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)

A serial prospective study of cellular immunity to HBsAg and liver-specific membrane lipoprotein was undertaken in 21 adults with acute hepatitis type B. Cellular immunity to HBsAg as determined by leucocyte migration inhibition with partially purified HBsAg as antigen was detected in all the patients during the recovery phase of the illness and was already detectable at the time of admission in 13 (62%) of the cases. In five of the remaining eight the titre of HBsAg in the serum at this time was high and in the whole series there was an inverse correlation between the degree of migration inhibition on admission and the peak HBsAg titre suggesting that antigen or possibly antigen/antibody complexes might be interfering with the demonstration of cellular immunity in vitro. Using a combination of minimum migration index recorded during the recovery period peak HBsAg titre, it was possible to compute the peak aspartate aminotransferase level with reasonable accuracy, a finding consistent with the hypothesis that the severity of the illness is related to both the number of infected hepatocytes and the vigour of the immune response to HBsAg. Evidence of an immune response to the liver-specific hepatocyte membrane lipoprotein was present in 50% of the patients tested at the time of admission, but was transient, having disappeared in every case by four weeks. The minimum migration index recorded with HBsAg as antigen was significantly lower in those with detectable sensitisation to the lipoprotein and it is possible that this autoimmune reaction is also generated by the interaction of T cells with viral antigenic determinants on the liver cell surface.
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PMID:Immune responses to the hepatitis B surface antigen and liver-specific lipoprotein in acute type B hepatitis. 85 83

A retrospective study concerning ten patients with autoimmune hepatitis (AiH), diagnosed during a 2 1/2-year period is presented. The age of the patients ranged from 25 to 82 years and nine of the patients were women. Their symptoms included jaundice, pruritus, fever, anorexia and fatigue during a few weeks to years. Seven patients had increased serum aspartate aminotransferase (ASAT) levels. The three patients with normal ASAT levels had hypoalbuminaemia, decreased level of prothrombin or high levels of serum immunoglobulin G. Moderate or high levels of smooth muscle antibody titer were detected in nine patients, while none had increased levels of anti-nuclear antibody titer. Histological features of moderate or severe chronic active hepatitis were demonstrated in nine patients. One patient presented with clinical and histological features of acute hepatitis. Prednisolone therapy was followed by biochemical improvement in all the patients. In one patient, maintenance therapy with prednisolone was combined with azathioprine.
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PMID:[Autoimmune hepatitis. Forms of manifestation, diagnosis and treatment]. 141 30

Because of widely differing reports on the significance of IgM anti-HBc in chronic hepatitis B virus (HBV) infection, paired sera and liver biopsies from 49 patients with chronic HBV infection were analysed for serum IgM anti-HBc, HBsAg titre, HBeAg/anti-HBe, HBV DNA, serum aspartate transaminase, intrahepatic HBcAg expression, and liver histology. High levels of IgM anti-HBc, in the diagnostic range of acute hepatitis B (greater than 1.2), were detected in seven patients (14.3%) and a total of 34 patients (69.6%) had an index of more than 0.2. No correlation was found between IgM anti-HBc and the serum markers of active viral replication or HBsAg titre but it correlated significantly with intrahepatic expression of cytoplasmic HBcAg (r2 = 0.165, P = 0.002). IgM anti-HBc also correlated with active liver histology (P = 0.015) but there was a considerable overlap of the IgM anti-HBc index values between the various disease groups, indicating a poor specificity. Serial assessment of IgM anti-HBc in eight patients treated with interferon-alpha (four responders) showed an increase in IgM anti-HBc in three out of four patients corresponding to the e-seroconversion period followed by a drop in IgM anti-HBc levels. However, an increase in IgM anti-HBc was also seen in one non-responder, indicating that this feature is not unique to interferon-alpha responders. These data indicate that serum IgM anti-HBc cannot be used alone as a certain diagnostic measure of HBV replication nor in the prediction of liver histology.
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PMID:Significance of serum IgM anti-HBc in chronic hepatitis B virus infection. 157 87

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

Using blood chemistry data from 77 cases of hypernutritional fatty liver diagnosed in our gastroenterological clinic, an automated quantitative interpretation was formulated. The reliability of this interpretation was confirmed in view of the following points: 1) Comparison with the degree of fatty infiltration of the liver seen in biopsy specimens or ultrasonographic findings. 2) The high rate of coincidence, sensitivity and specificity among the results. 3) Localization of almost all the cases of fatty or non-fatty liver into circumscribed areas by the value of standard deviation index (SDI) of glutamic oxaloacetic transaminase (GOT) i.e. aspartate aminotransferase (AST) and cholinesterase (CHE), respectively. 4) Graphic display of data and interpretation of a representative case of acute hepatitis at specified stages, and the comparison of this interpretation with clinical diagnoses and course of the disease. Moreover, two possible mechanisms for the elevation of the CHE level were discussed.
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PMID:Interpretation of patho-physiology by laboratory data (4). Cases of hypernutritional fatty liver. 178 Sep 13

