Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical specifity of an intraparticular virus-DNA of 5001 Bp associated with non-A, non-B hepatitis (HNANB) was evaluated. Investigations were done in liver biopsies and lymphocytes in 173 patients having acute or chronic HNANB (n = 107) or liver diseases of other etiology (n = 66). The sensitivity of the test system (polymerase chain reaction, southern-transfer, DNA-hybridisation with synthetic oligonucleotides) was less than 100 virus particles per probe. In all patients with acute HNANB (n = 5) (parenteral mode of infection) the DNA was found in 100% in liver and lymphocytes, and in 22 of 27 patients with acute sporadic HNANB. HNANB associated substance (HNANB-AS) (1.3 g/ml CsCl) excreted with feces was found in 50%, and 29.6%, respectively. In chronic HNANB the DNA was found in 83.3% in the liver (n = 42) and in 56.7% in lymphocytes (n = 30). The HNANB-AS was found in 45.6% (n = 68). In liver diseases with other etiologies as HNANB-infection (e.g. HBV, HAV, cholestasis, HBsAg pos.-liver cirrhosis) (n = 33) the DNA was found neither in liver biopsies nor in lymphocytes. In liver diseases of uncertain etiology, but with NANB-infection under discussion (e.g. nonspecific reactive hepatitis, fatty liver, HBV neg liver cirrhosis) the DNA was found in the liver in 24% (n = 25) and in lymphocytes in 40% (n = 5). In patients with clinically resolved HNANB no DNA was found in liver and lymphocytes (n = 5). All stools were negative for HNANB-AS in the latter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical studies of the specificity of detecting viral DNA in non-A, non-B hepatitis in liver tissue and lymphocytes]. 170 May 57

Immunological factors are important in the pathogenesis of a spectrum of hepatobiliary diseases. To characterize the nature of specific immunological responses in liver disease, we determined lymphocyte changes in liver tissue and in blood using flow cytometry. A total of 113 liver biopsy specimens was collected from patients with the following diseases: 19 chronic hepatitis B; 39 chronic non-A, non-B hepatitis; 27 alcoholic liver disease; 10 hepatic malignancy; 8 autoimmune hepatitis; 6 fatty liver and 4 primary biliary cirrhosis. The lymphocytes were isolated from the liver biopsy specimens by mechanical and enzymatic methods. The lymphocyte yield was 7,901 +/- 575 cells/mg of liver tissue. The viability of lymphocytes was 97.7% +/- 0.3%. Lymphocytes were stained with four pairs of two-color mixed fluorescein-conjugated monoclonal antibodies, including T4-T8 (CD4/CD8), T11-B1 (CD2-CD20), NKH1-T8 (CD56-CD8), IL-2R1-T11 (CD25-CD2), and the ratios were determined by an Epics Profile flow cytometer. Immunophenotyping of lymphocytes in whole blood samples was simultaneously analyzed. Variability in lymphocyte yield and different patterns of lymphocyte subsets were found in the liver biopsy specimens. The yields of lymphocytes from patients with chronic non-A, non-B and autoimmune hepatitis were highest, and the lowest yield was from patients with fatty liver. Patients with primary biliary cirrhosis, fatty liver and hepatic malignancy had relatively high ratios of CD4/CD8, CD56/CD8 and CD25/CD2; whereas patients with chronic hepatitis B, autoimmune hepatitis and non-A, non-B hepatitis had lower ratios of CD4/CD8, CD56/CD8 and CD25/CD2. No difference in lymphocyte ratios between the patients with cirrhotic and noncirrhotic alcoholic liver disease was found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunophenotyping of lymphocytes in liver tissue of patients with chronic liver diseases by flow cytometry. 171 36

A relatively noninvasive method is needed to evaluate the hepatic blood flow of patients with liver disease. We used per-rectal portal scintigraphy with 133Xe, and analysed the time-activity curves of the liver and portal vein. To do this, wash-out curves of the liver were plotted, and the hepatic blood flow and the ratio of the blood flow to the right lobe of the liver to that to the left lobe (R/L ratio) were calculated. The mean hepatic blood flow was 137 +/- 23 ml/100 g/min for four patients with fatty liver, 139 +/- 16 ml/100 g/min for seven patients with chronic persistent hepatitis, 120 +/- 15 ml/100 g/min for ten patients with chronic aggressive hepatitis, and 75 +/- 21 ml/100 g/min for 14 patients with cirrhosis. All seven patients with hepatic blood flow that was less than 100 ml/100 g/min and an R/L ratio less than 1.0 had cirrhosis. Only two of the 22 patients with hepatic blood flow that was greater than 100 ml/100 g/min and an R/L ratio greater than 1.0 had cirrhosis. Per-rectal portal scintigraphy can be used to measure the hepatic blood flow, but it was not useful for the diagnosis of fatty liver.
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PMID:Measurement of hepatic blood flow by use of per-rectal portal scintigraphy with 133Xe. 185 84

