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)

Quantitative determination of LP-X, abnormal serum low density lipoprotein, was performed on the sera of 620 patients with jaundice in two medical centers, one in Oklahoma City, Oklahoma, and the other in Birmingham, England. The results of serial assays over a period of 5 to 8 days after patient admission to hospital or after onset of jaundice, if this occurred in hospital, correlated best with the type and management of jaundice. In some cases of early cholestatic disease of extrahepatic origin LP-X may be absent, but after the observation period it was found that only 1 of 81 (98%) patients with obstruction of the extrahepatic bile duct system remained negative. Of the remainder, 74 (91%) had or developed levels of LP-X exceeding 300 mg per 100 ml. In addition, 43 (88%) of 49 subjects followed serially showed increases in LP-X concentration, with no change in 3 patients. Of 539 subjects with intrahepatic disease, 14 (26.5%) were LP-X positive and 27 (19.4%) of these had initial LP-X levels higher than 300 mg per 100 ml. During the follow-up period, 35 (74%) of 47 patients with intrahepatic disease showed a reduction of LP-X; of the remaining 12 patients 4 had mitochondrial antibody-positive primary biliary cirrhosis, and 6 had severe cholestasis associated with acute infectious hepatitis and high aspartate transaminase levels. Similar figures for alkaline phosphatase showed less consistent changes during the follow-up period. In this retrospective appraisal the trends and absolute levels of LP-X, in addition to the use of similarly followed levels of the routine liver function tests, allowed better differentiation of jaundice requiring surgical correction from that remediable by medical means exclusively than did the use of the routine liver function tests alone. In addition, LP-X is specific for liver dysfunction, whereas other routine liver function tests are not.
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PMID:Utilization of the quantitative assay of lipoprotein X in the differential diagnosis of extraphepatic obstructive jaundice and intrahepatic diseases. 17 11

A standard preparation of immune serum globulin containing a titer of immune adherence hemagglutination hepatitis A antibody of 1:3,200 neutralized the infectivity of MS-1 serum. An inoculation of MS-1 serum was followed by the following evidence of hepatitis A infection in eight of 14 seronegative recipients: (1) abnormal values for serum aspartate aminotransferase after an incubation period of 29-42 days, and (2) no detectable immune adherence hemagglutination hepatitis A antibody (less than 1:5) before exposure, and an eightfold or greater increase in antibody titer during convalescence. In contrast, inoculation of the mixture of MS-1 serum and immune serum globulin was followed by (1) normal values for aspartate aminotransferase in all eight seronegative recipients, and (2) evidence of an antibody response (indicating subclinical infection) in two of the eight. Under the conditions of this study, the use of the preparation of immune serum globulin described prevented or modified hepatitis A infection.
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PMID:Effect of human immune serum globulin on infectivity of hepatitis A virus. 18 98

Serum biochemical parameters were studied in 42 healthy wild-caught adult tamarins (S. mystax), males and females, to determine the normal values. Blood samples were drawn repeatedly, and the serum was tested for aspartate aminotransferase, alanine aminotransferase, isocitric dehydrogenase, serum glucose, serum urea, triglyceride, cholesterol, albumin, and total protein. The results indicated that serum chemistry values were similar to those reported as normal for both humans and other Callitrichidae species. The study of serum biochemical parameters in tamarins with experimental hepatitis A indicated that serum enzyme activities alone reflected the hepatic damage, while other biochemical parameters were of no real clinical importance. The experimental results showed the levels of serum urea to be indicative of the pathological involvement of the kidneys in experimental hepatitis A in some cases.
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PMID:[The biochemical indices of the blood serum in experimental hepatitis A in tamarins]. 132 56

Hepatitis A is an acute, necroinflammatory disease of the liver which results from infection by the hepatitis A virus (HAV). The mean incubation period is approximately 30 days. Although the disease is usually self-limited, the severity of illness is age-dependent. In children, hepatitis A is usually asymptomatic, while in adults, symptomatic infection is characteristic and jaundice is common. Fulminant hepatitis A is rare and is also age-dependent. The onset of hepatitis A is often abrupt and characteristic prodromal symptoms are followed, within a few days to a week, by dark urine and jaundice. Mild to moderate tenderness over an enlarged liver is usually detected. Serum alanine and aspartate aminotransferase levels usually both rise rapidly during the prodromal period, reach peak levels and then decrease by approximately 75% per week. Serum bilirubin concentrations reach peak levels later and decline less rapidly than serum aminotransferases. Nonetheless, the period of jaundice persists for < 2 weeks in approximately 85% of cases. Nearly all adult patients with clinically apparent disease experience complete clinical recovery with restoration of normal serum bilirubin and aminotransferase values by 6 months. Relapses and prolonged cholestasis are unusual manifestations of hepatitis A, and even in these circumstances, recovery is the rule and chronic hepatitis is not seen. The diagnosis of hepatitis A requires the detection of immunoglobulin M antibody to HAV in a patient who presents with, or has recently had, clinical features of hepatitis (icteric or anicteric disease) or in an individual with inapparent, asymptomatic infection in whom serum aminotransferase elevations may be detected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical manifestations and diagnosis of hepatitis A virus infection. 133 49

