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)

In this case report, a young woman with gallbladder sludge and acute pancreatitis due to acute hepatitis A (HAV) is presented. She was admitted to our hospital with abnormal hepatic enzymes. Five days prior to her admission, an initial abdominal ultrasound was performed at another hospital and revealed no abnormality, while her serum aspartate aminotransferase (AST) level was at the upper limit of normal (ULN) x 8. A second ultrasound was performed at our hospital and revealed a gallbladder wall thickness (9.3 mm), gallbladder sludge in the gallbladder lumen, pancreatic edema, ascites, and hepatomegaly while AST was at the ULN x 50. Magnetic resonance imaging and magnetic resonance cholangiopancreatography revealed imaging features of an acute stage of pancreatitis and gallbladder wall thickness with coexisting sludge in the gallbladder lumen. HAV infection was diagnosed by the detection of immunoglobulin M against HAV in the serum. The patient underwent two repeated abdominal ultrasound examinations on the 5th (AST was at the ULN x 3) and the 20th days (AST was at the normal) after her discharge, and both revealed normal findings. In our case, we observed reversible changes in the hepatobiliary and pancreatic system which was related to the severity of hepatic necro-inflammation. HAV-associated pancreatitis may be due to the formation of biliary sludge during the acute phase of the viral illness, but this association needs further investigation.
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PMID:Gallbladder sludge and acute pancreatitis induced by acute hepatitis A. 1790 17

The objective of this study was to investigate the effects of types of dialysis treatments on hepatitis C virus infection and the epidemiologic properties of hepatitis C virus (HCV) infection at three Baskent University hospitals, in Ankara, Adana, and Izmir, Turkey, in 655, 326, and 118 patients with end-stage renal disease, respectively. One hundred thirty patients with HCV viremia among 271 patients with end-stage renal disease seropositive for HCV were included in this cross-sectional study. HCV RNA-positive patients were classified according to the renal replacement therapies (hemodialysis or continuous ambulatory peritoneal dialysis), and viral load, transaminase levels, and distribution of genotypes were compared between these subgroups. In the continuous ambulatory peritoneal dialysis group, 26 of 165 patients (16%) were serum anti-HCV positive, and 11 of 26 patients (42%) were serum HCV RNA positive. Twenty-six percent of the patients undergoing hemodialysis were anti-HCV positive, and 49% were HCV RNA positive. The prevalence of genotype 1b was 68% and 73% for patients in the continuous ambulatory peritoneal dialysis and hemodialysis groups, respectively. No significant differences were found between the genotype 1b and the non-1b groups or between different dialysis types with regard to age and sex and serum aspartate transaminase, alanine aminotransferase, and HCV RNA levels. We conclude that HCV seropositivity may differ between different types of dialysis treatments, although viral load and genotypes may be similar in persons with end-stage renal disease and those without.
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PMID:Distribution of HCV genotypes in patients with end-stage renal disease according to type of dialysis treatment. 1686 30

Data were gathered from the records of 51 children of median age 1.5 years who survived more than 6 months after intestinal transplantation. Abnormal liver function tests (LFTs) were defined as serum aspartate aminotransferase (AST) greater than 100 IU/L or total bilirubin greater than 2.0 g/dL lasting more than 3 days. Temporary elevation was defined when LFTs returned to normal without graft loss or death. LFT elevation at the time of transplantation was not included as a temporary LFT elevation. Median follow-up was 36 months. In multivisceral transplant recipients, all patients (n = 34) showed abnormal LFTs at transplantation that normalized within a median period of 2 days. Temporary LFT elevations were seen in 20 of 34 (59%) in multivisceral transplantation and 5 of 17 (29%) in isolated intestinal transplantation. Median length of elevation was 14 days in multivisceral transplantation and 12 days in isolated intestinal transplantation. Peak AST was 353 +/- 190 IU/dL in multivisceral transplantation and 839 +/- 605 IU/dL in isolated intestinal transplantation (P = .0059). Events associated with temporary LFT elevations in multivisceral transplantation were total parental nutrition (TPN) (n = 8), dehydration (n = 2), viral infection (n = 2), others (n = 3), and nonspecific (n = 5). Events in isolated intestinal transplantation were posttransplant lymphoproliferative disorder (n = 2), TPN (n = 1), and nonspecific (n = 2). Temporary LFT elevations were commonly seen among pediatric intestinal recipients, which correlated with events other than rejection. Approximately half of the temporary LFT elevations were associated with no significant clinical events. They resolved spontaneously. Interestingly, the peak AST value was higher in isolated intestinal transplantation compared to multivisceral transplantation.
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PMID:Temporary elevation of serum transaminases after pediatric intestinal transplantation: incidence and clinical correlation in multivisceral transplant vs isolated intestinal transplant. 1690 75

