Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
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Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
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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)
Three patients with submassive hepatic necrosis developed acute liver failure during the severe reactivation of chronic hepatitis B. The activity of hepatitis B virus (HBV)
DNA polymerase
increased in all three patients immediately before the onset of hepatic failure. Liver biopsy specimens obtained before and after the episode of submassive hepatic necrosis showed progression to advanced liver cirrhosis. The nucleotide sequences of the precore and core regions of HBV-DNA were investigated in two of the three patients and in another two patients with piecemeal and bridging necrosis. The nucleotide and amino acid sequences of the HBV-DNA core region changed after reactivation in the the two patients with submassive hepatic necrosis, while the sequences in the other two patients with piecemeal necrosis remained unchanged before and after reactivation. These results suggest that the antigenicity of the HBV-DNA core region may have been changed before and after severe reactivation. Due to mutation at the core region, a different type of epitope would be expressed on the hepatocytes after submassive hepatic necrosis, which would not be a target for the cytotoxic T cell. This was evident by the continuation of the normal serum
GPT
for 5 and 9 years, respectively.
...
PMID:Mutation of the core region of HBV-DNA and submassive hepatic necrosis in patients with anti-HBe-positive chronic hepatitis B. 139 28
The nucleoside analog 2',3'-dideoxyinosine, currently being used to treat patients infected with the human immunodeficiency virus, has been shown to inhibit viral replication in certain cell culture systems of hepatitis B virus and the duck model of chronic hepatitis B infection. We studied the effect of dideoxyinosine on viral replication in patients with chronic hepatitis B. In the initial dose-finding phase, patients received sequential 2-wk courses of dideoxyinosine in escalating doses of 3, 6 and 9 mg/kg/day. In the second, long-term treatment phase, patients received dideoxyinosine at a dose of 9 mg/kg/day for 12 wk. Dideoxyinosine was given orally in three divided doses. The effects of dideoxyinosine on hepatitis B were assessed by serial measurements of
ALT
, hepatitis B virus DNA and
DNA polymerase
activity in serum. Six patients completed the dose-finding phase, and five patients continued into the long-term treatment phase. No significant differences were seen in serum aminotransferases, hepatitis B virus DNA levels or
DNA polymerase
activity at any time during treatment when compared with pretreatment levels. All patients remained positive for HBeAg during treatment and during 6 mo of follow-up. Thus at the doses tested, dideoxyinosine had no appreciable effect on viral replication in patients with chronic hepatitis B.
...
PMID:A pilot study of 2',3'-dideoxyinosine for the treatment of chronic hepatitis B. 139 94
In a 47-year-old male patient a tonsillar swelling was pointed out in May, 1991. Lymph node biopsy revealed that he had malignant lymphoma (diffuse large cell type). He had no hepatic dysfunction on admission, but because of positive hepatitis B (HB) antigen and negative HB antibody, he was diagnosed as an asymptomatic HB carrier. The staging examination showed that he had stage IIA lymphoma. Treatment with the COP-BLAM regimen was initiated on June 8. But the level of serum GOT and
GPT
increased to 286 IU/l and 392 IU/l, respectively. Serum
DNA polymerase
also increased to 9492 cpm. Interferon-alpha (3 x 10(6) units daily) was administered intramuscularly from June 8. Serum
DNA polymerase
decreased to zero on September 2, and his HBe antibody became positive indicating seroconversion. COP-BLAM chemotherapy without prednisolone was initiated from September 9 and complete remission was achieved. He was discharged from our hospital on September 25. It has been frequently reported that asymptomatic HB antigen carriers developed fulminant hepatitis during the course of chemotherapy. Our case suggests that it is necessary to continue chemotherapy in order to attain seroconversion by early use of interferon-alpha, when lymphoma patients display aggravated hepatic dysfunction and increased
DNA polymerase
levels.
...
