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 analyzed cancer mortality trends in 3282 elderly subjects from two general Italian populations with different life-style patterns taking part in the Cardiovascular Study in the Elderly (CASTEL). The aim of the study was to evaluate which predictors were able to influence cancer mortality. Age, gender, tobacco smoking, the presence of respiratory symptoms, increased serum levels of ALT and ALP, and the town of residence were powerful predictors. Subjects living in Chioggia (low income, rural) had significantly greater lung and liver cancer mortality, compared with those living in Castelfranco (industrial). The findings suggest that an incongruous life-style (smoking, alcohol consumption, poor hygienic conditions) may increase cancer mortality despite the favorable environmental conditions typical of rural Mediterranean areas.
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PMID:Cancer mortality trends in two cohorts of elderly people having different life-styles. 1033 38

The effects of cycloprodigiosin hydrochloride (cPrG-HCl), a new H(+)/Cl(-) symporter, were examined in liver cancer cell lines in vitro and in vivo. In the in vitro MTT assay, cPrG-HCl inhibited the growth of 6 liver cancer cell lines (Huh-7, HCC-M, HCC-T, dRLh-84, and H-35, hepatocellular carcinoma; HepG2, hepatoblastoma) in a dose- and time-dependent manner. The 50% inhibitory concentrations (IC(50)) at 72 hours' treatment for liver cancer cell lines were 276 to 592 nmol/L, while that for isolated normal rat hepatocyte was 8.4 micromol/L. The cPrG-HCl treatment of Huh-7 cells induced apoptosis as confirmed by the appearance of a subG(1) population, intranucleosomal DNA fragmentation, and chromatin condensation. cPrG-HCl raised the pH of acidic organelles and lowered pHi (below pH 6.8). In addition, the apoptosis in Huh-7 cells induced by cPrG-HCl was strongly suppressed when the cells were cultured with imidazole, a cell-permeable base. In the in vivo assay, nude mice bearing subcutaneous xenografted Huh-7 cells received 2 weeks of treatment with cPrG-HCl (1 or 10 mg/kg/d) subcutaneously. This treatment significantly inhibited tumor growth compared with the control after 8 days. The control mice were treated with 1% dimethylsulfoxide (DMSO) in saline (vehicle). A histopathological examination using the terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labeling (TUNEL) method showed apoptosis in the treated tumor cells. No pathological changes were observed in any organs, and the serum alanine transaminase levels remained within normal limits. These results suggest that cPrG-HCl may be useful for the treatment of hepatocellular carcinoma.
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PMID:Cycloprodigiosin hydrochloride, a new H(+)/Cl(-) symporter, induces apoptosis in human and rat hepatocellular cancer cell lines in vitro and inhibits the growth of hepatocellular carcinoma xenografts in nude mice. 1049 40

Chronic hepatitis C virus (HCV) infection is associated with a spectrum of liver diseases and a proportion of chronic cases progress through cirrhosis to hepatocellular carcinoma (HCC). The viral and host factors that are important in the clinical and histological progression of HCV infection are unclear. We investigated the effect of moderate (<80 g/day) and heavy (>80 g/day) alcohol intake on the histological and clinical progression of HCV infection and their associated risk of hepatic cancer in a group of Japanese patients. A number of other variables were assessed to evaluate their impact on disease progression. We recruited 120 patients with HCV infection and categorized them into four groups, based on alcohol consumption pattern. All clinical and biochemical profiles were collected from recorded files. Liver biopsies were analysed for the degree of fibrosis, presence of cirrhosis and histological activity of necroinflammation. Hepatic tumours were detected by the follow-up imaging analysis. There was no difference in the age, length of exposure to HCV infection and HCV RNA serum levels in the alcohol and alcohol-free groups. The histological grading of necroinflammation, serum levels of alanine aminotransferase and HCV RNA did not have any correlation with each other in the alcohol and alcohol-free group. There was a 1.5-2. 5-fold greater risk of liver cirrhosis and hepatocellular carcinoma in the alcohol intake group compared to the alcohol-free group. Kruskal-Wallis analysis among four groups demonstrated a significant transition to fibrosis (P < 0.05) for alcoholics with HCV infection. The increased risk of liver cancer in the alcohol group is independent of size and growth of tumours. The clinical manifestations of gastro-oesophageal variceal bleeding, ascites, and encephalopathy were also higher in the alcohol intake group. Alcohol consumption is an important risk factor in the histological and clinical progression of HCV infection and has no relation with HCV replication. Chronic HCV carriers should avoid excessive alcohol intake to reduce the acceleration of liver disease and risk of liver cancer.
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PMID:Effect of alcohol consumption on the progression of hepatitis C virus infection and risk of hepatocellular carcinoma in Japanese patients. 1086 50