The activities of serum malate dehydrogenase (MDH) and its mitochondrial isoenzyme (MDHm) were studied in sera of patients with liver disease. They proved to be more useful than those of aspartate aminotransferase (AST) and its mitochondrial isoenzyme for detection of hepatocellular carcinoma and acute circulatory failure, and for estimation of the severity of acute hepatitis. The N/T value measuring system, which is adaptable for autoanalysis and allows simultaneous determination of activities depending on NAD and thionicotinamide adenine dinucleotide (thio-NAD), yields both the total activity of MDH and the N/T value which was correlated significantly with MDHm/MDH (r = 0.748). Assay of MDH and its mitochondrial isoenzyme in association with the N/T value measuring system seems to be more useful and less time consuming for estimation of the severity of liver diseases than that of AST and its mitochondrial isoenzyme.
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PMID:Clinical usefulness of malate dehydrogenase and its mitochondrial isoenzyme in comparison with aspartate aminotransferase and its mitochondrial isoenzyme in sera of patients with liver disease. 217 15

Southern Taiwan experienced a dengue (type 1) outbreak in the autumn of 1988. One hundred and thirteen febrile patients suspected as having dengue infection were seen in the emergency room of the Kaohsiung Medical College Hospital. These patients were recruited for this study. Two hundred and eighty-six sequential serum aspartate transaminase (AST) and alanine transaminase (ALT) data from these patients were analyzed. Data analysis showed serum AST had increased daily and all data were out of normal range from day 6 of the illness. Compared to the AST level on the first day of the illness, the AST level was noted to elevate to an average of 9.25 folds on day 6. The sequential changes of AST were as follows: AST had elevated since the third ill-day in most cases and reached a peak on the 7th or 8th ill-day. It then declined gradually from the 8th ill-day and became normal about 3 weeks later. The changes of ALT level were about the same as AST but had later onset and lower peak. Abdominal sonographic examinations showed thickening of the gall bladder wall, splenomegaly and ascites in some patients during acute stage of the illness and recovered completely after patients recovered from the dengue attack. The sequential change of serum transaminase levels and sonographic findings were compatible. These findings may be used as a reference for the differential diagnosis among dengue fever, acute hepatitis and acute cholecystitis.
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PMID:Sequential changes of serum transaminase and abdominal sonography in patients with suspected dengue fever. 221 70

Argininosuccinate synthetase is an enzyme which has been found to be a specific marker for liver damage. In patients with acute hepatitis, the concentration in serum increases at the onset of the disease, but later decreases more quickly, so that the time required for normalization is shorter than that of alanine aminotransferase. This is probably caused by rapid clearance of argininosuccinate synthetase from the serum. Rapid clearance was demonstrated in experimental animals given purified enzymes intravenously. Argininosuccinate synthetase disappeared from the serum with a half life of about 15 min, while the half lives of alanine aminotransferase and aspartate aminotransferase were 4 and 5 h, respectively, under the same conditions.
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PMID:Clearance of argininosuccinate synthetase from the circulation in acute liver disease. 237 28

Although case reports of herpes simplex virus (HSV) causing acute hepatitis in otherwise healthy adults have appeared recently in the literature, a prospective study of the incidence of HSV-hepatitis in the general population hitherto has not been reported. In the present study, serum samples from 124 young adults attending a sexually transmitted disease clinic with either genital herpes infections (n = 86) or non-herpes sexually transmitted diseases (n = 38) (controls) were analyzed for liver enzyme abnormalities (including aspartate aminotransferase [AST] and alanine aminotransferase [ALT]). Twelve of eighty-six (14%) herpes-infected patients had mildly abnormal liver enzyme tests (less than or equal to twice the upper limit of normal) as opposed to only 1 of 38 controls (2.6%), (P less than .05). All individuals in the herpes-hepatitis group were anicteric, and only two complained of constitutional symptoms (malaise and fatigue). Liver enzyme tests were repeated in nine herpes-hepatitis patients 1 week after their genital lesions had resolved, and in six of nine patients the results had returned to within normal limits. Four patients subsequently returned at the onset of a recurrence of their genital herpes. In all four, serum ALT levels were elevated from the previous occasion, and in three of the four levels just exceeded the upper limit of normal. One patient was followed through three recurrences of his genital herpes. In that individual, the extent of liver enzyme abnormalities appeared to correlate with the presence or absence of his genital lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Genital herpes and hepatitis in healthy young adults. 301 68

A group of 295 adult male patients from Cairo, Egypt, with acute hepatitis were studied. Acute hepatitis A was diagnosed in 8 patients (2.7%), hepatitis B in 115 (38.9%), delta infection in 19 (6.4%) and possible Epstein-Barr virus or cytomegalovirus-mediated hepatitis in 7 patients (2.4%). The remaining 146 patients (49.5%) were considered to have hepatitis non-A non-B. The clinical presentation of the various causes of hepatitis was similar, although patients with hepatitis B and delta infection had significantly higher mean alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels than patients diagnosed as having hepatitis non-A non-B. Various risk factors for the acquisition of hepatitis were evaluated. A history of an injection for medical treatment and a history of anti-schistosomal therapy were significantly associated with delta infection when compared to patients with either hepatitis B or non-A non-B (P less than 0.05). Hepatitis non-A non-B is a major cause of acute hepatitis in adults living in Cairo, and an iatrogenic source of infection may be important in the epidemiology of delta infection.
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PMID:Acute sporadic hepatitis in adults living in Cairo, Egypt. 309 92


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