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)

Serial sera were collected prospectively during the clinical course of 13 HBsAg carriers with chronic liver disease and analyzed for ALT levels, pre-S1 and pre-S2 antigens and corresponding antibodies and other serological hepatitis B virus markers. In five patients, anti-pre-S1 and anti-pre-S2 antibodies became detectable in multiple serum samples, whereas in eight patients anti-pre-S was never detected or only appeared transiently during the follow-up. The first pattern was associated with normalization of ALT levels and undetectable pre-S antigens and viral DNA by the polymerase chain reaction assay at final follow-up. HBsAg clearance occurred in two of the five patients. The second pattern was one of persistence of HBsAg and pre-S antigens, associated with the presence of serum HBV DNA detectable by spot hybridization or polymerase chain reaction regardless of clinical outcome. These findings demonstrate the occurrence of anti-pre-S antibodies in chronic hepatitis B virus-induced liver disease and associate anti-pre-S appearance with the clearance of hepatitis B virus from serum.
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PMID:Anti-pre-S responses and viral clearance in chronic hepatitis B virus infection. 172 95

Serum level of osteocalcin (OC) is believed to be a specific biochemical parameter of bone formation. Decreased serum OC has been reported in alcohol-intoxicated subjects, in patients with primary biliary cirrhosis and in patients with chronic alcoholic liver disease. The question was, whether lower OC level could be detected in patients with nonalcoholic and non-cholestatic chronic liver disease. The serum OC was measured by RIA developed in our laboratory. Results were compared to age and sex matched controls. Decreased OC level was found in 35 out of 47 (74%) patients with non-alcoholic and non-cholestatic liver disease as chronic persistent hepatitis, chronic active hepatitis, fatty liver and cirrhosis, in 21 out of 26 (80%) patients with alcoholic liver disease and in 8 out of 15 (53%) primary biliary cirrhosis. None of the patients had elevated value. There was no correlation between the decreased OC level and the duration or severity of the liver disease and the laboratory parameters as bilirubin, AST, ALT, alkaline phosphatase, albumin, prothrombin, and serum 25-OH-D3 vitamin level. Decreased OC was found also in the patients without cirrhosis. The possible causes are discussed. Relying upon these findings it is supposed that chronic liver disease by itself can influence the osteoblast activity also by some unknown mechanism.
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PMID:[Decreased serum osteocalcin level in non-alcoholic and alcoholic chronic liver diseases]. 185 6

Chronic liver disease associated with hepatitis C virus (HCV) is an important cause of morbidity and mortality in hemophilia. We have used recombinant interferon alpha-2b (IFN alpha-2b) in a randomized controlled liver biopsy trial to treat hemophiliacs with chronic hepatitis. Eighteen patients entered the study, 16 of whom were subsequently shown to have antibodies to the HCV. All underwent liver biopsy at entry and were randomized to either treatment with self-administered IFN alpha-2b, 3 million units subcutaneously thrice weekly (n = 10) or no treatment (control group) (n = 8). Nine subjects had chronic active hepatitis, seven had chronic persistent hepatitis, and two had cirrhosis. Twelve months after entry into the study 17 patients underwent a second liver biopsy. All biopsies were coded, assessed, and scored according to the histologic severity of the liver disease. Ten patients were administered IFN for 1 year, and in four patients normalization of alanine aminotransferase (ALT) occurred compared with none in the untreated group. After the second liver biopsy, six of the eight initial no-treatment patients were treated with interferon 3 million units thrice weekly for 6 months, and normalization of ALT was seen in five patients. Biochemical relapse within 4 months of stopping IFN occurred in one of four patients treated for 1 year and in four of five patients treated for 6 months. IFN treatment was well tolerated. Although the histologic scores of the two groups were similar at entry into the study, after 12 months the biopsy appearances in the treated group were significantly improved compared with the controls (P less than .01). Histologic improvement was noted in the three interferon-treated human immunodeficiency virus antibody-positive patients and also in other patients who had no biochemical response. We conclude that low-dose recombinant IFN alpha is effective in normalizing transaminases and improving the histologic appearances in at least 50% of hemophiliacs with chronic hepatitis C.
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PMID:A randomized controlled trial of recombinant interferon-alpha in chronic hepatitis C in hemophiliacs. 191 56

