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)

This paper reported 96 cases with chronic hepatitis B treated by a double-blind method. There were 51 cases of observation group(OG) and 45 cases of control group (CG). OG was treated with Jiedu Yanggan Gao consisting of Artemisia capillaris, Taraxacum mongolicum, Plantago seed, Cephalanoplos segetum, Hedyotis diffusa, Flos Chrysanthemi Indici, Smilax glabra, Astragalus membranaceus, Salviae miltiorrhizae, Fructus Polygonii Orientalis, Radix Paeoniae Alba, Polygonatum sibiricum, etc.). CG was prescribed with three charred medicinal herbs (charred Fructus Crataegi, charred Fructrus Hordei Germinatus, charred fermented mixture of several medical herbs and wheat bran). The average duration of treatment was five months. All 96 cases belong to the virus-duplication-type with positive HBsAg for over one year. Among them 65.5% of cases HBeAg, DNAP and HBV-DNA were positive. 20.8% of cases were positive in two out of the above tests. 13 data were compared statistically between two groups, and proved to be comparable (P greater than 0.05) before treatment. 27.3% and 66.7% of cases' ALT, AST returned to normal respectively in OG after treatment. However, in CG they were 9.1% and 22.2% (P less than 0.05). TTT returned to normal in 52% cases of OG and 44% in CG (P greater than 0.05). 20% cases HBeAg shifted to negative in OG, but 6.7% in CG. Cases with negative DNAP in OG occupied 34.2%, but 10.8% in CG. 31.6% cases' HBV-DNA changed to negative in OG, while 17.6% in CG. After comprehensive judgement, the total effective rate was 74.5% in OG and 24.4% in CG respectively (P less than 0.001). Eight cases were basically cured in OG and one case in CG. After one year's follow-up, one recurred in eight patients of OG, however the only one cured in CG still relapsed.
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PMID:[Clinical study of 96 cases with chronic hepatitis B treated with jiedu yanggan gao by a double-blind method]. 236 64

Seventy-six children aged 1-13 years who were known to be positive for hepatitis B surface antigen and hepatitis B e antigen in serum for at least 6 months and who had biopsy-proven chronic hepatitis have been followed longitudinally for 1-12 years (mean, 5 years). Twenty-three of them are now young adults. Eight patients had acute type B hepatitis 12-24 months before entering the study, while 68 patients came to observation during a chronic phase. At the beginning of follow-up, all 76 children were positive in serum for hepatitis B virus DNA, and 44 (58%) had chronic active hepatitis, associated with cirrhosis in two cases. During follow-up, 23 (30%) patients remained hepatitis B e antigen-positive, most with unchanged biochemical and histological features. The other 53 (70%) cases seroconverted to hepatitis B e antibody and cleared hepatitis B virus DNA from serum, including 7 of 8 (87%) patients with acute hepatitis at presentation. After seroconversion, alanine aminotransferase levels normalized in all patients and remained normal in 49 patients (92.5%) throughout a mean observation period of 3 years. Five of these children, including 2 of 7 (29%) with previous acute hepatitis, eventually cleared hepatitis B surface antigen from their sera. Finally, 4 (7.5%) patients experienced a mild increase of alanine aminotransferase levels several months after seroconversion in the absence of hepatitis B virus replication or of delta virus superinfection. Clinical and virological parameters did not significantly differ between patients with or without acute onset; however, seroconversion occurred earlier, and the rate of hepatitis B surface antigen clearance was greater in the former than in the latter group. The present data indicate that approximately two thirds of children with hepatitis B e antigen- and hepatitis B virus DNA-positive chronic hepatitis clear hepatitis B virus DNA from their sera before reaching adulthood. After termination of viral replication, most patients achieve a sustained biochemical remission, suggesting the disappearance of disease activity. Reactivation of virus replication after hepatitis B e antibody seroconversion has never been observed in this series, although mild alanine aminotransferase level abnormalities could be detected in a minority of cases.
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PMID:Long-term outcome of chronic type B hepatitis in patients who acquire hepatitis B virus infection in childhood. 237 83