In two cases of hepatic arterial flow interruption after hepatopancreatic surgery, continuous PGE(1) infusion from the superior mesenteric artery (SMA) was applied to oxygenate the liver through the portal vein. Case 1 was a 69-year-old woman with a non-functioning islet cell tumor of the pancreas. She underwent pancreatic resection following hepatic arterial infusion of anticancer drugs. Serum alanine aminotransferase (ALT) was elevated to 5500 IU/l on postoperative day (POD) 2; angiography revealed complete celiac artery obstruction. Continuous PGE(1) was administered from SMA at a rate of 0.01 &mgr;g/kg/min for 7 days. Serum ALT was normalized within 2 weeks and the peak level of serum total bilirubin (T. Bil) was 4.5 mg/dl. Case 2 was a 66-year-old man suffering from metastatic liver cancer. Complete obstruction of the proper hepatic artery was noted at the time of liver resection after hepatic arterial chemotherapy. Serum ALT was elevated to 2930 IU/l on POD 1, and PGE(1) infusion from SMA was done for the succeeding 7 days. Necrotic area was so vast that serum T. Bil rose to 19 mg/dl. However, it decreased with time. Both cases required 3 months for necrotic liver shrinkage. Doppler ultrasonography revealed that PGE(1) infusion actually increased portal blood flow. In conclusion, based on the preceding experimental backgrounds and clinical experiences, continuous PGE(1) infusion via the SMA can be a useful measure to prevent severe liver damage after hepatic arterial flow interruption through portal blood oxygenation.
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PMID:Two cases of hepatic artery interruption after hepatopancreatobiliary surgery treated by prostaglandin E(1) infusion via the superior mesenteric artery. 1264 44

Transarterial chemoembolisation of liver tumours is typically followed by elevated body temperature and liver transaminase enzymes. This has often been considered to indicate successful embolisation. The present study questions whether this syndrome reflects damage to tumour cells or to the normal hepatic tissue. The responses to 256 embolisations undertaken in 145 patients subdivided into those with hepatocyte-derived (primary hepatocellular carcinoma) and nonhepatocyte-derived tumours (secondary metastases) were analysed to assess the relative effects of tumour necrosis and damage to normal hepatocytes in each group. Cytolysis, measured by elevated alanine aminotransferase, was detected in 85% of patients, and there was no difference in the abnormalities in liver function tests measured between the two groups. Furthermore, cytolysis was associated with a higher rate of postprocedure symptoms and side effects, and elevated temperature was associated with a worse survival on univariate analysis. Multivariate analysis demonstrated that there was no benefit in terms of survival from having elevated temperature or cytolysis following embolisation. Cytolysis after chemoembolisation is probably due to damage to normal hepatocytes. Temperature changes may reflect tumour necrosis or necrosis of the healthy tissue. There is no evidence that either a postchemoembolisation fever or cytolysis is associated with an enhanced tumour response or improved long-term survival in patients with primary or secondary liver cancer.
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PMID:Postchemoembolisation syndrome--tumour necrosis or hepatocyte injury? 1456 11

Although hepatitis C virus (HCV)-related cirrhosis has been suggested as a risk factor for intrahepatic cholangiocarcinoma (ICC), few sizeable studies have tested this hypothesis. We investigated ICC risk factors, with special reference to HCV infection. We conducted a hospital-based case-control study including 50 ICC patients and 205 other surgical patients without primary liver cancer. HCV seropositivity was detected in 36% of ICC patients and 3% of controls. By univariate analysis, the odds ratio (OR) for association of anti-HCV antibodies with development was 16.87 (95% confidence interval (CI), 5.69 to 50.00). History of blood transfusion or diabetes mellitus, elevated serum total bilirubin, elevated aspartate aminotransferase and alanine aminotransferase, decreased serum albumin and decreased platelet count were identified as other possible ICC risk factors. By multivariate analysis, anti-HCV antibodies (adjusted OR, 6.02; 95% CI, 1.51 to 24.1), elevated alanine aminotransferase, decreased serum albumin, and decreased platelet count were found to be independent risk factors for ICC development. As liver status worsened, the adjusted OR for ICC tended to increase. HCV infection is a likely etiology of ICC in Japan.
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PMID:Hepatitis C virus infection as a likely etiology of intrahepatic cholangiocarcinoma. 1524 96

