Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-eight (5.0%) of 966 healthy Zambian blood donors were positive for hepatitis B surface antigen (HBsAg) when tested by the turkey erythrocyte passive haemagglutination (TEPHA) method. Twenty-six were investigated in detail, but only one blood donor was found to have liver disease, and this was thought unlikely to be causally related to HBsAg (alcohol-induced fatty infiltration). It is recommended however, that blood donors should be screened for HBsAg. Positive individuals should be rejected but their serum tested for aspartate transaminase (AST), and, if elevated, a liver biopsy performed. This ideal policy is not practicable in all tropical hospitals.
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PMID:Hepatitis B surface antigenaemia: incidence and significance in Zambian blood donors. 26 76

Response to hepatitis B virus (HBV) infection [HBV surface antigen (HBsAg) and antibody to HBsAg (anti-HBs)], serum iron, total iron-binding capacity, hematological status (erythrocytes, Hb, and hematocrit), and evidence of liver damage (serum glutamic pyruvic transaminase; aspartate aminotransferase, L-aspartate:2-oxoglutarate aminotransferase, EC 2.6.1.1) were determined for 201 patients on chronic renal dialysis. Four factors-serum iron level, transminase level, sex, and HBV response [i.e., infected-HBsAg(+) (HBsAg positive), anti-HBs(+) (anti-HBs positive), or no response]-were analyzed simultaneously to test the hypothesis that serum iron is higher in those with HBsAg in their serum than in those without HBsAg, independent of the transaminase level. Four independent, statistically significant two-factor interactions were identified. (i) Serum iron is higher in those HBsAg(+). (ii) Serum iron is higher in those with increased transaminase. (iii) Transaminase is higher in those HBsAg(+). (iv) Males are more likely to be HbsAg(+) and females are more likely to be anti-HBs(+). Also, those who are HBsAg(+) have significantly higher percent iron saturation (serum iron/total iron-binding capacity). That is, the hypothesis was supported by the findings. Several additional biological hypotheses are suggested, including a possible role of increased iron levels in susceptibility and response to HBV infection and the possible relationship between higher iron levels and the likelihood of HBV infection progressing to primary hepatocellular carcinoma. In addition, further tests of the initial hypothesis in nonhospitalized populations with endemic HBV infection are proposed.
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PMID:Serum iron levels and response to hepatitis B virus. 28 82

A prospective, double blind placebo-controlled trial was carried out on twenty-nine patients with hepatitis B. Thirteen received transfer factor and sixteen placebo. There were no significant differences between the two groups in any clinical or laboratory measurements made, although a rapid early reduction of serum aspartate transaminase levels by transfer factor is possible. Similarly, no significant changes were delineated by the in vitro measurements of lymphocyte function. Transfer factor did not alter the natural course of hepatitis B.
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PMID:Transfer factor and hepatitis B: a double blind study. 47 25

Eight patients with chronic hepatitis B infection (seven with chronic active hepatitis and one with chronic persistent hepatitis) were treated with daily intramuscular injections of human leucocyte interferon for periods of 5 to 8 weeks and in one case for 5 months. In one patient there was a marked fall in virus-associated DNA polymerase activity and in the number of DNA containing viral particles during each of two courses of interferon. Hepatitis Be antigen (HBeAg) also disappeared, the aspartate transaminase levels fell and liver histology improved. In the four other patients with detectable DNA polymerase activity there was an early fall but this was transient and in one of these patients there was a continuing rise in activity despite treatment. One other patient became HBeAg negative but hepatitis B surface antigen (HBsAg) titres were mostly unaffected by treatment. A marked decrease in T-lymphocyte mediated cytotoxicity towards HBsAg coated target cells was demonstrated and raises the possibility that an immunosuppressant action of interferon may offsets its direct anti-viral action but may also account for the improvement in liver function which occurred in some patients.
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PMID:Effects of human leucocyte interferon on hepatitis B virus replication and immune responses in patients with chronic hepatitis B infection. 50 26

