Higher Serum Aspartate Aminotransferase Research Articles

Distribution of liver haemosiderin iron in 187 patients with various types of hepatic diseases.

The purpose of this study was to evaluate the distribution of haemosiderin iron in various regions of the liver (central, intermediary and peripheral hepatocytes, Kupffer cells, portal macrophages and bile duct epithelial cells) in 174 patients with different hepatic diseases (alcoholic cirrhosis (n = 49), alcoholic steatosis (n = 60), non-alcoholic cirrhosis (n = 16), acute hepatitis (n = 20), clinically overt untreated hereditary haemochromatosis (n = 3), miscellaneous disorders (n = 26)), and in 13 subjects with a normal liver biopsy. Furthermore, the relationship between liver haemosiderin iron, biochemical iron status markers and biochemical liver tests was investigated. In haemochromatosis iron was consistently present in all examined regions of the liver, and in 43% of patients with alcoholic liver disease haemosiderin was present in at least one region of the liver lobule. In 65% of patients with acute hepatitis, haemosiderin was present in macrophages and Kupffer cells. In other hepatic diseases and in normal livers, haemosiderin was rarely seen. Regression analyses showed a correlation between iron status markers in most patients, except in those with high serum aspartate aminotransferase levels. In conclusion, haemosiderin iron is distributed in a typical pattern in haemochromatosis, alcoholic liver disease and acute hepatitis. Both histochemical liver iron and serum ferritin are of value as indirect markers of liver iron stores in patients with moderate hepatocellular damage.

Correlation between hepatitis B viremia and the clinical and histological activity of chronic delta hepatitis

To analyze the serological, clinical and histological significance of hepatitis B virus (HBV) replication among a group of patients with chronic delta hepatitis (CDH), we have studied the clinical and the histological activity in 49 patients with CDH. The HBV-DNA was analyzed by dot-blot and polymerase chain reaction (PCR). Concomitant infection with hepatitis C virus (HCV) was analyzed by reverse transcriptase (RT)-PCR, HDV replication by dot-blot, and human immunodeficiency virus (HIV) infection by enzyme-linked immunosorbent assay. The subjects were divided into three groups according to HBV-DNA status: group I: 14 patients HBV-DNA dot-blot positive; group II: 29 patients HBV-DNA positive only by PCR, and group III: 6 patients HBV-DNA negative by dot-blot and PCR. We have found HBV-DNA by dot-blot in 28.5% of patients, and by PCR in 87.7%. Also 22 patients were anti-HCV positive (86.3% had HCV-RNA by RT-PCR). The first group (HBV-DNA dot-blot positive) had significantly higher serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) than those in the second and third groups. Likewise, serum ALT and AST were significantly higher in the second group (HBV-DNA positive by PCR) than in those of the third group. Histological inflammatory activity was significantly higher in the group of patients with HBV-DNA detectable by dot-blot. The prevalence of serum HDV-RNA and IgM anti-HDV were similar in the three groups. These results were similar in the anti-HCV-positive and -negative patients. In conclusion, these data suggest that: (1) persistence of HBV replication is a major determinant of severe liver damage in chronic delta hepatitis, and (2) HCV and HIV infections do not influence the natural history of CDH.

Evidence against hepatitis viruses as important causes of severe autoimmune hepatitis in the United States

To determine if the hepatitis viruses are important etiologic factors in autoimmune hepatitis, the clinical, immunoserologic, virologic and HLA phenotypes of 105 of the latter patients were assessed prospectively and compared to 45 patients with chronic viral hepatitis. Patients with autoimmune hepatitis were more often women with higher serum aspartate aminotransferase and immunoglobulin levels than patients with viral disease. Only eight patients (8%) were seropositive for anti-HBc and anti-HBs (four patients) or anti-HCV (four patients) and none with anti-HCV were reactive by second generation immunoassay or recombinant immunoblot assay. Smooth muscle (90 vs. 22%, P < 0.001) and antinuclear (70 vs. 22%, P < 0.001) antibodies were more common in patients with autoimmune hepatitis and the titers more frequently exceeded 1:80 (84 vs. 11%, P < 0.0001). Patients with autoimmune hepatitis were more often positive for HLA B8 (48 vs. 20%, P < 0.01) and DR3 (49 vs. 20%, P < 0.003) and they more frequently had the HLA A1-B8-DR3 phenotype (38 vs. 10%, P < 0.003). Only one of the 120 patients tested for anti-LKM1 was seropositive. We conclude that in an American referral population autoimmune hepatitis usually lacks virologic markers and has a distinctive clinical, immunoserologic and HLA phenotype. Hepatitis viruses are not important immunogenic stimuli for non-organ specific antibodies and they are unlikely to be important causes of this form of autoimmune hepatitis.