The authors examined the aminoterminal type III procollagen peptide level of serums and killer-cell activity peripheric blood lymphocytes with 75 patients suffering from ethanol originated liver diseases as well as control samples from 40 healthy volunteers. Determination of type III procollagen peptide (Fab) took place by the RIA method. The cytotoxic activity of killer-cells was tested against human red blood cells. Both in fatty liver and chronic alcoholic hepatitis the level of type III procollagen peptide increased, while in liver cirrhosis the same level reached a value three times of the normal. At the same time in cirrhosis hepatitis an increased killer-cell activity could be observed. Type III procollagen peptide values were also analysed in view of the cytotoxic capacity of killer-cells. At first ill, then healthy control individuals were divided into three groups according killer-cell activity values. Results have shown that in the group with a high level killer-cell activity average type III procollagen peptide values were significantly greater as compared to those of the medium or low level activity groups. These results might indicate a relation between a conditional antibody-dependent cellular cytotoxicity reaction and increasing collagen synthesis.
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PMID:[Serum aminoterminal type III procollagen peptide level and killer cell activity in patients with alcoholic liver diseases]. 195 78

In 230 patients (90 females, 140 males aged between 20 and 73 years, average age 47.8 years) with and without exception histologically and/or laparoscopically ascertained chronic liver diseases (degenerative damages of liver parenchyma in 45, fatty liver stage I in 28, fatty liver stage II in 36, cholangiohepatitis in 4, chronic persisting hepatitis in 31, chronic active hepatitis in 57 and liver cirrhosis in 59 cases) the incorporation of the aminophenazon breathing test in the so-called laboratory chemical liver spectrum was controlled. The restriction of the microsomal biotransformation established by means of the aminophenazon breathing test behaved parallel to the degree of severity of the disease. The aminophenazon breathing test was performed in the modification after Haustein and Schenker (1985). The largest delays in the decomposition were found in the complete cirrhotic transformation of the liver. The unequivocally pathologic result of the aminophenazon breathing test in severe irreversible damages of the liver parenchyma was confirmed by the formation of correlations with parameters of the conventional laboratory spectrum of the liver. Thus the restriction of the performance of the synthesis of the liver for coagulation factors and albumins was parallel to the loss of function of the mixed functional oxidases. In all patients with chronic liver diseases a connection between the value of the thromboplastin time (Quick's test) and result of the breathing test was found. Positive linear correlation between serum albumin and results of the breathing test could also be proved particularly in the group of the severe chronic inflammatory liver diseases. In chronic fibrosing liver diseases there were positive inverse correlations between gamma-globulin concentration in the serum and thymol turbidity test on the one hand as well as the aminophenazon breathing test on the other. There were no correlations between liver enzyme and aminophenazon breathing test. The results of the own investigations incorporate the aminophenazon breathing test as indicator of a severe liver cell damage which at the same time is established by the pathological result of the so-called synthesis parameters of the liver.
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PMID:[The diagnostic value of the aminophenazone breath test in chronic liver diseases]. 196 92

Lymphocytic dipeptidylaminopeptidase IV (DP-IV; E.C.3.4.14.5.) is described as a marker enzyme of immunostimulant T-lymphocytes as well as functional characteristic of IL-2-producing cells. Mononuclear cells of periphere blood (MNC) were isolated by density gradient centrifugation followed by enzymcytochemical staining of DP-IV positive cells and measuring of DP-IV enzyme activity using chromogenic substrates. As relative sign of single cell DP-IV activity we calculated average DP-IV activities of DP-IV positive cells. Blood samples from 14 patients with acute virus hepatitis, 30 cases of chronic active liver disease, 61 cases with liver cirrhosis of various kind and 19 patients with fatty liver and toxic hepatitis were investigated. As standard of comparison we used a group of healthy blood donors. By this way significant differences of described DP-IV parameters between some groups of liver disease were evident. Using an aetiologic classification of investigated liver diseases we found highly significant increased single cell activities in hepatitis-B associated cases in comparison to remarkable lower lower values in autoimmune cases. Different hypothesis about changes of lymphocytic dipeptidylaminopeptidase IV as a part of disturbed immunoregulation in chronic liver diseases were discussed.
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PMID:[Dipeptidylpeptidase IV activity in human lymphocytes in hepatobiliary diseases]. 197 80

An arabinogalactan-coated ultrasmall superparamagnetic iron oxide (AG-USPIO) preparation specific for asialoglycoprotein (ASG) receptors on hepatocytes was used as a magnetic resonance (MR) imaging contrast agent in the evaluation of a spectrum of benign liver diseases in animal models. The activity of hepatocyte ASG receptors, which directly reflects liver function, was directly assessed by measuring liver relaxation times in vitro and MR signal intensity in vivo. The following measurements allowed three-dimensional assessment of liver function: (a) liver relaxation time, (b) native MR signal intensities of liver, (c) response of liver to the AG-USPIO probe (percentage decrease of liver signal intensity after intravenous administration of 10 mumol/kg of AG-USPIO: normal liver 55%, fatty liver 57%, acute hepatitis 36%, chronic hepatitis 29%, and cirrhosis 46%), and (d) redistribution of hepatocyte-specific AG-USPIO to the spleen (present in hepatitis and cirrhosis but not in normal liver and fatty liver). The results of this study indicate that cellular hepatic abnormalities can be detected and quantitated with MR receptor imaging.
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PMID:Asialoglycoprotein receptor function in benign liver disease: evaluation with MR imaging. 199 16