Six patients with hepatitis B surface antigen-positive (HBsAg-pos) chronic liver disease have been treated with transfer factor (TF) prepared from leucocytes of normal blood donors with no history of hepatitis, and with TF from subjects recently recovered from type B hepatitis. In three patients there were transient elevations of aspartate transaminase (AsT) after 'specific' TF, representing damage or destruction of hepatocytes, and in two of these patients there was coincidental complement consumption, suggesting that TF had stimulated production of antibody. In one other patient there was an increase in E-rosetting lymphocyte (ERL) concentration representing a change in T-lymphocyte reactivity. One of the two patients who had no measured response to TF had a primary liver cell carcinoma and was receiving prednisolone therapy. TF prepared from subjects who have recently recovered from type B hepatitis may have temporarily altered the immunological status of patients with HBsAg-pos chronic liver disease, but it did not have a beneficial therapeutic effect.
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PMID:Transfer factor in the attempted treatment of patients with HBsAg-positive chronic liver disease. 60 32

Cellular immunity to the hepatitis B surface antigen (HBsAg) and a liver-specific lipoprotein was studied, using the leucocyte migration test, in 38 asymptomatic blood donors found to have HBsAg in the serum. Sensitization to HBsAg was found in 26% and was related to the presence of liver damage, being detected in 47% of those with elevated serum aspartate aminotransferase but in only 13% with normal enzyme levels. The frequency of sensitization to this antigen in those with chronic persistent or chronic aggressive hepatitis on biopsy was also higher than in those with unrelated or minimal changes. The findings using the liver-specific lipoprotein as antigen were similar and there was a correlation between the results obtained with this and the hapatitis B surface antigen. This study supports the hypothesis that a T-lymphocyte response to hepatitis B virus antigen can initiate an autoimmune reaction to antigens such as liver-specific lipoprotein on the hepatocyte surface, and that this reaction may be of importance in the production of chronic liver damage. In the absence of the T-cell response, the autoimmune reaction cannot occur and the virus is able to establish a harmless symbiotic union with the host.
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PMID:Cell-mediated immunity to hepatitis B surface antigen in blood donors with persistent antigenaemia. 108 Jan 25

Two hundred and forty-three patients receiving renal replacement therapy (RRT) and 20 renal unit staff were tested for antibodies to hepatitis C (HCV). Three patients (1.2%) were positive by the first generation test kit, the lowest rate in patients receiving RRT reported in the literature to date. These three, and eight other patients tested positive by the second generation kit, a prevalence rate of 4.5%. Anti-HCV antibody positivity was associated with higher mean serum alanine aminotransferase (p = 0.0003) and aspartate aminotransferase (p = 0.018) levels. However, only one of the 11 anti-HCV positive patients had liver transaminase levels more than twice the upper limit of the laboratory reference range. Anti-HCV positivity was associated with a higher mean number of units of blood transfused (p = 0.035). None of 20 staff were anti-HCV positive. Twenty-five of 212 (11.7%) patients reported a history of liver disease; none of these were anti-HCV positive. Hepatitis B surface antigen was detected in eight of 215 (3.7%) patients, of which three were e antigen positive. There was evidence of past hepatitis B infection in 53 of 215 (24.7%) patients, more frequently in Maoris (p = 0.001). Overall, significantly raised liver transaminases were present in three of 198 (1.5%) patients and in no staff. This unit has a remarkably low prevalence of antibodies to HCV, an observation supported by the low rate of abnormal serum liver enzymes.
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PMID:Prevalence of antibodies to hepatitis C virus in patients receiving renal replacement therapy, and in the staff caring for them. 128 95

