 7 p. 100 of the controls, respectively. In addition, a second course of vidarabin was administered to the 12 patients who were still HBe Ag positive 6 months after the first course. During the next 6 months, 8 patients lost DNA polymerase and 4 lost HBe Ag. Altogether, the final score of durable inhibition of HBV replication was 11/15 (73 p. 100) within one year. The above results demonstrate that one course of vidarabin can significantly improve ALT and liver inflammatory activity but the effect upon HBV replication is only transient. A second course does however increase efficacy on HBV replication without additional side effects.
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PMID:[Vidarabine treatment of chronic active hepatitis associated with hepatitis B virus multiplication. A randomized multicenter study]. 330 17

Twelve hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), hepatitis B virus DNA polymerase (HBV-DNAp) and hepatitis B virus DNA (HBV-DNA) positive patients with chronic active hepatitis (CAH) were treated with doses of either 20 X 10(6) IU/m2 or 10 X 10(6) IU/m2 body surface of recombinant interferon (rIFN)-alpha-2A, I.M., twice a week, during a period of 6 months. No appreciable differences with respect to clinical history, liver function tests and markers of HBV replication between the two groups were apparent at the time of entry into the trial. At the third month of treatment HBV-DNAp became negative in 10 out of 12 patients (83%). After a 15-month follow-up, HBV-DNAp, HBV-DNA and HBeAg were negative in 7 out of 12 patients (38%) (responders). Furthermore, at 24 months, 2 non-responder patients became HBV-DNA and HBV-DNAp negative and one responder lost serum HBsAg. In addition, HBsAg concentration, GPT level and histological Knodell's index decreased significantly in the responder patients, while no changes were observed in non-responders. Five out of six patients who received a low rIFN dose responded to the treatment, and only 2 out of 6 with a higher dose. No unacceptable toxicity was noted in any of the 12 patients. All of them completed the course of treatment. The results suggest that long-term rIFN-alpha-2A therapy has an antiviral effect in CAH due to HBV infection and is well tolerated.
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PMID:Prolonged (6 months) treatment of chronic hepatitis B virus infection with recombinant leukocyte A interferon. 343 94

Serum levels of antibody to hepatitis B core antigen and IgM antibody to hepatitis B core antigen were tested in 15 patients who participated in a randomized, placebo-controlled trial of a 28-day course of prednisolone therapy. During treatment, serum levels of antibody to hepatitis B core antigen and IgM antibody to hepatitis B core antigen decreased in all 10 treated patients, but in none of five controls (p less than 0.05). Also during therapy, ALT activity decreased by an average of 50% and serum IgG levels by 30% (both p less than 0.05). Serum levels of hepatitis B virus DNA and DNA polymerase activity did not change significantly. Four to 10 weeks after discontinuation of prednisolone, a rebound of serum ALT and IgM antibody to hepatitis B core antigen levels occurred, which usually resolved within the subsequent months of follow-up evaluation. In three patients, however, there was a prolonged exacerbation of the disease following prednisolone withdrawal; in these three, levels of IgM antibody to hepatitis B core antigen and ALT remained elevated above pretreatment values. The close correlation between changes in serum ALT activity and IgM antibody to hepatitis B core antigen levels suggests that corticosteroids can modulate disease activity in chronic type B hepatitis by suppression of the host-immune response to hepatitis B virus antigens.
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PMID:Effect of corticosteroid therapy on levels of antibody to hepatitis B core antigen in patients with chronic type B hepatitis. 355 25

The incidence of HBV-DNA polymerase, HBV-DNA and serum and liver HBcAg in 104 chronic HBsAg carriers was studied. HBV-DNA was the most frequently detected marker, followed by HBcAg and HBV-DNAp. According to their individual or combined presence, four different serological patterns of viral replication were discerned: 53 patients had all these markers, 30 had HBV-DNA but lacked HBV-DNAp (15 with and 15 without HBcAg) and 21 had no such markers detectable. The simultaneous positivity for all of those markers was observed only in HBeAg-positive patients. HBV-DNA alone or along with HBcAg was found in a similar incidence irrespective of the HBe system. Liver HBcAg was found in all but four patients with and in four without HBV-DNA. Viral DNA concentration was significantly (p less than 0.001) higher when HBV-DNAp tested positive. Indeed, HBeAg rather than anti-HBe patients had higher (p less than 0.005) levels of HBV-DNA. In HBeAg-positive patients, the nuclear HBcAg staining was significantly (p less than 0.05) higher when HBV-DNAp tested positive. In DNA polymerase-negative patients, but positive for HBV-DNA, those with or without HBcAg had a similar percentage of core antigen staining. The same distribution was seen in anti-HBe, HBV-DNA-positive patients. However, the mean percentage of hepatocytes displaying cytoplasmic HBcAg did not differ significantly among patients with HBV-DNA, irrespective of the HBe system and the HBV-DNAp status. Such patients had significantly (p less than 0.001) higher ALT levels than those without viral DNA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Identification of different degrees of hepatitis B virus (HBV) replication by serological (HBV-DNAp, HBcAg and HBV-DNA) and histological (HBcAg) methods. 361 85

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


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