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 study maximum urinary iron elimination with continuous desferrioxamine subcutaneous infusion was obtained in thalassemia major patients with chronic persistent or active hepatitis with lower doses (60 mg/kg) than those necessary in patients without hepatitis (80 mg/kg). Since dose-response curves were highly variable the treatment schedule should be tailored to the individual needs of each patient. Both groups may achieve iron balance but chronic hepatitis patients have more frequently a net urinary iron excretion. In patients with chronic hepatitis no correlation was found between serum ferritin levels or serum ferritin/aspartate aminotransferase ratios and transfusional iron overload while serum ferritin/aspartate aminotransferase ratios were seen to be correlated with liver iron stores.
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PMID:Iron chelation in transfusion-dependent thalassemia with chronic hepatitis. 680 Feb 2

Lyme disease, caused by a tick-transmitted spirochete, typically begins with a unique skin lesion, erythema chronicum migrans. Of 314 patients with this skin lesion, almost half developed multiple annular secondary lesions; some patients had evanescent red blotches or circles, malar or urticarial rash, conjunctivitis, periorbital edema, or diffuse erythema. Skin manifestations were often accompanied by malaise and fatigue, headache, fever and chills, generalized achiness, and regional lymphadenopathy. In addition, patients sometimes had evidence of meningeal irritation, mild encephalopathy, migratory musculoskeletal pain, hepatitis, generalized lymphadenopathy and splenomegaly, sore throat, nonproductive cough, or testicular swelling. These signs and symptoms were typically intermittent and changing during a period of several weeks. The commonest nonspecific laboratory abnormalities were a high sedimentation rate, an elevated serum IgM level, or an increased aspartate transaminase level. Early Lyme disease can be diagnosed by its dermatologic manifestations, rapidly changing system involvement, and if necessary, by serologic testing.
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PMID:The early clinical manifestations of Lyme disease. 685 26

In a one-year prospective study we assessed the incidence of Reye's syndrome in children presenting with the acute onset of vomiting after a prodromal upper-respiratory-tract infection or varicella, and with serum alanine or aspartate aminotransferase levels at least three times higher than normal, and a paucity of neurologic findings. Of 25 patients meeting the above criteria, 19 had liver biopsies yielding adequate tissue for diagnostic purposes. Biopsy specimens from 14 of these 19 patients (74 per cent) were diagnostic of Reye's syndrome, according to rigorous light-microscopical, histochemical, and ultrastructural criteria. None of the biopsy specimens contained evidence of other acute pathologic processes, including hepatitis. A wide spectrum of mitochondrial alterations existed at the ultrastructural level, ranging from mild to severe lesions that were indistinguishable from those seen in comatose patients with Reye's syndrome. Our findings suggest that the clinical complex of vomiting, hepatic dysfunction, and minimal neurologic impairment after varicella or an upper-respiratory-tract infection usually represents Reye's syndrome. This syndrome occurs more frequently than previously recognized.
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PMID:Grade I Reye's syndrome. A frequent cause of vomiting and liver dysfunction after varicella and upper-respiratory-tract infection. 686 12

We postulated that three tests could be used to advantage in the prognosis of patients with alcoholic liver disease. Ninety-eight patients who entered the hospital in hepatic failure, and who survived that illness, were observed for an average of 3.5 years after discharge. At the time of entry, most had jaundice, ascites, edema, and hepatosplenomegaly. Biopsy of the liver disclosed both cirrhosis and hepatitis in 75-80%. Neither clinical features nor laboratory tests could differentiate these patients at the time of entry. However, as early as 3 months after hospitalization, the clinical course and laboratory tests served to distinguish two groups: group 1 comprised 46 patients in whom the serum bilirubin was less than 2 mg/dl; the aspartate aminotransferase less than 55 mU/ml; and the alkaline phosphatase less than 125 mU/ml. In 40 (87%) of these 46 patients, clinical findings improved concomitantly with laboratory tests. Group 2 comprised 52 patients in whom one or more of these three tests showed persistent abnormality; only 12 (23%) of the 52 patients in this group improved clinically and three subsequently died. Although the majority of patients (76%) in group 1 reported abstinence on follow-up, 44% of group 2 patients also claimed abstinence. Complications of liver disease, shunt surgery, and continuing alcoholism contributed to liver failure. Early identification of such patients should aid in the management of alcoholic liver disease.
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PMID:Predicting clinical recovery from alcoholic liver disease. 688 50