The impact of dengue on liver function was studied by biochemical tests on 125 male and 145 female patients diagnosed with this disease during an outbreak that extended from November 1987 to December 1988. Abnormal levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, alkaline phosphatase, and gamma-glutamyl transpeptidase (G-GT) were observed in 93.3%, 82.2%, 7.2%, 16.3% and 83.0% of the patients, respectively. The elevation of transaminases was mild to moderate in most cases, but was 10-fold greater than the normal upper limit for AST and ALT in 11.1% and 7.4% of the patients, respectively. Initially, the level of AST was greater than that of ALT, increasing to maximum levels nine days after the onset of symptoms, then decreasing to normal levels within two weeks. Results of the biochemical tests did not differ significantly between the cases with and without hepatitis B or hepatitis C virus infection, but significantly higher elevations of AST, ALT, and G-GT were observed in patients with episodes of bleeding. Liver biopsies of two patients showed features of lobular hepatitis. Of the five fatal cases, three died of hepatic failure. It is concluded that dengue fever may cause hepatic injury and transaminase elevation similar to that in patients with conventional viral hepatitis. In epidemic or endemic areas, dengue fever infection should be considered in the differential diagnosis of hepatitis.
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PMID:Liver biochemical tests and dengue fever. 135 50

To evaluate indications for new therapies such as liver transplantation and antiviral therapy, survival of histologically proven hepatitis B surface antigen (HBsAg)-positive cirrhosis of the liver was assessed in a cohort of 98 patients followed up for a mean of 4.3 years. The overall survival probability was 92% at 1 year, 79% at 3 years, and 71% at 5 years. Variables significantly associated with the duration of survival were age, serum aspartate aminotransferase levels, presence of esophageal varices, and all five components of the Child-Pugh index (bilirubin, albumin, coagulation factors, ascites, encephalopathy). Multivariate analysis showed that only age, bilirubin, and ascites were independently related to survival. Survival of patients with decompensated cirrhosis (determined by the presence of ascites, jaundice, encephalopathy, and/or a history of variceal bleeding) and those with compensated cirrhosis at 5 years was 14% and 84%, respectively. For patients with compensated liver cirrhosis, hepatitis B e antigen (HBeAg) positivity was also a prognostic factor with a 5-year survival of 72% for HBeAg-positive cirrhosis and 97% for HBeAg-negative cirrhosis; the risk of death was decreased by a factor of 2.2 when HBeAg seroconversion occurred during follow-up. It is concluded that liver transplantation should be considered for patients with decompensated HBsAg-positive liver cirrhosis and antiviral therapy for patients with HBeAg-positive compensated cirrhosis.
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PMID:Survival and prognostic indicators in hepatitis B surface antigen-positive cirrhosis of the liver. 142 89

We report the development of severe hepatotoxicity in a patient on zidovudine therapy who received 3.3 g of acetaminophen in less than 36 hours. Three days later, the patient's serum aspartate aminotransferase level was 5,724 U/L, alanine aminotransferase was 3,124 U/L, lactate dehydrogenase was 12,675 U/L, alkaline phosphatase was 84 U/L, and total bilirubin was 20 mumol/L. These values substantially improved over the ensuing 4 days. Serologic results for hepatitis B, hepatitis A, and cytomegalovirus were all negative. The pattern and time sequence of transaminase elevation in this patient are consistent with acute acetaminophen hepatotoxicity, especially since zidovudine-induced hepatotoxicity is described as producing cholestasis rather than acute hepatitis. We hypothesize that our patient's susceptibility to acetaminophen-dependent hepatotoxicity may have been augmented by competitive utilization of glucuronidation by other drugs such as zidovudine and/or trimethoprim-sulfamethoxazole with subsequent increased cytochrome P450-dependent metabolism of acetaminophen. Additionally, due to malnutrition and/or to human immunodeficiency virus infection per se, our patient may have had decreased hepatic reserves of glutathione with which to conjugate the toxic acetaminophen product of the P450 system. Although severe acetaminophen-associated hepatotoxicity has not previously been reported in patients receiving zidovudine, we suggest that clinicians be aware of this potential interaction and counsel malnourished patients, especially those with concomitant hepatic disease, to exercise caution when taking both these medications.
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PMID:Severe hepatotoxicity in a patient receiving both acetaminophen and zidovudine. 836 34


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