PMID:[Successful interferon-alpha treatment of hepatitis B developing during chemotherapy of malignant lymphoma]. 143 50
We have evaluated the problem of autoantibodies such as antinuclear antibodies (ANA), smooth muscle antibody (SMA) and antibodies to thyroid microsomal (TMA) and to thyroglobulin (TGA) related to interferon therapy in 27 patients with chronic hepatitis B. Anti-interferon antibody was also studied by Western blot method. Eight patients had ANA and 2 had SMA during interferon therapy. However, 6 of the 8 patients were ANA positive and one of the 2 was SMA positive prior to interferon treatment. No patients developed TMA, TGA or anti-interferon antibody. Eight (29.6%) of the 27 patients had clearance of both
DNA polymerase
and HBeAg and persistent normalization in
alanine aminotransferase
levels with interferon therapy. Seven of the 8 responders developed none of the autoantibodies related to interferon therapy. These results suggest that the presence of ANA or SMA during treatment may affect the therapeutic response to interferon.
...
PMID:[Autoantibodies related to interferon therapy in chronic hepatitis B may affect the therapeutic response to interferon]. 172 18
Seventeen patients with chronic hepatitis B were treated with a 4-week administration of glycyrrhizin followed by a 4-week treatment with human lymphoblastoid interferon, then followed for 6 months after the end of treatment. All were positive for hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), and hepatitis B virus-associated
DNA polymerase
(DNA-p) for at least 6 months before entry. All patients were Japanese and none of them were homosexuals. Eleven patients lost DNA-p activity and 10 of them lost HBeAg. Three of these 10 patients had antibody to HBeAg. In 10 patients who became HBeAg-negative,
alanine aminotransferase
levels after glycyrrhizin administration were higher and initial DNA-p activities relatively lower than the levels found in seven patients who remained HBeAg-positive. The immunomodulator provided by a short course of glycyrrhizin before administration of human lymphoblastoid interferon may be an effective treatment for patients with chronic hepatitis B.
...
PMID:Glycyrrhizin withdrawal followed by human lymphoblastoid interferon in the treatment of chronic hepatitis B. 176 47
Serum
DNA polymerase
activity (DNA-P) was detected in 27.6 per cent of non-A, non-B (NANB) hepatitis patients, 8.7 per cent of patients with alcoholic liver disease (ALD), 8.6 per cent of hepatitis B surface antigen (HBsAg)-positive patients and 19.0 per cent of HBsAg-negative blood donors with elevated serum
glutamic-pyruvic transaminase
(SGPT) concentrations. In contrast, none of the patients with hepatitis A, drug-induced liver injury or non-alcoholic fatty liver had DNA-P in their sera in the acute phase of the illness. All HBsAg-positive samples with detectable DNA-P were strongly positive for hepatitis B virus (HBV) DNA, but the samples from patients with NANB hepatitis and ALD and HBsAg-negative blood donors had no HBV DNA. Sensitivity to actinomycin D showed the heterogeneity of DNA-Ps in HBsAg-negative blood donors; the enzyme activity of one type was inhibited by 100 micrograms/ml of actinomycin D, whereas the other was not. The preference for exogenous template primers of these DNA-Ps was different to those of HBV and human retroviruses. The results reveal the prevalence of serum DNA-P in NANB hepatitis patients and suggest that two distinct agents are relevant to the aetiology of NANB hepatitis.
...
PMID:Prevalence and heterogeneity of serum DNA polymerase activity in patients with non-A, non-B hepatitis and HBsAg-negative blood donors with elevated SGPT. 212 73
Twenty patients with hepatitis B e antigen (HBeAg) -positive chronic hepatitis, who received 40 mg of prednisolone per day for three weeks followed by withdrawal, were studied for changes in
alanine aminotransferase
(
ALT
), triiodothyronine (T3), thyroxine (T4), and hepatitis B virus
DNA polymerase
(HBV-DNAp) levels determined before and during prednisolone treatment and after its withdrawal. A decreased HBV-DNAp level of less than 100 cpm/ml three to five weeks after withdrawal was considered a sign of efficacy and was shown in 10 patients (50%). Significant differences were found between
ALT
levels, between T3 levels, and between the T3/T4 ratios assayed in the third and fourth weeks in total (P less than 0.02) and in the group in which efficacy was demonstrated (P less than 0.01). The T3/T4 ratio in the third week in the effectively treated group was significantly less than that in the noneffectively treated group (P less than 0.05). Prednisolone withdrawal effective for HBV-DNAp was shown in the patients with a decreased T3 level and the T3/T4 ratio at the third week and an increase in the ATL level after the withdrawal. The
ALT
level increased after the T3 level decreased. Changes in the T3 level or the T3/T4 ratio represent a marker for effectiveness of prednisolone withdrawal and for determination of combination therapy after steroid withdrawal.