We studied the effect of putrescine on acute liver failure caused in rats by two injections of 1 gm/kg D-galactosamine. The hepatic polyamine level rose only slightly in the D-galactosamine-injected rats treated with glucagon and insulin, and [3H]thymidine incorporation into DNA increased little; these hormones did not improve the survival rate. When D-galactosamine-injected rats were given putrescine, the putrescine concentration in the liver increased and the survival rate of the rats was significantly higher than that of control rats given only D-galactosamine. Putrescine administration tended to lower the serum level of alanine aminotransferase in rats injected with D-galactosamine, so the polyamine might have a protective effect on hepatocytes. Putrescine significantly increased [3H]thymidine incorporation in the liver; thus it accelerated liver regeneration. Difluoromethylornithine decreased the level of putrescine in the liver, decreasing both [3H]thymidine uptake and the survival rate. In the rats treated with D-galactosamine, in which liver damage was so severe that treatment with glucagon and insulin was ineffective, the intraperitoneal administration of putrescine increased the survival rate in acute liver failure. This probably resulted mainly from activation of liver regeneration and possibly from a protective effect of putrescine on the liver.
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PMID:Effects of putrescine on D-galactosamine-induced acute liver failure in rats. 239 Oct 73

Female Sprague-Dawley rats were given 0, 168, 840, 2550 or 4200 mg/kg of 1,4-dioxane 21 and 4 h before sacrifice. Hepatic DNA damage (by the alkaline elution technique), ornithine decarboxylase activity (ODC), reduced glutathione content, cytochrome P-450 content and serum alanine aminotransferase activity (ALT) were determined. Treatment with 1,4-dioxane increased hepatic DNA damage and cytochrome P-450 content at doses of 2550 and 4200 mg/kg. Large increases in the activity of hepatic ODC were observed at 840, 2550 and 4200 mg/kg of 1,4-dioxane. Thus the data suggest that 1,4-dioxane is a weak genotoxic carcinogen in addition to being a strong promoter of carcinogenesis (a non-genotoxic carcinogen).
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PMID:Is 1,4-dioxane a genotoxic carcinogen? 239 85

Primary human hepatocytes were used to study bile salt hepatotoxicity and the hepatoprotective potential of ursodeoxycholate in vitro. Hepatocytes were obtained by collagenase perfusion of healthy human liver tissue and were treated with glycochenodeoxycholate for 24 hr 1 day after plating. Clear signs of cytotoxicity were observed at concentrations of about 100 mumol/L glycochenodeoxycholate. Toxicity was determined by release of alkaline phosphatase, gamma-glutamyl transferase, AST, ALT or lactate dehydrogenase into the culture medium, by measuring DNA synthesis of the cultured liver cells and by testing the viability of the hepatocytes using trypan-blue dye exclusion. Addition of ursodeoxycholate, which by itself proved to be of little toxicity, significantly reduced the hepatotoxic effects of glycochenodeoxycholate: 72% +/- 6% of the cells survived treatment with 500 mumol/L glycochenodeoxycholate alone, but addition of 100 mumol/L ursodeoxycholate increased the survival rate to 87% +/- 4% (p less than 0.05). Moreover, all enzymes tested were secreted at a significantly lower level when ursodeoxycholate was present. Similarly, the cellular DNA synthesis was maintained at significantly higher levels as a result of ursodeoxycholate treatment. We conclude that (a) primary human hepatocytes are a suitable model for studying hepatotoxicity of bile salts in vitro, (b) ursodeoxycholate reduces hepatotoxicity of other bile salts and (c) ursodeoxycholate can act hepatoprotectively by itself (i.e., alteration of the metabolism of other bile salts is not necessarily required).
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PMID:Ursodeoxycholate reduces hepatotoxicity of bile salts in primary human hepatocytes. 240 54