The two categories of anti-albumin antibodies (AAA), namely precipitins (AA-P) and agglutinins (AA-Aggl), were investigated in 260 patients with morphologically diagnosed chronic liver diseases (CLD). A parallelism was observed between AA-P titre and the severity of chronic hepatitis as revealed by clinical diagnosis. Thus, significant differences in AA-P titre were noticed between chronic persistent hepatitis (CPH) and chronic aggressive hepatitis (CAH) and between CAH and liver cirrhosis (LC). No correlation was found between AA-P positivity and either HBsAg presence or disease activity, maximum AA-P values being registered in decompensated, inactive LC. AA-P positivity was found associated with a higher degree of liver cell dysfunction. In every category of CLD a striking association was also observed between AA-P positivity and raised serum aspartate transaminase and bilirubin levels, thus suggesting a common pathogenic substrate, namely liver cell membrane damage. These correlations were also observed after immunosuppressive therapy which would argue for the maintenance of AA-P diagnostic value. AA-Aggl showed raised incidences and titres in CAH patients, the values decreasing in LC. Therefore, the main diagnostic value is attributed to AA-P.
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PMID:Anti-albumin antibodies in chronic liver diseases: diagnostic significance of these antibodies in patients with conventional or immunosuppressive therapy. 697 71

A systemic BCG infection in mice induced multiple small granulomas located mainly in the periportal areas of the liver. Following systemic challenge of such mice with purified protein derivative of tuberculin (PPD), a rapidly developing hepatitis with diffuse intralobular mononuclear cell infiltration was precipitated, accompanied by high levels of aspartate transaminase in peripheral blood, hypoglycemia, focal hepatocyte necrosis, and accumulation of fibrinogen in liver. Bacterial lipopolysaccharide (LPS) also provoked acute hepatic damage both in BCG-infected mice and in mice pretreated with Corynebacterium parvum. PPD was not active in the latter. There were also lymphoid cell destruction and fibrinogen accumulation in the spleen of BCG-PPD-treated mice. Possible involvement of inflammatory and hepatotoxic mediators is suggested, and a T-lymphocyte-macrophage regulatory role in the pathogenesis of hepatitis is discussed.
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PMID:Tuberculin hypersensitivity hepatitis in mice infected with Mycobacterium bovis (BCG). 702 5

Quadratic multiple discriminant analysis of 25 commonly ordered laboratory tests resulted in correct classification of 100% of nonalcoholics without overt liver disease, 98% of alcoholism treatment program patients with presumed mild liver involvement, 96% of alcoholics with liver disease, and 89% of nonalcoholics with liver disease. Direct comparison of the biopsy-verified alcoholic and nonalcoholic liver disease groups resulted in 100% discrimination, and removal of traditionally evaluated liver tests from the battery of 25 tests did not substantially alter the original classification accuracy. Alcoholic and nonalcoholic liver disease was still 100% differentiable when equated for number of patients with cirrhosis, hepatitis, and hepatitis combined with cirrhosis or fibrosis. Additional utility of the quadratic discriminant approach was demonstrated when 83% alcoholic and 83% nonalcoholic liver disease cases were diagnosed correctly in a prospective manner. In contrast, use of aspartate aminotransferase to alanine aminotransferase ratios (ie, SGOT to SGPT) identified correctly 75% and 33% of patients, respectively.
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PMID:Biochemical and hematologic correlates of alcoholism and liver disease. 713 77

