Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-six of 388 patients (6.7%) followed prospectively after open-heart surgery developed non-A, non-B hepatitis. Of these 26, 12 had an elevated (often fluctuating) serum alanine aminotransferase (SGPT) for greater than 1 year. Liver biopsy, done in eight of 12, showed chronic active hepatitis in six and chronic persistent hepatitis in two; one patient with chronic active hepatitis had early cirrhosis. Anicteric patients with peak SGPT greater then 300 IU/L were at greatest risk of developing chronic hepatitis. Chronic non-A, non-B hepatitis was symptomatically mild and unaccompanied by physical signs or laboratory evidence of autoimmune disease or severe chronic liver disease. In all 12 patients there was spontaneous improvement in serum transaminase over a period of 1 to 3 years, and four patients had sustained normalization of SGPT. Thus chronic active hepatitis is a common sequela of acute non-A, non-B hepatitis but may have a better prognosis than chronic active hepatitis of other causes.
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PMID:The chronic sequelae of non-A, non-B hepatitis. 46 17

Neopterin is a pyrazino-pyrimidine compound which is biosynthesized by macrophages. Increased concentrations of neopterin have been reported in conditions causing a stimulation of cellular immunity, such as viral and other infections, graft versus host disease, autoimmune disease and different malignancies. Recently, urinary neopterin levels have been found increased in patients with acute viral hepatitis and NANB chronic hepatitis. In the present study, neopterin serum levels have been measured in 23 cirrhotic patients (6 HBV related, and 17 cryptogenetic cirrhosis, 7 of them occurring in alcoholic subjects) and in 24 normal subjects. Mean values of serum neopterin were significantly increased in cirrhotics (3.92 +/- 3.28 ng/ml versus 1.24 +/- 0.51 ng/ml in controls, p less than 0.01). Serum neopterin values were not found to be significantly different in cirrhotics assessed in three different clinical classes according to Child's classification and in cirrhotics with and without serological findings of active disease. In fact, in cirrhotic patients, serum neopterin levels did not correlate with the values of serum AST, ALT, ALP, GGT and gamma-globulin. These data show that increased levels of serum neopterin occur in cirrhotic patients, but there is no relation between serum neopterin values and the activity or the clinical severity of the disease. The results are consistent with the hypothesis that activated macrophages are involved in all stages of liver cirrhosis irrespective of its aetiology.
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PMID:Serum neopterin levels in liver cirrhosis. 263 48

The association between liver/kidney microsomal antibody type 1 and adult cases of hepatitis C virus-related chronic liver disease has been firmly established. In the presence of both markers, evidence of autoimmunity (liver/kidney microsomal antibody type 1) and actual viremia (serum HCV RNA), the therapeutic dilemma arises between steroids, which are beneficial to autoimmune but deleterious to viral diseases, and interferon-alpha, which may exacerbate an autoimmune disorder. Six patients with liver/kidney microsomal antibody type 1 and serum HCV RNA were given interferon-alpha: three showed a response pattern similar to that observed in autoantibody-negative chronic hepatitis C cases; the other three developed a sharp transaminase peak, which was not followed by HCV RNA clearance. Considering the brisk flare-up of liver cell necrosis, interferon-alpha treatment proved to be dangerous in the above three liver/kidney microsomal antibody type 1/HCV RNA positive cases. Subsequent steroid administration reduced alanine aminotransferase peaks, but may be harmful in viral infections. Therapeutic alternatives are needed: they will probably include pure antivirals (exerting no immunostimulatory effects) with or without immunosuppressive drugs.
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PMID:Interferon therapy in liver/kidney microsomal antibody type 1-positive patients with chronic hepatitis C. 798 9

The purpose of this study was to determine the etiology of elevated alanine aminotransferase (ALT) in a population of asymptomatic volunteer blood donors. Subjects with an ALT value > 2.25 sd above norm (> 55 IU/liter) from the donated unit, were prospectively evaluated over a six-week interval. The subjects consisted of blood donors (78% male, 22% female) beginning basic military training at Lackland Air Force Base. Of 44,160 individuals screened, 19,877 (45%) voluntarily donated blood, 99 (0.5%) of which had confirmed ALT elevation. Of these (90 male/9 female), an associated condition or explanation was made in 12%: four with acute hepatitis B, four positive for anti-HCV, two with autoimmune disease, one with cholelithiasis and one associated with acute appendicitis. In 87 the ALT elevation could not be explained using available testing methods but may represent individual variation from a non-Gaussian distribution, be of nonhepatic origin (muscle), or of hepatic disease not detected by the diagnostic algorithm used. To increase the diagnostic yield, it is suggested that at least two elevated ALT values be established in this population over a period of time (yet undefined), before an extensive hepatic investigation is pursued.
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PMID:Serum alanine aminotransferase (ALT) elevation in asymptomatic US Air Force basic trainee blood donors. 826 13