The influence of diets containing faba bean or casein as sources of protein were studied in rats at two stages of development. A significant impairment of growth rate, carcass, liver and skeletal muscle were found in young and adult rats fed for a period of 10 days on raw legume. Urinary urea output and the activities of three amino acid degrading enzymes: arginase, alanine aminotransferase and arginine succinate synthetase were all affected by the dietary protein and the stage of development. Urinary creatinine excretion was higher in the adult rats, while serum cholesterol was slightly increased in the young ones. Changes in plasma zinc may be attributed to a reduced zinc bioavailability to rats from the faba bean diet. Other biochemical parameters measured (glucose, triglycerides and plasma proteins) remained unchanged in all the experimental groups. Liver DNA and RNA content (mg/g tissue) decreased with age in both dietary groups, which were accompanied by an increase in tissue size. Furthermore, liver RNA concentration (primarily a measure of protein synthesis capacity) was enhanced in the adult legume fed rats. In this context, it is suggested that other organs (particularly muscle, with lower amino acid requirements for protein synthesis as a consequence of the stunting of growth) could contribute to increase the amino acid supply to liver in the animals fed on the faba bean diet.
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PMID:Induced biochemical and physiological changes in young and adult growing rats fed on a vegetable or animal protein diet. 243 60

We investigated the efficacy of a short course of prednisone therapy in 20 patients with histologic evidence of chronic active hepatitis B. Sixteen of 20 prednisone-treated patients who were initially serum hepatitis B virus DNA-positive had a transient elevation of their serum ALT activity on withdrawal of prednisone. Subsequently, 14 of these 16 patients (87.5%) became persistently negative for serum hepatitis B virus DNA, and 10 also lost their HBeAg. In addition, there was a significant fall in serum ALT levels and HBsAg titers up to 12 months of follow-up in the prednisone-treated group. Five of 20 (25%) prednisone-treated patients experienced a transient episode of hepatic decompensation coinciding with the peak of enzyme elevation. To contrast, only 3 of 15 (20%) initially hepatitis B virus DNA-positive matched untreated patients followed during the same time period became negative for serum hepatitis B virus DNA, and no significant changes in serum ALT values or HBsAg titers were noted over the 12-month study period. Thus, patients with chronic active hepatitis B appear to be responsive to immunologic manipulation with prednisone as indicated by a pronounced rebound immune response and clearance of hepatitis B virus DNA with improvement in liver disease activity.
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PMID:A pilot study on the effects of prednisone withdrawal on serum hepatitis B virus DNA and HBeAg in chronic active hepatitis B. 243 91

Two types of clinical events, acute exacerbation and uneventful course, precede spontaneous HBeAg seroconversion to its antibody (anti-HBe) in chronic type B hepatitis. To examine the possible mechanism responsible for these two types of clinical events, serial serum specimens from 75 patients who underwent spontaneous HBeAg seroconversion were assayed for hepatitis B virus DNA by slot blot hybridization with 32P-labeled cloned hepatitis B virus DNA as probe. Of these 75 patients, 47 (62.7%) had episodes of acute exacerbation (ALT greater than 300 IU per liter) within 3 months prior to HBeAg seroconversion. All of these 47 patients had high hepatitis B virus DNA levels (greater than 1,000 pg per ml) at the onset of acute exacerbation. Their serum hepatitis B virus DNA disappears shortly before or simultaneously with the HBeAg clearance in 27 patients (57.4%) and persisted but with decreasing levels for 2 to 40 months in 20 patients. Most of these patients had high alpha-fetoprotein levels or evidence of bridging hepatic necrosis. In contrast, the serum hepatitis B virus DNA was undetectable for a minimum of 3 (3-17) months in the 28 patients who had an uneventful course before HBeAg seroconversion. Twenty of these 28 patients had well-documented episodes of acute exacerbation with high hepatitis B virus DNA levels, but with normal alpha-fetoprotein and little evidence of extensive necrosis as far back as 6 to 27 months before HBeAg seroconversion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes of serum hepatitis B virus DNA in two types of clinical events preceding spontaneous hepatitis B e antigen seroconversion in chronic type B hepatitis. 243 1