Incidence and properties of aspartate aminotransferase-immunoglobulin complexes in patients with a high serum aspartate to alanine aminotransferase ratio

Sera of 260 patients with high serum aspartate aminotransferase ( l-aspartate: 2-oxoglutrate aminotransferase, EC 2.6.1.1; AST)/alanine aminotransferase ( l-alanine: 2-oxoglutrate aminotransferase, EC 2.6.1.2; ALT) ratio (>2.0) and high serum AST (> 45 IU/1) were selected and tested for the presence of immunoglobulin complexed-AST, by using immunoprecipitation reaction and counterimmunoe-lectrophoresis. The macromolecular AST was confirmed by size-exclusion high-performance liquid chromatography (HPLC). 34 patients out of 260 were found to have AST-immunoglobulin complexes (13.1%). The classes of AST-linked immunoglobulins were identified to be α in 28 cases (82.4%, P < 0.01), mixed type of α and γ in 5 cases (14.7%) γ in one case (2.9%). Positive frequency was the highest in liver malignancies, either primary (9/26, 34.6%) or metastatic (7/17, 42.2%), followed by other malignancies (6/55, 10.9%) and chronic liver diseases (4/22, 18.2%). Thus, it can be strongly suggested that the immunoglobulin A complexed-AST is frequently found in association with liver malignancies.

The role of maternal alcohol damage on ethanol teratogenicity in the rat.

To study the severity and degree of in utero alcohol effects in relation to the rate of maternal alcohol damage, multiparous 1-year alcohol-fed rats were used, with an appropriate pair-fed control group. During pregnancy, alcoholic dams showed relatively high acetaldehyde levels (41 +/- 19 mumol/l) and blood alcohol levels of 22.8 +/- 14 mmol/l. They also showed marked histological alterations in liver as well as high serum aspartate-aminotransferase, alanine-aminotransferase, alkaline phosphatase, glutamate dehydrogenase, and gamma-glutamyltransferase activities. The increase in serum enzyme levels did not correlate with an increase in hepatic enzyme levels since only glutamate dehydrogenase was enhanced in liver after 1 year of alcohol intake. In addition, except for an increase in low Km aldehyde dehydrogenase activity, there were no changes in liver alcohol metabolizing enzymes in chronic alcohol vs. pair-fed females. Alcoholic rats showed a high incidence of damage in their progeny (resorptions, immature fetuses, decrease in fetal weight, etc.), and rats with the highest serum levels of the above enzymes (especially glutamate dehydrogenase and gamma-glutamyl transferase) had severely affected progeny. Rats with minimal histological liver damage, in contrast, did not show resorptions. Thus, the results presented suggest that the stage of maternal alcohol illness, as indicated mainly by the extent of liver damage, plays an important role in the frequency and severity of in utero alcohol effects in the rat.

Clinical Course of Chronic Lobular Hepatitis&lt;subtitle&gt;REPORT OF FIVE CASES&lt;/subtitle&gt;

The clinical course, and biochemical, immunological, and liver histological changes in five patients with chronic lobular hepatitis are described. All were male (ages 17 to 44 years) and presented with an acute viral hepatitis-like illness. In two of these patients liver function tests have never returned entirely to normal and in both prednisone has been necessary to maintain control of the disease. In the other three the subsequent clinical course has been characterized by remission and relapse. Up to four relapses have occurred with a return of symptoms and strikingly high serum aspartate aminotransferase concentrations (844 to 2800 iu/l), and two of the three patients have required prednisone to induce remission. The remissions appear to be complete and have lasted for up to five years. During relapse the changes in liver histology on biopsy have invariably been indistinguishable from those of acute viral hepatitis, no case showing progression to cirrhosis even after eight and a half years. All cases had non-organ specific auto-antibodies (antinuclear, antimitochondrial, or anti-smooth muscle) demonstrable in the serum and four had hyperglobulinaemia (52 to 79 g/l). These findings together with the initial presentation, the changes on liver biopsy, and the relapsing course would all be consistent with a persistent virus infection.

Pitfalls in the diagnosis of jaundice due to carcinoma of the pancreas or biliary tree.

Analysis of 56 patients with obstructive jaundice due to carcinoma of the pancreas or extrahepatic biliary tree showed that unexpected features were present in 25%. Presentation with painless jaundice was uncommon, and the symptoms were more often non-specific, with malaise, anorexia, and vomiting. Abdominal pain was frequent, and the condition was found in young patients. One-fifth presented with serum alkaline phosphatase levels of less than 30 K.A. units. Some had high serum aspartate aminotransferase levels, more characteristic of hepatocellular jaundice. A mathematical model may be helpful in correctly weighting these various criteria.