The disposition of phenazone (antipyrine), a low extraction compound with low protein binding, is known to be altered in the presence of various types of hepatic dysfunction. As such, its pharmacokinetics may be useful in the objective characterisation of altered liver function. Understanding the known effects of various liver disease states upon the disposition of this probe may provide insight into future applications. This article provides a review of background information about normal plasma phenazone pharmacokinetics, urinary metabolite disposition and tabulations of reported total body clearances of the drug in the presence of cirrhosis, fatty liver, hepatitis and cholestasis in humans. An estimate is made of the sensitivity and specificity of phenazone testing for the verification of the presence of cirrhosis based on this compiled literature.
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PMID:Quantifying hepatic function in the presence of liver disease with phenazone (antipyrine) and its metabolites. 202 2

We investigated lipopolysaccharide-induced tumor necrosis factor production in vitro by peripheral blood monocytes from patients with various liver diseases. Tumor necrosis factor production was found to be significantly reduced in patients with chronic hepatitis B (n = 17; 135 +/- 30 pg tumor necrosis factor/ml; mean +/- S.E.M.) and patients with chronic non-A, non-B hepatitis (n = 15; 212 +/- 22 pg tumor necrosis factor/ml) compared with healthy control individuals (n = 47; 411 +/- 40 pg tumor necrosis factor/ml; p less than 0.0005 and p less than 0.01, respectively). This reduced tumor necrosis factor production was not only seen with an optimal stimulating concentration of lipopolysaccharide (100 ng/ml) but also with suboptimal concentrations (0.1 ng/ml). In contrast to patients with chronic viral hepatitis, monocytes from patients with alcohol-induced cirrhosis (n = 26; 444 +/- 49 pg tumor necrosis factor/ml), primary biliary cirrhosis (n = 7; 412 +/- 81 pg tumor necrosis factor/ml) and alcohol-induced fatty liver changes (n = 5; 401 +/- 62 pg tumor necrosis factor/ml) produced normal amounts of tumor necrosis factor when stimulated with an optimal concentration of lipopolysaccharide. Lipopolysaccharide (0.1 ng lipopolysaccharide/ml)-stimulated peripheral blood monocytes of patients with chronic hepatitis B (n = 15; 102 +/- 32 pg/ml) or non-A, non-B hepatitis (n = 13; 97+/- 16 pg/ml) could not be induced to produce more tumor necrosis factor either when prestimulated with gamma-interferon (170 +/- 45 pg/ml and 149 +/- 32 pg/ml, respectively), a lymphokine known to activate monocytes, or with the cyclooxygenase inhibitor indomethacin to reduce the suppressive effect of prostaglandin E2 (148 +/- 40 pg/ml and 153 +/- 45 pg/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired lipopolysaccharide-inducible tumor necrosis factor production in vitro by peripheral blood monocytes of patients with viral hepatitis. 212 37

24 patients with alcoholic intake were classified according to the amount of alcohol ingestion; clinical symptoms and signs, liver function tests (bilirubin, aminotransferases and prothrombin time) were analyzed. In all patients a percutaneous liver biopsy was performed and tissue stained by hematoxylin-eosin, wilder reticulin and Mallory trichromic. 9 Histologic criteria were analyzed. 4 groups according to the histology were identified. Group 1 (5 patients) hepatic fibrosis and/or fatty liver. Group 2 (5 patients) alcoholic hepatitis. Group 3 (10 patients) cirrhosis. Group 4 (4 patients) normal. 20% of patients with fatty liver, 80% of alcoholic hepatitis and 100% of cirrhotics referred ingestion or more than 160 g of ethanol and important correlation between liver histological damage and alcohol ingestion. Telangiectasia was the most common clinical finding and present in all hepatitis, 70% of cirrhotics and only 20% of fatty livers. Hemosiderosis was found in 60% of cirrhotics and in alcoholic hepatitis. Only 40% of patients with fatty liver and inflammatory cells while this was evident in all patients with alcoholic hepatitis and those with cirrhosis. Mallory bodies were identified in only 20% of cirrhotics and in none of the alcoholic hepatitis. The results suggest that there are significant differences from a histological and clinical point of view that distinguish alcoholic liver disease as seen in Venezuela from that reported in other countries.
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PMID:[Alcoholic liver disease in Venezuela. Clinical hepato-functional and histopathologic course]. 215 50


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