Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Salicylamide glucuronide (SAMG) in 0-6 and 6-12 hours-urine specimens was determined after oral administration of salicylamide in 7 normal volunteers (NV), in 51 cases of various liver diseases and hyperbilirubinemias, and in 19 cases after drug administration, to predict the in vivo drug metabolism in man and its change by drugs. Maximal glucuronide formation was obtained by 1.0 g of salicylamide administered to NV; thus, this dosage was used in the present study. SAMG as percent of total salicylamide, the percent of SAMG, from 0-6 hours-urine specimens was high and constant in NV (71.3 +/- 8.3 (Mean +/- S.D.)). 0-0.08% of the total salicylamide was confirmed as free salicylamide in 0-12 hours-urine specimens of NV. The percent of SAMG of 0-6 hours-urine specimens was 57.2 +/- 8.6 in acute hepatitis, 66.6 +/- 10.9 in chronic hepatitis, and 48.6 +/- 10.7 in liver cirrhosis (mean +/- S.D.). Free salicylamide increased slightly in liver diseases. Serum bilirubin levels tended to be inversely correlated with the percent of SAMG. In most cases of Gilbert's syndrome, the percent of SAMG remained at a normal level. The percent of SAMG in cases with unconjugated hyperbilirubinemias of other geneses were almost within normal limits. Bucolome and phenobarbital increased the percent of SAMG in patients with various liver diseases. After rifampicin or phenytoin administration, the percent of SAMG of the patients with lung tuberculosis or epilepsy did not surpass that of NV.
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PMID:Salycylamide glucuronide formation in liver disease and its change by drugs. 1 Feb 19

The activities of several glycosidases (beta-galactosidase, beta-glucosidase, N-acetyl-beta-glucosaminidase) were demonstrated in human bile. The enzyme activities are increased about 100 times after exclusion of bile salts and other small molecular compounds by Sephadex G-50 gel filtration. The use of 4-methylumbelliferyl derivatives as substrates was useful as measurement of the bile enzyme activities are not altered in the presence of bile pigments. Enzyme characteristics of bile glycosidases were determined: pH optimum and isoelectric point. The bile glycosidase activities were also measured in various hepatobiliary disorders (cholelithiasis, cancer of gallbladder, acute hepatitis, liver cirrhosis and fatty liver). The glycosidase activities in bile from patients with liver diseases, as well as with cholelithiasis, were generally decreased. Isoelectric focusing patterns of biliary glycosidases were similar for specimens from patients with hepatobiliary disorders as compared to normal.
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PMID:Bile lysosomal enzymes: characteristics and pathological significance for various hepatobiliary disorders. 1 80

A group of 165 geriatric patients is compared with a control group of 114 younger patients concerning different frequency of laparoscopic diagnoses. As it was suspected from the clinical view aged patients predominently suffered from posthepatic cirrhosis and from cirrhosis of unknown origin, from recurrent cholecystitis, obstructive jaundice, metastases and carcinosis of peritoneal cavity. Younger patients much more frequently showed toxic liver damage starting from fatty liver and ending up with fatty liver cirrhosis. Persistent acute hepatitis non associated with HBSAg was scarcely seen with the aged group. It was a frequent diagnosis with the younger control group. There are explanations given for the differing endoscopic results concerning aged persons and younger control persons.
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PMID:[Laparoscopic findings in aged patients (author's transl)]. 2 56

Chronic liver disease developing after acute hepatitis type B is well documented, but is not thought to occur after acute hepatitis due to other viruses. However, follow-up of 29 patients in a haemodialysis unit who contracted HBsAg-negative acute hepatitis during 1968-70 revealed 8 cases with raised serum-aminotransferase levels dating from that time. Liver biopsy in 7 of these disclosed chronic aggressive hepatitis in 3, of whom 2 had already progressed to advanced cirrhosis. Chronic persistent hepatitis was present in 2 others, and the remaining 2 had non-specific hepatitis in association with massive iron overload. Immunological studies demonstrated a higher frequency of cellular immunity to HBsAg in those who had previously had acute hepatitis than in those who had not, although the prevalence of humoral antibody was similar in the two groups. One possible explanation for these findings is the presence of immunological cross-reaction at a cellular level between the hepatitis B virus and that responsible for the initial outbreak.
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PMID:Chronic liver disease developing after outbreak of HBsAG-negative hepatitis in haemodialysis unit. 5 71