To describe the clinical features of dengue cases in Japan, a retrospective study was conducted on 62 laboratory-confirmed Japanese dengue cases presented to Tokyo Metropolitan Komagome Hospital between 1985 and 2000. Age distribution was from 18 to 62 years old (mean, 31.5 years). All cases were imported from abroad and diagnosed as dengue fever. Clinical manifestations included fever (100%), headache (90%), and skin rash (82%). Laboratory examinations revealed leukocytopenia (71%), thrombocytopenia (57%), elevated levels of serum aspartate aminotransferase (78%), and lactate dehydrogenase (71%). Antibody responses were consistent with that of secondary flavivirus infection in 60% of cases. Severity of symptoms in patients with primary dengue antibody response and those with secondary flavivirus antibody responses didn't show statistical significance. Dengue virus infection should be taken into consideration in the differential diagnosis of febrile patients who recently entered Japan from tropical or subtropical countries.
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PMID:Clinical features of 62 imported cases of dengue fever in Japan. 1696 23

Protein adducts are useful biomarkers for assessing exposure, metabolism and risk of carcinogens. Aflatoxin B1-albumin adducts (AAA) and protein carbonyl content (PCC) have long been used for assessing aflatoxin exposure and oxidative stress to proteins, and the quantitative data are almost exclusively expressed per mg protein. Given the large variation in protein concentrations in plasma among populations, this may not be the most appropriate method. The objective was to test the hypothesis that AAA and PCC should be expressed per mL plasma in population studies. AAA and PCC were analyzed among 402 subjects from three regions of China with a gradient in hepatocellular carcinoma (HCC) mortality ranging from 21 to 97 per 100,000. When biomarker values were expressed per mL plasma, the AAA level was significantly associated with plasma PCC (r = 0.262, P < 0.001), and adjusted levels of AAA and PCC paralleled HCC mortalities in the three regions, suggesting a role for aflatoxin-related oxidative stress in hepatocarcinogenesis in this population. In addition, there were statistically significant associations between both protein biomarkers, expressed per mL plasma, and the levels of alanine aminotransferase and aspartate aminotransferase in hepatitis B virus-infected subjects, suggesting roles for aflatoxin exposure, oxidative stress and hepatitis B virus infection in the development of HCC. The present data suggest that interindividual variation in plasma protein concentration may influence the dosimetry and relevant interpretation of protein biomarkers.
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PMID:Is correction for protein concentration appropriate for protein adduct dosimetry? Hypothesis and clues from an aflatoxin B1-exposed population. 1723 31

One of the main difficulties in studying dengue virus infection in humans and in developing a vaccine is the absence of a suitable animal model which develops the full spectrum of dengue fever, dengue haemorrhagic fever, and dengue shock syndrome. It is our proposal to present morphological aspects of an animal model which shows many similarities with the dengue infection in humans. BALB/c mice were intraperitoneally infected with non-neuroadapted dengue virus serotype 2 (DENV-2). Histopathological and morphometrical analyses of liver tissue revealed focal alterations along the infection, reaching wide-ranging portal and centrolobular veins congestion and sinusoidal cell death. Additional ultrastructural observations demonstrated multifocal endothelial injury, platelet recruitment, and alterated hepatocytes. Dengue virus antigen was detected in hepatocytes and in the capillar endothelium of the central lobular vein area. Liver function tests showed high levels of aspartate transaminase and alanine transaminase enzyme activity. Lung tissue showed interstitial pneumonia and mononuclear cells, interseptal oedema, hyperplasia, and hypertrophy of the bronchiolar epithelial cells. DENV-2 led to a transient inflammatory process, but caused focal alterations of the blood-exchange barrier. Viremia was observed from 2nd to 11th day p.i. by isolation of DENV-2 in C6/36 mosquito cell line inoculated with the supernatant of macerated liver, lung, kidney, and cerebellum tissues of the infected mice.
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PMID:Morphological studies in a model for dengue-2 virus infection in mice. 1729 87

Hepatitis is caused by hepatitis viruses, but hepatitis or hepatocellular enzyme abnormalities is sometimes associated with infection by the hepatiticomimetic viruses. The direct and indirect effects of infection with hepatiticomimetic viruses were examined in two human hepatocyte systems. Poliovirus, adenovirus, and herpes simplex virus (HSV) induced cytopathology in Hep G2 cells. Measles virus caused no change in hepatocytes. Poliovirus infection did not affect cellular protein synthesis, and the peak of hepatocellular enzyme release coincided with the peak of virus release. The increase in adenovirus protein synthesis correlated with the decrease of transferrin synthesis, and enzyme release was not prominent. HSV induced viral protein synthesis with enhanced processing and inhibition of synthesis of alpha1-antitrypsin. The peak of enzyme release was later than the peak of virus release. In primary hepatocytes, poliovirus, adenovirus, and induced extensive cytopathology and enzyme release, and VZV caused cytopathology and significant but minute enzyme release. The ratio of lactate dehydrogenase to aspartate aminotransferase release was larger in poliovirus infection in both hepatocytes than in HSV or VZV infection. Although poliovirus and adenovirus are released by cytolysis and HSV and VZV are secreted by exocytosis of cytoplasmic vacuoles, enzyme release was independent of the type of virus release. Adenovirus showed strong cytotoxicity but did not modify the membrane nor cause enzyme release. Enzyme release was associated with modification of the surface membrane due to apoptosis with poliovirus and necrosis with HSV. Consequently hepatocellular injury by viral infection did not reflect the amount or pattern of hepatocellular enzyme release.
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PMID:Infection and direct injury in human hepatocyte explants and a hepatoblastoma cell line due to hepatiticomimetic (non-hepatitis) viruses. 1731 34