Twenty-one of 40 patients with chronic non-A, non-B hepatitis (37 anti-HCV positive) were randomised to receive interferon alpha 2b (3 million units subcutaneously thrice weekly for 24 weeks) and then to be observed for six months. Among the other 19 patients (controls) randomised to be observed without treatment for 12 months, eight have subsequently been treated with interferon for six months. One treated patient and three controls were lost to follow-up. A return to normal serum alanine aminotransferase levels which lasted until the end of the treatment period occurred in 18 (64%) of the 28 patients given interferon (and in 13 of 21 (62%) randomised to treatment), but only in one of the 16 untreated controls (p less than 0.001). Multivariant analysis indicated that, compared with the ten nonresponders, the 18 patients who responded to interferon were more likely to have acquired infection by intravenous drug abuse than by blood transfusion (p less than 0.05), and were more likely to have histologically less severe chronic liver disease (p less than 0.01). Thus, all 13 patients with less severe liver disease histologically responded to interferon, but only five of 15 patients with cirrhosis or bridging fibrosis responded. Among 17 responders followed for more than four months, five (28%) are still in remission a median of 13 months (range four months to 24 months) after stopping interferon. The characteristics which favoured a response during treatment also appeared to distinguish those who experienced sustained post-treatment remission.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Can the response to interferon treatment be predicted in patients with chronic active hepatitis C? 195 24

Antibodies to hepatitis C virus, hepatitis B serology and liver enzymes were examined in 137 Finnish haemophiliac patients to detect signs of chronic viral hepatitis and its possible aetiological associations. The prevalence of raised alanine aminotransferase values was 37%. These were significantly associated with hepatitis C seropositivity but not with hepatitis B antibodies, severity of haemophilia or the type of clotting factor used in replacement therapy. The prevalence of hepatitis C seropositivity was 50%; it was significantly associated with severe haemophilia and with the use of large pool concentrates. The hepatitis C virus seems to be the major cause of chronic liver disease transmitted by clotting factors also in Finland, despite a somewhat lower seroprevalence than described elsewhere so far.
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PMID:Antibodies to hepatitic C virus and chronic liver disease among Finnish patients with haemophilia. 196 89

Hydrophobic bile acids have been shown to be hepatotoxic, whereas treatment with ursodeoxycholic acid, a hydrophilic bile acid, has improved liver function indices in patients with chronic liver disease. Taurine administration has also been suggested to be useful for chronic hepatitis, taurine-conjugated bile acids being more hydrophilic than glycine-conjugated bile acids. To determine if taurine and ursodeoxycholic acid are beneficial and if their effects are additive, a double-blind, randomized trial was designed comparing the effects of ursodeoxycholic acid, taurine, and a combination of the two on indices of liver injury in 24 patients with chronic hepatitis. They were assigned at random to two of the four following treatments: ursodeoxycholic acid (600 mg/day), taurine (1.5 g/day), ursodeoxycholic acid plus taurine (600 mg + 1.5 g/day) or placebo, given in two successive cycles of 2 mo each, according to a balanced incomplete-block design. Ursodeoxycholic acid became the predominant biliary bile acid when administered alone or in combination with taurine, and taurine conjugate levels increased during taurine administration. Ursodeoxycholic acid reduced aspartate aminotransferase (35%), alanine aminotransferase (33%), and gamma-glutamyl transpeptidase (41%), whereas taurine alone did not. The addition of taurine to ursodeoxycholic acid produced only minor changes in the effects of ursodeoxycholic acid alone. Results were confirmed by the administration of ursodeoxycholic acid, in a successive open phase of the study, to the entire patient population, which was large enough for different subsets of patients to be compared. Serum bile acids were measured at entry and during the open phase: primary bile acids did not change, whereas ursodeoxycholic acid levels increased from trace amounts to very high levels, especially in patients with more severe histological disease. It is concluded that ursodeoxycholic acid, but not taurine, improves enzymatic indices of liver injury in chronic hepatitis.
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PMID:Effects of ursodeoxycholic acid and taurine on serum liver enzymes and bile acids in chronic hepatitis. 196 71