Additional antigenic sites, distinct from those present on spherical 20 nm diam. particles of hepatitis B surface antigen (HBsAg), are exposed on the surface of Dane particles and tubular forms of HBsAg. The immunological relationship of these sites to e-antigen, an antigen detected earlier in HBsAg-positive sera from patients with chronic hepatitis, cirrhosis or acute hepatitis but not in healthy HBsAg-carriers, was established by immune electron microscopy and affinity chromatography. These findings suggest that e-antigen may be potentially useful in active immunization against hepatitis B.
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PMID:Identification of additional antigenic sites on Dane particles and the tubular forms of hepatitis B surface antigen. 5 22

One hundred liver biopsies from 100 patients with clinical presumptive diagnosis of hepatitis were examined by immunofluorescence for the presence of hepatitis B surface antigen (HBSAg) and hepatitis B core antigen (HBcAg). Of the 60 HBsAg-positive livers, 51 were diagnosed as chronic hepatitis on histological grounds, 6 as acute hepatitis, and 3 as "near-normal liver." From the 60 tissue-positive cases, 3 subjects were HBsAg seronegative. HBcAg was detected in 44 livers, all of which also had HBcAg in the localized in the cytoplasm and the membranes of the hepatocytes, and HBcAg in the nuclei and in 4 cases also in the cytoplasm. Predominant HBsAg expression in the cytoplasm was observed in near-normal liver, chronic persistent hepatitis, and cirrhosis with little activity. This correlated with the amount of ground glass hepatocytes in the biopsies. HBcAg and membrane-localized HBsAg were minimal in those conditions. HBcAg was most prevalent in patients with chronic aggressive hepatitis and active cirrhosis treated with immunosuppressive drugs, whereas the amounts of HBsAg and HBcAg in nontreated patients of those two groups and in acute hepatitis with signs of transition to chronicity were almost equal. HBsAg expression in liver cell membranes was most prominent in active forms of chronic hepatitis (chronic aggressive hepatitis and in active cirrhosis) and in acute hepatitis with signs of transition to chronicity. This observation correlated in the presence of HBcAg in the biopsies of those patients. In acute hepatitis both HBsAg and HBcAg were detected rarely and no membrane expression of HBsAg was observed. The over-all results show a significant relationship between the different degrees of accumulation of HBsAg and HBcAg in the liver and the various histological types of hepatitis and further suggest an interplay of both hepatitis B virus and host immune response in the development and pathogenesis of hepatitis B.
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PMID:Differential distribution of hepatitis B surface antigen and hepatitis B core antigen in the liver of hepatitis B patients. 5 75

Alpha-fetoprotein (AFP) was determined by a new radioimmunoassay in the sera of patients with different liver diseases. Compared to a normal group (n = 140, AFP levels below 15 ng/ml), most elevated AFP concentrations were found in 18 patients with primary liver cancer (PLC), 7 of whom showed Ouchterlony-positive levels (above 10,000 ng/ml). In 3 cases with liver cirrhosis, PLC was first suggested by high AFP levels between 1000 and 3600 ng/ml and later confirmed by histology. On the other hand, only 6 from 15 patients with other primary tumors and liver metastasis had AFP concentrations between 20 and 111 ng/ml. In 90% of 102 patients with liver cirrhosis AFP levels below 20 ng/ml were determined, while 13 cases showed elevated values up to 134 ng/ml. A transitory AFP increase between 20 and 238 ng/ml was seen in 32% of 63 cases in the early stage of acute hepatitis but 65% of 31 these cases in follow-up studies. 3 of 7 cases of chronic hepatitis gave similar results. The maximal AFP levels developed following the maximal transaminase activities by 5-18 days and coincided with a decrease of cholinesterase activity. The radioimmunological determination of AFP is recommended for earlier detection of the development of PLC in liver cirrhosis patients.
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PMID:[Significance of serum alpha-fetoprotein determination. Experiences with our own radioimmunoassay]. 6 Nov 54