Acute hepatitis C in immunocompetent individuals is rarely symptomatic and rarely biopsied. Thus, the histologic descriptions of acute hepatitis C remain limited. The histology of 5 cases of acute hepatitis C in adults were studied by selecting cases from the consult and surgical pathology files of a single institution. The 5 individuals, 3 males and 2 females, had an average age at biopsy of 50+/-17 years. They presented with jaundice and other nonspecific abdominal symptoms. The time interval from clinical presentation to biopsy ranged from 2 to 18 weeks. The average alanine aminotransferase/aspartate aminotransferase/alkaline phosphatase at the time of biopsy was 308/73/85 U/L. The average total bilirubin was 5.2 mg/dL. Each individual had a single liver biopsy. The histologic findings of the 2 cases biopsied in close temporal proximity to the initial clinical presentation showed similar histologic findings of mixed portal infiltrates with lymphocytes and neutrophils along with bile ductular proliferation that raised the possibility of down stream biliary tract disease. The lobules showed canalicular cholestasis and mild to moderate inflammation. In the third and fourth case, obtained 8 weeks after presentation, the biopsies showed mild to moderate portal and lobular lymphocytic inflammation, findings that were also present in the last case, obtained 18 weeks after presentation. In conclusion, early after acute hepatitis C viral infection, biopsies can have a cholestatic pattern whereas later biopsies tend to show mild nonspecific portal and lobular lymphocytic inflammation. Proper histologic diagnosis can be aided by an awareness of the various histologic findings, which vary depending on the time interval from clinical symptoms to biopsy.
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PMID:Histology of symptomatic acute hepatitis C infection in immunocompetent adults. 1805 33

Nonspecific chronic hepatitis and increased activities of serum aminotransferases have been reported in cetaceans (dolphins, porpoises, and whales). We identified bottlenose dolphins in our current population with episodic increases in serum aminotransferases, specifically alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and we hypothesized that hematologic and serum biochemical changes in these animals may provide clues as to potential causes of liver disease in cetaceans. A retrospective case-control study involving 1,288 blood samples collected during 1998-2006 from 18 dolphins (six cases and 12 age- and sex-matched healthy controls) was conducted to compare eosinophil and platelet counts; and serum proteins, albumin, globulins, bilirubin, gamma glutamyltransferase (GGT), cholesterol, triglycerides, glucose, iron, and erythrocyte sedimentation rates. Bottlenose dolphins with increased ALT and AST activities were more likely to have higher serum globulins, bilirubin, GGT, iron, glucose, triglycerides, and cholesterol levels, greater erythrocyte sedimentation rates, and lower platelet counts compared to healthy controls. Our findings suggest that dolphins with chronic increases in aminotransferases may have a chronic hepatitis involving iron overload with similar etiologies and pathophysiology compared to terrestrial mammals. Areas for future research include predisposing metabolic risk factors; associations between iron overload and a diabetes-like condition; and a potential overlap syndrome involving autoimmune responses that may or may not be associated with viral infection.
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PMID:Assessment of increased serum aminotransferases in a managed Atlantic bottlenose dolphin (Tursiops truncatus) population. 1843 64

Clinical manifestations of severe dengue diseases include thrombocytopenia, vascular leakage, and liver damage. Evidence shows that hepatic injury is involved in the pathogenesis of dengue infection; however, the mechanisms are not fully resolved. Our previous in vitro studies suggested a mechanism of molecular mimicry in which antibodies directed against dengue virus (DV) nonstructural protein 1 (NS1) cross-reacted with endothelial cells and caused inflammatory activation and apoptosis. In this study, the pathogenic effects of anti-DV NS1 antibodies were further examined in a murine model. We found, in liver sections, that anti-DV NS1 antibodies bound to naive mouse vessel endothelium and the binding activity was inhibited by preabsorption of antibodies with DV NS1. Active immunization with DV NS1 resulted in antibody deposition to liver vessel endothelium, and also apoptotic cell death of liver endothelium. Liver tissue damage was observed in DV NS1-immunized mice by histological examination. The serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were increased in mice either actively immunized with DV NS1 protein or passively immunized with antibodies obtained from DV NS1-immunized mice. Furthermore, histological examination revealed mononuclear phagocyte infiltration and cell apoptosis in mice passively immunized with antibodies obtained from mice immunized with DV NS1. Increased AST and ALT levels were observed in mice passively immunized with purified immunoglobulin G (IgG) from dengue patients compared with normal control human IgG-immunized mice. The increased AST and ALT levels were inhibited when dengue patient serum IgG was preabsorbed with DV NS1. In conclusion, active immunization with DV NS1 protein causes immune-mediated liver injury in mice. Passive immunization provides additional evidence that anti-DV NS1 antibodies may play a role in liver damage, which is a pathologic manifestation in dengue virus disease.
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PMID:Liver injury caused by antibodies against dengue virus nonstructural protein 1 in a murine model. 1867 79


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