Using our ELISA kit for GST-alpha, we tested the serum GST-alpha levels of patients with hepatitis A, acute hepatitis B (HB), chronic active HB, chronic persistent HB and liver cirrhosis. Serum GST-alpha levels in all these groups of patients were significantly higher than those in the controls (P < 0.01). Serum GST-alpha levels was closely (P < 0.01) correlated with serum alanine transaminase (ALT) levels in various groups of patients except chronic persistant HB. The combined application of the two markers, GST-alpha and ALT, raised the sensitivity of detection for liver diseases. In detection of chronic persistent HB patients, the GST-alpha marker was more sensitive than ALT (P < 0.01). The follow-up data of GST-alpha and ALT markers in serum showed that the GST-alpha level could reflect the clinical progression of liver disease more exactly as observed in 79 liver cancer patients in then GST-alpha and ALT positive rate were 81% and 61% respectively (P < 0.01). In 30 persons with positive HBsAg, the positive rates of GST-alpha and ALT were 70% and 37%, respectively. These results indicated that, (1) the detection of GST-alpha combined with ALT was capable of increasing the sensitivity for recognizing hepatocellular damage; (2) the elevation of serum GST-alpha level mainly resulted from the increased expression of GST-alpha in liver cells during hepatocarcinogenesis, thus, the GST-alpha is thought to be a tumor marker for liver cancer; (3) GST-alpha measurement offers advantage over ALT for the detection of minor degree of hepatocellular damages. GST-alpha may act as an early, sensitive and specific enzyme marker.
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PMID:[Studies on the relationship between purified alpha class glutathione S-transferase (GST-alpha) and hepatocellular damage]. 1561 36

Inactive carriers forms the largest group in chronic HBV infected patients. Around 300 million people are inactive carriers The inactive HBsAg carrier state is diagnosed by absence of HBeAg and presence of anti-HBe, undetectable or low levels of HBV DNA in PCR-based assays, repeatedly normal ALT levels, and minimal or no necroinflammation, slight fibrosis, or even normal histology on biopsy. Inactive cirrhosis may be present in patients who had active liver disease during the replicative phase of infection. The prognosis of the inactive HBsAg carrier state is usually benign. Long-term follow- up (up to 18 years) of these carriers has indicated that the vast majority show sustained biochemical remission and very low risk of cirrhosis or hepatocellular carcinoma (HCC). Rarely, patients, even noncirrhotics, may develop liver cancer during the inactive HBsAg carrier state. In addition, approximately 20 to 30% of persons in the inactive HBsAg carrier state may undergo spontaneous reactivation of hepatitis B during follow-up. Multiple episodes of reactivation or sustained reactivation can cause progressive hepatic damage and even hepatic decompensation.
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PMID:Hepatitis B virus: inactive carriers. 1619 Nov 99

Hepatitis C is a major public health problem. General screening is not advisable and should be limited to risk groups. The gold standard for the assessment of disease severity is liver biopsy. AST and ALT do not correlate with histology. Serum HCV RNA by qualitative assay and HCV genotype should be determined prior to therapy. Response to antiviral therapy should be assessed by testing AST, ALT and qualitative HCV RNA. Repeat liver biopsy is not necessary. The incidence of HCC related to HCV infection is rising. Early detection by a cost effective screening program is essential. In patients with liver cirrhosis caused by hepatitis C, alpha fetoprotein and liver sonography should be done every 6 months. Upper GI endoscopy is recommended every 1-4 years in cirrhotic patients. Over 350 000 000 people are infected with HBV worldwide, and chronic HBV infection is the leading cause of liver cancer and tenth leading cause of death. HBs Ag, HBeAg and HBV DNA positive patients should be monitored for 6 months before treatment. Patients treated with antiviral therapy should be tested for HBAg, HBeAg and HBV DNA at the end of treatment and every 6 months thereafter to assess virologic response. Monitoring of serum HBV DNA is done by PCR. Patients treated with lamivudine should be tested for YMDD mutation. Ultrasound and AFP monitoring are recommended for detection of HCC, but results are not always reliable. Approximately 40% -70% of HIV infected patients have coinfection with HCV, HBV and HDV. HIV/HCV coinfected patients have an increased risk of progressive liver disease and should be treated accordingly.
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PMID:[Monitoring patients with chronic hepatitis during and after therapy]. 1638 Dec 36

Twenty-one patients with chronic hepatitis C were treated with a mistletoe preparation as monotherapy (either Iscador or Abnoba viscum) during one year. The treatment was well tolerated. Patients entering the study with elevated transaminases had a significant improvement, both for AST (aspartate aminotransferase) (p = 0.01) and for ALT (alanine aminotransferase) (p = 0.04). Quality of life significantly improved (p = 0.006) in patients with a low initial quality of life. Although one patient obtained a complete virological response, few effects on viral load were seen in the whole group. These results suggest an effect comparable to glycyrrhicin treatment: improvement of liver inflammation and thus possibly reduction of the long term complications, viz cirrhosis and liver cancer. Mistletoe preparations have the advantage of easy administration and low cost.
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PMID:Exploratory study on the effects of treatment with two mistletoe preparations on chronic hepatitis C. 1643 29


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