...
PMID:Triiodothyronine level and triiodothyronine/thyroxine ratio in HBeAg-positive chronic hepatitis patients treated with prednisolone withdrawal. 239 Sep 25
Two years or more after 35 patients (29 men and six women) with chronic hepatitis B were treated by interferon, we studied relationships of age,
ALT
activity, activity of serum
DNA polymerase
associated with the hepatitis B virus, serum levels of hepatitis B e antigen and activity of 2',5'-oligoadenylate synthetase in peripheral blood mononuclear cells when treatment started in comparison with treatment results. Seventeen patients were given human lymphoblastoid interferon-alpha; the other 18 patients were given interferon-beta. We measured the activity of 2',5'-oligoadenylate synthetase in these mononuclear cells and found the rate of increase in vivo and in vitro; the correlation between the two was r = 0.68. This enzyme activity in the patients who became negative for
DNA polymerase
after interferon treatment increased more both in vivo and in vitro than in patients who did not became negative. Also, both the in vivo and in vitro activity increased more in patients who became negative for the e antigen after interferon therapy than in those who remained positive. In the first group, interferon was considered to be effective; in the second, ineffective. Of the patients who became negative, some developed e antibodies and some did not; the increase in this enzyme activity in the two groups was not significantly different. The increase in the activity of 2',5'-oligoadenylate synthetase activity could be used to predict the results of interferon treatment and is an index that can be used before treatment to predict the response.
...
PMID:Relationship of the effects of interferon on chronic hepatitis B and the induction of 2',5'-oligoadenylate synthetase. 247 40
Thirty-five patients with active chronic hepatitis B (ACH-B) were evaluated. They were in stable replicative phase (HBeAg +;
DNA polymerase
and
ALT
stable in two determinations at least one month apart) and had not been infected by delta virus or HIV-1. Thirty-four patients were heterosexual and no patient was a drug abuser except one. The 23 initial cases were followed up for 15 months without therapy. The subsequent 12 cases were treated with maximal doses of 2.5 megaunits/m2 of lymphoblastoid alpha interferon (IFN-L) daily for two weeks and three times a week during 10 more weeks. While in the controls only two cases (8.69%) lost the DNA-polymerase activity and HBeAg, 5 treated patients (41.66%; p less than 0.05) developed seroconversion to nonreplicative phase. No patient from the control series lost the HBsAg; however, this happened in 2 treated patients (16.66%). These results show that IFN-L is effective in heterosexual patients with ACH-B in replicative phase without delta virus or HIV-I co-infection.
...
PMID:[Treatment of chronic hepatitis B with lymphoblastoid alpha interferon]. 261 34
The future of patients with chronic hepatitis (HC) due to B virus depends above all on the tendency of the interaction between viral activity and immune response. Viral activity (replication) (RV) can be expressed in these patients by two variants: a) "complete" or "early", associated with the presence in serum of HBsAg, HBeAg, and significant
DNA polymerase
activity, and b) "incomplete" or "late", in which anti-HBe is found in serum and there are scant or no histopathologic changes ("healthy carriers" in some cases). In prolonged infections viral replication declines gradually, although viral capsid protein continues to be synthesized and DNA-HBV is integrated into the genome. Viral replication per se does not condition the histologic damage (DH) expressive of liver cirrhosis with HBV (HCB). Other publications take a different view of this problem. The increase in viral replication often is proportional to a rise in serum
GPT
(an expression of histologic damage), but viral replication is not always associated with a progressive disease course. The immune defense leads to cytolysis and subsequent elimination of the HB virus. Some patients with high HBsAg levels have little active forms of liver cirrhosis; the DNA-HBV integrated would be capable of producing HBsAg but not HBcAg. It is precisely this that induces the response of cytotoxic T lymphocytes at the level of the hepatocyte surface. The presence in serum of anti-HBe IgM would be related to the expression of HBcAg on the hepatocyte membrane and/or the liberation of HBcAg particles by lysed hepatocytes. The relationship between the degree of histologic damage and serum aminotransferase levels is better established.
...
PMID:[Viral replication, histologic damage and enzymatic activity in chronic hepatopathies caused by B virus]. 266 54
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