Progression of acute type B hepatitis to chronic liver disease and cirrhosis is well recognized, whereas no progression of acute type A hepatitis has as yet been documented. The natural history of acute non-A, non-B hepatitis has not been previously characterized. Ten cases of chronic liver disease were identified in 44 cases of acute non-A, non-B post-transfusion hepatitis. Age, sex, severity of acute illness, and prevalence of preoperative antibodies to known hepatitis-producing agents did not differ between the group whose hepatitis progressed to chronicity and the group whose hepatitis resolved. Less progression of acute hepatitis to chronic liver disease was seen in those patients receiving immune serum globulin preoperatively than in those receiving an albumin placebo (P = 0.009). Only 3 patients had clinical symptoms of hepatitis at the time of liver biopsy, and elevations of liver enzymes and gamma-globulin were mild. However, liver biopsy specimens in 8 of 10 patients showed chronic active hepatitis and an additional biopsy specimen showed cirrhosis. Acute non-A, non-B post-transfusion hepatitis often progresses to chronic active hepatitis. Preoperative gamma-globulin prophylaxis significantly reduces this progression. Identification and characterization of this viral agent(s) will further aid in the prevention of this undesirable complication of blood transfusion.
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PMID:Development of chronic liver disease after acute non-A, non-B post-transfusion hepatitis. Role of gamma-globulin prophylaxis in its prevention. 6 67

When normal lymphocytes were stimulated with PHA in the presence of serum taken from patients with various liver diseases, lower lymphocyte transformation was seen in many cases. The occurrence of a serum inhibitory factor in liver diseases tends to increase with the progress of the disease from acute hepatitis to cirrhosis of the liver. No such inhibitory factor was detected in two asymptomatic HBs-antigen carriers. When the inhibitory factor was fractionated by DE-52 column chromatography, an active component was obtained and shown to have mobilities from alpha2-globulin to beta-globulin in cellulose acetate membrane electrophoresis. However, two active fractions were separated by DEAE-cellulose column chromatography with stepwise increases of the concentration of the acetate buffer and their mobilities were consistent with those of alpha1-globulin and alpha2-globulin, respectively. In 11 cases of acute hepatitis which were followed for at least 6 months, three out of four inhibitory factor positive cases developed into the chronic form and the other became a protracted case. On the other hand, six out of seven inhibitory factor negative cases completely recovered and the remaining case followed a protracted course.
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PMID:Studies on an inhibitory factor to phytohemagglutinin-induced lymphocyte transformation found in the serum of patients with various liver diseases. 8 90

The incidence of primary liver cell carcinoma was investigated in a prospective study over 6 yr and 5 mo in 403 clinically unselected patients derived from a homogeneous population by means of serial determination of alpha 1-fetoprotein (AFP) by radioimmunoassay. The diagnosis of liver cirrhosis was proved in 90% by laparoscopy and/or histology and/or autopsy. The incidence of primary liver cell carcinoma in liver cirrhosis in the clinically studied patients was 4.47%, significantly lower than in the autopsy material (11.03%; p less than or equal to 0.025). In the follow-up study, all patients with increasing AFP concentrations exhibited a primary liver cell carcinoma. A transitory rise of AFP (higher than 50 ng/ml) was observed in 15.1% of patients with liver cirrhosis without primary liver cell cancer. In contrast to the results of animal experiments, this transitory rise of AFP was not followed by malignant transformation of the cirrhotic tissue. Posthepatitic liver cirrhosis was observed in 21.57%, postalcoholic liver cirrhosis in 42.93%, and cryptogenic liver cirrhosis in 27.30%. Liver cirrhosis of other etiology occurred in 8.19%. The incidences of primary liver cell cancer in these 4 groups were 4.94, 4.62, 5.45, and 0%, respectively. These differences are not statistically significant, although in absolute figures postalcoholic liver cirrhosis is the main cause of primary liver cell carcinoma in this sample from West Germany. HBs antigen-positive liver cirrhosis was more often associated with primary liver cell cancer than HBs antigen-negative liver cirrhosis (6.58 versus 3.96%); this difference also is not statistically significant. Observations of larger groups of patients may show a higher risk of developing primary liver cell carcinoma in those with a combination of alcohol abuse and HBs antigenemia and/or acute hepatitis in the history. Patients without these 2 risk factors had an incidence of primary liver cell carcinoma of 2.61%; those with 1 risk factor, 5.77%; and those with both risk factors, 10.71%.
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PMID:Etiology of human liver cancer: controlled prospective study in liver cirrhosis. 8 98


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