A group of 24 patients underwent a 7-14-day course of continuously infused Cyclosporin A (2 mg.kg-1.day-1) to treat a severe attack of ulcerative colitis. In 19 of them, including eight treated with total parenteral nutrition, we retrospectively analyzed the serum aminotransferase (AST/ALT) levels at the beginning and at the end of Cyclosporin infusion. The baseline levels of AST/ALT in the group were 19.9 +/- 3.2 and 31.4 +/- 6.4; on stopping Cyclosporin infusion, they were 43 +/- 15.8 and 119 +/- 56, respectively. Six patients showed an ALT change above 1.5 times the upper limit of reference. They included five of the eight patients treated with total parenteral nutrition (62.5%). In one of six, ALT rose to 1000 U/l and was accompanied by full-blown febrile cholangitis (proven by liver biopsy). This episode was preceded by excessive accumulation of Cyclosporin in blood. The development of liver toxicity was independent of the length of Cyclosporin treatment, nor did it impair drug efficacy. Thus, in these patients total parenteral nutrition and Cyclosporin were synergistic, causing twice the frequency of liver damage (62.5%) reported for ulcerative colitis patients on total parenteral nutrition alone (37%). Total parenteral nutrition should not be used to support patients needing Cyclosporin for autoimmune disease. However, too high a dose of Cyclosporin may cause liver disease per se.
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PMID:Hepatotoxicity of intravenous cyclosporin A in patients with acute ulcerative colitis on total parenteral nutrition. 860 12

Elevated concentrations of plasma proinflammatory cytokines have been detected in patients with alcoholic hepatitis (AH) and in a model of lipopolysaccharide-induced hepatitis in ethanol-fed Wistar rats. These cytokines have been implicated in the pathogenesis of the liver damage. Considering the likely involvement of the immune system in AH, and the frequent use of Lewis rats in autoimmune disease models, Lewis rats were examined in the model to determine whether they would more closely mimic the immune status of a chronic alcoholic and be a preferable strain for use in future experiments. Lipopolysaccharide-induced hepatic tumor necrosis factor-alpha, interleukin-1alpha, interleukin-1beta, and interleukin-6 mRNA expression was examined in both rat strains. The overall pattern of histological (panlobular piecemeal necrosis) and biochemical liver damage (plasma ALT levels), and cytokine expression was similar in both strains. Thus, it would appear that, despite the known susceptibility of Lewis rats to autoimmune phenomena, they do not respond to the experimental regime significantly better than Wistar rats. This study confirms that unknown mediators are contributing to the liver damage seen in this model and possibly in AH.
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PMID:A comparison of lipopolysaccharide-induced hepatitis in ethanol-fed Wistar and Lewis rats. 980 38

The proto-oncogene product bcl-2 is known to inhibit apoptotic cell death, and its dysregulation might play a critical role in the development of autoimmune disease. To elucidate the role of bcl-2 in autoimmune hepatitis (AIH), its expression in peripheral blood mononuclear cells (PBMC) and in liver-infiltrating lymphocytes (LIL) was investigated. Increased bcl-2 expression in PBMC was found in AIH patients compared with that in chronic hepatitis C (CHC) patients and in healthy controls. The level of bcl-2 expression significantly correlated with serum ALT level. Further analysis showed that CD4+ T cells are enriched in bcl-2-expressing PBMC. To characterize the Th1/Th2 profile of bcl-2-expressing CD4+ T cells, intracellular interferon-gamma (IFN-gamma) and IL-4 were analysed. The results revealed that most of the bcl-2-expressing cells were found to be IFN-gamma-secreting Th1 cells. In three patients for whom their clinical courses could be followed, bcl-2 expression was decreased after the initiation of immunosuppressive therapy with corticosteroids. However, the level of IFN-gamma + cells was not altered. Immunohistochemical analysis also showed that large amounts of bcl-2+ cells were observed in periportal area in the liver. In conclusion, bcl-2-expressing cells were shown to be increased in peripheral blood and liver in AIH and the bcl-2 product was expressed mainly in CD4+ Th1-type cells, suggesting that these cells might promote the cellular immune response and contribute to the development of hepatitis and hepatocellular damage in AIH.
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PMID:Increased bcl-2 expression in lymphocytes and its association with hepatocellular damage in patients with autoimmune hepatitis. 1020 18

