Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Having constructed the serological diagnostics of Hepatitis A and B viruses there remained non identified agent(s): named "Non-A, non-B". The non-A, non-B infecting parenterally is a Flavivirus, with lipoid envelope and a diameter of 30-60 nm, as stated very early. After having known the simple filament RNS genome, named as Hepatitis C. In the same time it was tried to isolate the antigen and antibody from ill people, without success. There were not usable the surrogate markers too (anti-HBc and ALT). One part of the synthetized polypeptides from little fragments of C virus genome was apt to antibody-detection. In the acute state there was 20-40, in the chronic state 60-80% anti-HCV positive during the illness. This seropositivity is not equal of healing, neither the potency to infect. The infectivity is showed by the nucleic acid's presence (of the virus) in the blood (PCR), the perfect healing by the neutralizing antibody.
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PMID:[Advances in the diagnosis of non-A non-B viral hepatitis]. 163 Jul 99

Seventy-seven blood samples from normal controls aged 0-8 years and 93 blood samples from children of similar ages with various viral hepatitis were investigated by measuring plasma superoxide dismutase (EC 1.15.1.1) using chemiluminescence immunoassay (CLIA). Total and Cu,Zn-SOD activities of normal controls of group 2 (1-8 years old) were significantly higher than that of normal controls of group 1 (0-1 year old) (P less than 0.01, P less than 0.01), while there were no differences of Mn-SOD activities between the two groups. Total, Cu,Zn- and Mn-SOD activities significantly increased in the acute phase (0-4 weeks after onset) and dropped to the normal levels in the restoration phase (4th week later) for 29 children with cytomegalovirus hepatitis (CMVH), in comparison with group 1. Only Mn-SOD activities were significantly increased in the acute phase (with increased ALT levels) and restoration phase (with normal ALT levels) for 18 children with hepatitis A (HA). Total and Cu,Zn-SOD activities significantly decreased and Mn-SOD activities significantly increased in both the active (with increased ALT levels) and the inactive phases (with normal ALT levels) for 36 children with chronic persistent hepatitis (CPH). Only Cu,Zn-SOD activities fell significantly in both active and inactive phases for 10 children with chronic active hepatitis (CAH).
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PMID:Plasma superoxide dismutase measurement in children with viral hepatitis. 164 17

An enzyme immunoassay was used to detect antibodies to hepatitis C virus (anti-HCV) in 261 patients and 69 staff members of a hemodialysis unit. The prevalence of anti-HCV was 46.7% in patients and 2.9% in staff members (p less than 0.001). The prevalence of anti-HCV increased significantly with increasing duration of hemodialysis (p less than 0.001), but was not related to age, sex, history of blood transfusion, status of hepatitis B or hepatitis A virus infection, or serum ALT. Patients with hepatitis episode increased with increasing duration of hemodialysis and showed a significantly higher prevalence of anti-HCV than those without (63.1 vs. 34.7%, p less than 0.001). The prevalence of anti-HCV in patients with hepatitis also increased with increasing duration of hemodialysis (p = 0.05). Thus, HCV appears to be the major cause of hepatitis in hemodialysis patients. Besides strict infection control measures, further studies are needed to determine the mode of HCV infection and its prevention in the hemodialysis unit.
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PMID:Prevalence of antibodies to hepatitis C virus in the hemodialysis unit. 166 Feb 21

Current notions on the role of the thymol test (TT) in the diagnosis of viral hepatitis A are discussed. Changes in TT results over the course of the disease are presented, starting from the incubation period up to the second-third week; these values are compared to those of hepatitis A specific markers. The earliest TT shifts in hepatitis A are detectable already 15-18 days before the first clinical manifestations, when this parameter surpasses the upper threshold of the range of normal values. The incubation period TT values are 6.9-8.4 U S-H, those during the 3 weeks of the acute period are 9.1-9.7 U S-H. This test earlier reacts to liver inflammation than alanine aminotransferase (a hepatic enzyme) measurement, which fact recommends TT for active early detection of hepatitis A patients in epidemic foci in collective bodies. One more TT advantage over the detection of hepatitis A specific markers in epidemic foci is that it permits the diagnosis of hepatitis whatever its etiology.
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PMID:[Current concepts of the role of the thymol test in the laboratory diagnosis of viral hepatitis A]. 169 32

The development of spontaneous outbreak of hepatitis A (HA) among African green monkeys kept under strict isolation conditions was studied. It was shown that in the case of introduction of HAV the infection involved all the susceptible monkeys, running a course with and without any increase in the level of activity of serum alanine aminotransferase (ALT) After inoculation of commercial gamma-globulin only the infection without the ALT activity increase developed and some monkeys had no signs of HA at all. Experimental reinfection with HAV was produced in monkeys having anti-HAV titres of less than or equal to 1:3500.
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PMID:[Development of an infection in monkeys as a result of their sequential natural and experimental exposure to the hepatitis A virus]. 169 29