We studied 145 children with acute lymphocytic leukemia (ALL) in remission who had been off chemotherapy for at least 2 years, to assess the prevalence of hepatitis delta virus (HDV) infection, and to determine whether HDV infection was associated with more severe chronic liver disease. The prevalence of chronic HBV infection was 41.5% (60/145). The prevalence of HDV infection among these patients with chronic HBV infection was 50% (30/60). Eighty-five patients were HBsAg-negative. There was evidence that HDV-infected children had more severe chronic liver disease than did HBsAg-positive, anti-HDV-negative patients: (1) their serum ALT levels were significantly more likely to be elevated at long-term follow-up (27/30 vs. 10/26, p = 0.0001); (2) their mean ALT levels were significantly higher 3 years after the cessation of chemotherapy (128 vs. 84 IU/L, p = 0.001); and (3) they were more likely to have either chronic acute hepatitis or cirrhosis when liver biopsy was done (18/23 vs. 6/18, p = 0.0038). Children who were HBsAg-negative had the lowest alanine aminotransferase (ALT) levels and were least likely to have chronic active hepatitis or cirrhosis (3/31). We conclude that infection with HDV in children with ALL is associated with serious chronic liver disease. In long-term survivors, HDV infection is a major cause of morbidity and an adverse prognostic factor in terms of leukemia-free survival.
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PMID:Delta virus and childhood leukemia. 202 65

Hepatitis C virus (HCV) is the predominant etiologic agent of posttransfusion non-A, non-B hepatitis, characterized by undulating elevation of alanine aminotransferase (ALT) and chronic liver disease. A commercial enzyme-linked immunosorbent assay detected antibodies to HCV (anti-HCV) in 11 specimens among 101 nontransfusable plasma units obtained from asymptomatic, volunteer blood donors with elevated levels' of ALT. Using a combined reverse-transcription polymerase chain reaction (RT-PCR) assay developed by us, HCV RNA was detected in 0.6 ml of plasma from 8 of 11 (73%) of the anti-HCV-positive but in none of the 90 anti-HCV-negative specimens. The relatively low concentration of HCV RNA could be detected in the remaining three anti-HCV-positive specimens when 2.4 ml of plasma was analyzed. The plasma concentration of virions was estimated to range from 10(2) to 5 x 10(7)/ml. Direct sequencing performed on the PCR-amplified HCV cDNAs (210 base pairs) from three specimens revealed heterogeneity between 2.5 and 8.6% at the nucleotide level and less than 4% at the amino acid level. Our findings demonstrate that RT-PCR can be performed with 2.4 ml of plasma, providing an assay for the direct detection of HCV RNA and confirming the existence of an asymptomatic carrier state for HCV infection in the apparently healthy anti-HCV-positive donors.
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PMID:Detection, semiquantitation, and genetic variation in hepatitis C virus sequences amplified from the plasma of blood donors with elevated alanine aminotransferase. 217 25

Markers of hepatitis B virus (HBV) and immune response against them were studied in 18 chronic asymptomatic carriers, 8 patients of the virus induced chronic liver disease (CLD), and 7 patients of chronic alcoholic liver cirrhosis, who were also chronic HBV carriers (CALC). The LMI responses to HBeAg were elevated in HBeAg and/or HBV-DNA positive chronic asymptomatic carriers, (median response 31.5%), along with elevation of serum alanine aminotransferase (sALT) levels (59-150 IU/l). On the other hand the LMI responses to this antigen, in HBeAg and HBV-DNA negative chronic carriers were in the normal range (median response 12%) and their sALT levels were also normal (7-50 IU/l). The CLD and CALC patients did not show any relation between their LMI to HBeAg and sALT levels. In contrast no relation between LMI to HBsAg and sALT levels was observed in any group. The LMI responses to HBsAg in CLD patients were elevated (median response 38%) and the responses of chronic asymptomatic carriers and CALC patients were either in the normal range or poor (median responses, 18 and 7% respectively), irrespective of their sALT levels. These results suggest that T cell responses to both the antigens may be involved in liver cell damage.
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PMID:Immune response to hepatitis B viral antigens in chronic infection & its relationship with liver necrosis. 222 52

Evidence is accumulating that ursodeoxycholic acid (UDCA), an agent widely employed for gallstone dissolution, exerts therapeutic effects in chronic liver disease. UDCA is thought to act mainly by reducing the detergent properties of bile, making it less toxic for the liver cells. Confirming the results of preliminary observations double-blind, placebo-controlled trials have shown that UDCA significantly decreased serum concentrations of liver enzymes such as alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and gamma-glutamyl transferase in primary biliary cirrhosis and other cholestatic conditions, as well as in chronic active hepatitis. A substantial improvement in liver histology has also been detected in UDCA-treated patients with primary biliary cirrhosis. The effect of UDCA in chronic hepatitis is currently a matter of investigation.
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PMID:Treatment of chronic liver disease with ursodeoxycholic acid. 229 32


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