Previous studies have shown that "xenobiotic" compounds such as the environmental pollutant alpha-hexachlorocyclohexane (alpha-HCH) and the synthetic sex steroid cyproterone acetate (CPA) induce growth of rat liver by hypertrophy and hyperplasia. After withdrawal of the growth stimuli, liver hypertrophy was usually found to be readily reversible. Conflicting observations were made concerning the fate of liver hyperplasia: hepatic hyperplasia persisted when induced by alpha-HCH but was found to be partially reversible when induced by CPA. The present study confirms the reversibility of hepatic hyperplasia induced by CPA in rats: about 30% of liver DNA present at maximal liver enlargement disappeared within 6 days after cessation of CPA treatment. Simultaneously, a dramatic increase in the rate of cell elimination by apoptosis was found. Glutamate-pyruvate transaminase and alkaline phosphatase in serum did not show major increases, suggesting that cell death was not due to lytic membrane damage. Furthermore, if treatment with CPA was continued or resumed, the enhanced DNA content persisted and the number of apoptotic bodies was greatly reduced. These observations suggest that the occurrence of cell death is due to withdrawal of the growth stimulus CPA. It may reflect a regulatory phenomenon serving to maintain homeostasis of cell number. Further studies showed that CPA is rapidly eliminated from rat liver and serum: t 1/2 in the liver is about 11 h. In contrast, alpha-HCH was previously found to be eliminated more slowly: t 1/2 approximately 144 h. The present study revealed that alpha-HCH, CPA and nafenopin lower the number of apoptotic bodies. This suggests that inducers of liver growth can inhibit hepatocellular death by apoptosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth, regression and cell death in rat liver as related to tissue levels of the hepatomitogen cyproterone acetate. 243 63

Seventy HBsAg-positive patients, including 24 with primary hepatocellular carcinoma, 34 with chronic active hepatitis, 12 with chronic persistent hepatitis and 30 asymptomatic healthy hepatitis B virus carriers were tested for anti-HBc IgM using the Corzyme-M test. Anti-HBc IgM was detected in 50% of the primary hepatocellular carcinoma patients, 26.5% of the chronic active hepatitis patients, 25% of the chronic persistent hepatitis patients, but in none of the healthy hepatitis B virus carriers. There was no correlation between the presence of anti-HBc IgM and HBeAg, hepatitis B virus DNA, ALT or alpha-fetoprotein levels in either the chronic active hepatitis or chronic persistent hepatitis patients. However, a significantly higher positive rate of anti-HBc IgM was noted in the HBeAg-positive or HBV DNA-positive primary hepatocellular carcinoma patients than in those with negative markers of viral replication, but no correlation was noted between the presence of anti-HBc IgM and serum ALT or alpha-fetoprotein levels in these primary hepatocellular carcinoma patients. Also, no differences in positivity for HBeAg, HBV DNA or levels of serum ALT were noted when patients with high titers of anti-HBc IgM were compared to those with low titers. Thus, anti-HBc IgM cannot distinguish between HBsAg-positive patients with chronic active hepatitis, chronic persistent hepatitis or primary hepatocellular carcinoma, does not correlate with serum ALT or alpha-fetoprotein levels and is only associated with markers for viral replication in primary hepatocellular carcinoma patients. Based on this, anti-HBc IgM appears to have a limited usefulness for diagnosis of either chronic hepatitis B or primary hepatocellular carcinoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is anti-HBc IgM a useful clinical test in patients with HBsAg-positive chronic hepatitis or primary hepatocellular carcinoma? 245 29


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