Thirty-four pregnant women with hepatitis A and their neonates were investigated on serum anti-HAV IgM, ALT (GPT) and clinical manifestations (with 34 randomized controls) during the outbreak of viral hepatitis A in Shanghai. The result showed no evidence of maternal-infant transmission of hepatitis A, and no birth defect was found. Sufficient rest and proper diet for and close surveillance of the pregnant woman were suggested to ensure the well-being of mother and child. In addition, we found immune gamma-globulin given to the neonates born of mothers with hepatitis A may be beneficial to avoid horizontal transmission of hepatitis A.
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PMID:Survey of 34 pregnant women with hepatitis A and their neonates. 169 88

A 17-year-old male patient with T-cell type lymphoblastic lymphoma in complete remission underwent high dose chemotherapy (busulfan 16 mg/kg and cyclophosphamide 120 mg/kg) followed by autologous bone marrow transplantation (ABMT). The patient had been taking oral acyclovir (200 mg x 5) daily from seven days prior to the ABMT (day -7). On day +24, he complained of epigastralgia and general malaise, and the next day his GOT and GPT rose to 570 U/l and 397 U/l, respectively. Although he had no mucocutaneous lesions, hepatitis caused by a herpes virus was suspected, and high dose intravenous acyclovir (10 mg/kg x 3/day) was immediately started. His GOT, GPT and total bilirubin reached peaks of 2,870 U/l on day +26, 1,830 U/l on day +27 and 10.3 mg/dl on day +39, respectively, and rapidly improved thereafter. Serological analyses on IgG antibody titers to herpes simplex virus type 1 using an enzyme-linked immunosorbent assay revealed specific increases (454-fold before transplantation to 3,830-fold on day +46). Antiviral antibody titers to cytomegalovirus, varicella-zoster virus and Epstein-Barr virus showed no significant changes. The serologic markers of hepatitis B virus, hepatitis A virus and hepatitis C virus were all negative. The results indicate the patient's severe icteric hepatitis to have been caused by a reactivation of herpes simplex virus type 1 due to immunosuppression after high dose chemotherapy with ABMT. It is suggested that prompt commencement of high dose intravenous acyclovir is required to treat severe herpes simplex virus hepatitis affecting immunocompromised patients.
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PMID:Severe herpes simplex virus hepatitis following autologous bone marrow transplantation: successful treatment with high dose intravenous acyclovir. 175 18

The prevalence of hepatitis A-, B- and C-markers has been studied in patients at a Norwegian rehabilitation centre for drug addicts. The prevalence of hepatitis C-antibodies was fairly constant in the years 1976 (56%), 1985 (78%) and 1988-89 (73%), but may be decreasing in younger addicts. The data suggest a highly variable incidence of HAV with few infections in recent years. The prevalence of hepatitis B-markers, which has been calculated from 1975 to 1988-89, reached a maximum of 93% in 1986. Since then a significant decrease in prevalence has been observed among younger patients, suggesting that the HIV campaign has led to improved hygiene precautions among intravenous drug addicts. A strong correlation was observed between positive markers for HBV and presence of anti-HCV, and, similarly, between the presence of anti-HAV and markers for HBV and HCV. Anti-HCV was significantly associated with pathological ALT-values.
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PMID:[Hepatitis A-, B- and C-markers among Norwegian drug addicts in the period 1975-89]. 190 31

3089 healthy persons, aged 4 to 27 years, have been inoculated in 3 batches with attenuated live hepatitis A vaccine (H2 strain) since May, 1987. Each subject received 10(8.5) TCID dosage subcutaneously in the upper arm. None of the recipients developed any local or systemic reaction during a 42-day followup after vaccination. The serum enzyme activities, including SGPT/ALT and LDH5, were within normal range during the 4th to 16th weeks of serial tests after inoculation. The study of hepatitis A virus (HAV) shedding in feces of 4 subjects showed that no hepatitis A antigen (HAAg) was detected with antigen capture ELISA, but infectious HAV was recovered from stool-cell cultures in three of four recipients. No patient with hepatitis A was found within 6 months after vaccination in the institution where the HAV vaccine was used. In addition, no immunological evidence was seen that the HAV vaccine recipients can transmit HAV after the investigation of serological epidemiology at a class in which the HAV vaccine was tested. It is suggested that the potential of hepatitis A related to HAV vaccine among the non-vaccinated persons is rare. Seroconversion occurred at a mean time of 2 to 5 weeks after inoculation, and the positive rate of specific antibody was 95.6%.
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PMID:[Safety observation of attenuated live hepatitis B vaccine (H2 strain) in humans]. 196 72


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