alpha-Glutathione S-transferase (alpha-GST; EC 2.5.1.18) has been advocated as a better marker of hepatocellular damage than the transaminases in toxic and autoimmune hepatitis. We have assessed the potential interest of plasma alpha-GST determination in 94 anti-hepatitis C virus-positive patients with histologically proven chronic hepatitis C (34 women, 60 men, ages 40.0 +/- 11.9 years). Blood samples were assayed for aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltransferase, alkaline phosphatase, and alpha-GST on the same day a liver biopsy was performed. alpha-GST concentrations were significantly above reference values in 64% of patients (compared with 58% for AST, 68% for ALT), and this increase was seen in 52% of patients with normal values for transaminases and a Knodell score > 3. Furthermore, there was a significant correlation between alpha-GST and lobular necrosis score (r = 0.31; P < 0.01). Our findings suggest that association of plasma alpha-GST with ALT may improve the biochemical assessment of liver damage in patients with chronic hepatitis C.
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PMID:Plasma alpha-glutathione S-transferase assessed as a marker of liver damage in patients with chronic hepatitis C. 749 11

In order to evaluate the persistence of antibodies against hepatitis C virus (HCV) in a chronic hemodialysis population, we studied 151 HBsAg-negative patients. Anti-HCV titers were evaluated every 3 months over 1 year, and the serum alanine aminotransferase/serum aspartate aminotransferase ratio monthly from the start of hemodialysis. The anti-HCV titers (ELISA C100-3) remained stable in 127 patients and fluctuated in 24, without an evident correlation with hepatic function. Using our criteria, we found 85 patients with non-A, non-B hepatitis, 57 of them with biochemical criteria of chronic hepatic disease. There was a strong correlation between antibodies to HCV and non-A, non-B hepatitis (chi 2; p < 0.05) which was more marked in those patients with biochemical criteria of chronic hepatic disease (chi 2; p < 0.001). We concluded that the anti-HCV titer is reliable as a long-term marker of hepatitis C virus infection.
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PMID:Persistence of antibodies to hepatitis C virus in a chronic hemodialysis population. 752 4

The liver has an important role in thyroid hormone metabolism and the level of thyroid hormones is also important to normal hepatic function and bilirubin metabolism. Besides the associations between thyroid and liver diseases of an autoimmune nature, such as that between primary biliary cirrhosis and hypothyroidism, thyroid diseases are frequently associated with liver injuries or biochemical test abnormalities. For example, thyroid diseases may be associated with elevation of alanine aminotransferase and alkaline phosphatase, which is mainly of bone origin, in hyperthyroidism and aspartate aminotransferase in hypothyroidism. Liver diseases are also frequently associated with thyroid test abnormalities or dysfunctions, particularly elevation of thyroxine-binding globulin and thyroxine. Hepatitis C virus infection has been connected with thyroid abnormalities. In addition, antithyroid drug therapy may result in hepatitis, cholestasis or transient subclinical hepatotoxicity, whereas interferon (IFN) therapy in liver diseases may also induce thyroid dysfunctions. These thyroid-liver associations may cause diagnostic confusions. Neglect of these facts may result in over of under diagnosis of associated liver or thyroid diseases and thereby cause errors in patient care. It is suggested to measure free thyroxine (FT4) and thyroid-stimulating hormone (TSH) which are usually normal in euthyroid patients with liver disease, to rule out or rule in coexistent thyroid dysfunctions, and consider the possibility of thyroid dysfunctions in any patients with unexplained liver biochemical test abnormalities. It is also advisable to monitor patients with autoimmune liver disease or those receiving IFN therapy for the development of thyroid dysfunctions, and patients receiving antithyroid therapy for the development of hepatic injuries.
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PMID:Clinical associations between thyroid and liver diseases. 754 16


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