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

A 71-yr-old male presented with a 2-month history of fever, malaise, and weight loss. Physical exam revealed chorioretinitis. Laboratory studies were notable for elevated levels of alkaline phosphatase, gamma-glutamyl transpeptidase, aspartate transaminase, and alanine transaminase. Immunoglobulin G antibody to Toxoplasma gondii was positive to a dilution of 1:4096, whereas serologic studies for hepatitis A virus, hepatitis B virus, cytomegalovirus, Epstein-Barr virus, human immunodeficiency virus, Brucella, and Tularemia were negative. A percutaneous biopsy of the liver revealed hepatic granulomas. Culture of the biopsy specimen was negative for growth of mycobacteria or fungi. Spontaneous improvement in clinical and laboratory parameters occurred over a 4-month period.
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PMID:Toxoplasmic chorioretinitis and hepatic granulomas. 222 Jul 41

The effect of PG on patients with fulminant and subfulminant viral hepatitis (FHF) was studied. 17 patients presented with FHF secondary to hepatitis A (n = 3), hepatitis B (n = 6), and non-A, non-B (NANB) hepatitis (n = 8). 14 of the 17 patients had stage III or IV hepatic encephalopathy (HE). At presentation the mean aspartate transaminase (AST) was 1,844 +/- 1,246 U/liter, bilirubin 232 +/- 135 mumol/liter, prothrombin time (PT) 34 +/- 18, partial thromboplastin time (PTT) 73 +/- 26 s, and coagulation Factors V and VII 8 +/- 4 and 9 +/- 5%, respectively. Intravenous PGE1 was initiated 24-48 h later after a rise in AST (2,195 +/- 1,810), bilirubin (341 +/- 148), PT (36 +/- 15), and PTT (75 +/- 18). 12 of 17 responded rapidly with a decrease in AST from 1,540 +/- 833 to 188 +/- 324 U/liter. Improvement in hepatic synthetic function was indicated by a decrease in PT from 27 +/- 7 to 12 +/- 1 s and PTT from 61 +/- 10 to 31 +/- 2 s, and an increase in Factor V from 9 +/- 4 to 69 +/- 18% and Factor VII from 11 +/- 5 to 71 +/- 20%. Five responders with NANB hepatitis relapsed upon discontinuation of therapy, with recurrence of HE and increases in AST and PT, and improvement was observed upon retreatment. After 4 wk of intravenous therapy oral PGE2 was substituted. Two patients with NANB hepatitis recovered completely and remained in remission 6 and 12 mo after cessation of therapy. Two additional patients continued in remission after 2 and 6 mo of PGE2. No relapses were seen in the patients with hepatitis A virus and hepatitis B virus infection. Liver biopsies in all 12 surviving patients returned to normal. In the five nonresponders an improvement in hepatic function was indicated by a fall in AST (3,767 +/- 2,611 to 2,142 +/- 2,040 U/liter), PT (52 +/- 25 to 33 +/- 18 s), and PTT (103 +/- 29 to 77 +/- 44 s), but all deteriorated and died of cerebral edema (n = 3) or underwent liver transplantation (n = 2). These results suggest efficacy of PGE for FHF, and further investigation is warranted.
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PMID:Biochemical and clinical response of fulminant viral hepatitis to administration of prostaglandin E. A preliminary report. 279 44

Normal ranges for gamma glutamyl transferase (GGT) in chimpanzees were determined and categorized according to age and sex. Enzyme patterns presented for 36 cases of non-A, non-B (NANB) hepatitis and compared to others with hepatitis A and/or B show that the response of this enzyme to these viral agents in chimpanzees is comparable to that seen in human patients. The value of GGT determinations, in addition to aspartate aminotransferase and alanine aminotransferase for the differentiation of various types of viral hepatitis, is described.
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PMID:The clinical chemistry of chimpanzees: II. Gamma glutamyl transferase levels in hepatitis studies. 286 23

The possible development of hepatotoxic effects as a result of high dosages of isoniazid, rifampin, pyrazinamide, and ethionamide was assessed in 56 young children (median age, 22 months) treated for severe tuberculous meningitis (TBM). Only one of the 56 children became jaundiced, probably as result of hepatitis A infection. Of 33 children observed for at least eight weeks, only five (15%) had normal serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyl transferase levels throughout, but in only three patients were AST or ALT values greater than 200 U/L, and enzyme levels tended to normalize toward the end of the period. In this group of 33 children, those at stage III TBM had higher enzyme levels than did those at stage II. The remaining 23 children were observed for a mean period of only four weeks, and 18 (75%) had at least one abnormal liver function test result.
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PMID:Hepatic toxicity during chemotherapy for severe tuberculosis meningitis. 288 66

Increased alanine and aspartate aminotransferase (ALT and AST) serum levels are usually considered expressions of cellular necrosis, especially in hepatocytes. They represent cellular damage due to burn which, according to many authors, becomes normal before discharge of patients. We studied 43 consecutive burned patients, both during and after recovery, from a minimum of 120 to a maximum of 640 days, and an average of 18.62 blood samples were taken from each patient. Hepatitis A and B markers were tested. Results showed a 67.44% increase in aminotransferases in patients during recovery and a 25.58% increase after discharge. No neopositivity was observed for hepatitis A and B markers. We therefore conclude that the increase of enzymes during recovery expresses a toxic-infective phase and this increase, contrary to what was believed, does not always drop to normal values at time of discharge. Instead, after discharge, higher values can be a manifestation of a Non-A Non-B hepatitis.
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PMID:Alanine and aspartate aminotransferase serum levels in burned patients: a long-term study. 361 54


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