A 71-year-old man with chronic atrial fibrillation was treated with aspirin because of a right cerebral infarction. Oral anticoagulation was not initiated because of a secondary hemorrhagic transformation. Six years later after a left cerebral transient ischemic attack aspirin was replaced by ticlopidine. Two weeks after starting ticlopidine he experienced abdominal cramps and diarrhea. Also dark urine and gray-colored stools were noticed, so that the patient stopped taking ticlopidine. 40 days after starting ticlopidine he was admitted to our hospital because of cholestatic jaundice. Serum alkaline phosphatase (305 U/l) and gamma GT (143 U/l) were elevated, the total bilirubin was 18.6 mg/dl at peak. GOT and GPT were 2.7 fold increased. After exclusion of a viral infection and autoimmune disease liver biopsy was performed, which showed a centroacinar cholestasis compatible with a drug-induced liver damage. 79 days after discontinuation of the drug laboratory signs of cholestasis had disappeared. In patients in whom long-term therapy with ticlopidine is indicated regularly laboratory tests and clinical examinations should be done to recognize infrequent side effects such as the cholestatic hepatitis in time.
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PMID:[Cholestatic hepatitis as a rare side effect of therapy with ticlopidine]. 1096 56

Twelve patients with chronic hepatitis C received interferon-alpha at doses of 3 million units (11 patients) or 6 millions units (1 patient) 3 times per week for 52 weeks. The patients were evaluated for clinical response, and total blood cell count, B and T lymphocyte count, subtyping of CD4+ and CDS+ lymphocytes, blastic transformation of lymphocytes after stimulation with phytohemagglutinin and concanavalin-A, and liver function tests. Liver biopsies with immunohistochemical methods were done before and after treatment in 7 patients. Blood tests were done every 4 weeks in all 12 patients. Serum beta-2-microglobulin was measured before treatment and after 32 and 52 weeks. Patients with liver disease due to other causes (autoimmune disease and HIV infection) were excluded. The following results were obtained: 1) Four patients improved with treatment (4/12 = 33%) during the 52 week treatment period; 3 of them responding completely and one partially. Two others who were not considered responders maintained ALT levels below 1.5x the normal range after the end of therapy. One of these had received the higher dose of interferon-alpha. Histopathologically, 10 patients improved (10/12 = 83%), one presented progression of the disease and one did not show significant changes with treatment; 2) Immunological evaluation before and after treatment did not show significant differences except for total blood lymphocyte count, which was decreased after treatment; 3) T and CD4+ lymphocyte counts in liver tissue were significantly decreased after treatment, but there was no change in the pattern of their distribution within the hepatic parenchyma. These findings confirm that interferon-alpha is effective in patients with hepatitis C, and suggest that the drug has a predominantly antiviral effect in chronic hepatitis caused by C virus, and that the hepatocellular damage observed in these cases is mainly due to the cytopathic effect of the virus rather than immunopathologic processes.
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PMID:Response in Patients with Chronic HCV Hepatitis to Treatment with Interferon-alpha. 1109 15

Following an acute episode of undifferentiated collagenosis/autoimmune disease with joint pain, a 50-year-old female patient with known long-standing chronic hepatitis B was treated orally with corticosteroids (30 mg prednisolone in decreasing doses over a period of six months). During this treatment, exacerbation of hepatitis B and massive flare-up under simultaneous treatment with lamivudine occurred (GOT 530 U/L, GPT 791 U/L). Serology was positive for HBs-Ag and anti-HBc-lgM. HBV-DNA titer was > 400,000 copies/ml in polymerase chain reaction. Considering the increased risk of reactivation of autoimmune phenomena during a six months therapy with interferon-alpha, an intensive combination therapy with interferon-beta and -gamma (2 weeks: 1 x 3 MIU nIFN-beta Fiblaferon i.v.; 3 weeks: 1 x 3 MIU nIFN-beta i.v. plus 1 x 50 microg rIFN-gamma Imukine) was carried out over five weeks. After two months this resulted in a complete viral and biochemical response. During an observation period of twelve months no reactivation of the autoimmune disease occurred.
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PMID:[Severe exacerbation of chronic hepatitis B during therapy with corticosteroids and lamivudine therapy and successful short-term combination therapy with interferon-beta and interferon-gamma]. 1277 56


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