摘要:

AbstractA randomized double‐blind, placebo‐controlled efficacy trial of hepatitis B immune globulin (HBIG) for prevention of the mother‐to‐infant transmitted HBsAg carrier state was conducted in Taiwan where the carrier rate in the general population is 15 to 20%. HBIG was given immediately after birth to infants of e antigen positive HBsAg carrier mothers, and all infants were followed for at least 15 months. Among 61 placebo recipients, the carrier rate was 92%; compared with 26% among 57 infants who received 0.5 ml HBIG at birth, 3 months, and 6 months, and 54% among 67 infants who received a single 1.0 ml dose of HBIG at birth only. Efficacy was 71 and 42%, respectively, for the two treatment schedules. The most common response of HBIG‐treated infants was passive‐active immunization which was 27% in the single‐dose group and 61% in the three‐dose group. Some of the infants who became carriers were probably infected as HBIG protection waned, and we expect that higher efficacy can be achieved by hepatitis B vaccine in conjun

ISSN:0270-9139    

DOI:10.1002/hep.1840030201

出版商:W.B. Saunders    

年代:1983

数据来源: WILEY

摘要:

Abstracttime sequence, relative reactivity, and persistence of anti‐HBc IgM were assessed in patients with HBsAg‐positive viral hepatitis. A solid‐phase immunoassay was developed using the IgM capture procedure with anti‐m̈ated polystyrene beads. HBcAg was purified from serum Dane particles and used as a probe with 125I‐labeled anti‐HBc IgG. This immunoassay exhibited a pronounced prozoning phenomenon, and relative titers of sera differed widely depending upon the dilution of serum tested. When all sera were tested at 1:5,000 dilution, results were comparable in different patient groups.HBc IgM persisted at detectable levels for up to 2 years, and it was necessary to establish relative titers to discriminate current from remote infections. A cut‐off assay value was established, and in 12 cases of acute hepatitis B virus (HBV) infection, antibody exceeded this value for about 6 months after onset of HBs antigenemia. A similar profile of anti‐HBc IgM persistence was observed in seven patients who developed an HBsAg chronic carrier state. Long‐term viral replication did not sustain elevated IgM class‐specific antibody levels.studies suggest that anti‐HBc IgM analyses may be useful for differentiating recent and current HBV infections from remote infections, eliminating HBV as the agent for non‐A, non‐B hepatitis in asymptomatic HBsAg carriers, and detecting HBV as the etiologic agent during silent (

ISSN:0270-9139    

DOI:10.1002/hep.1840030202

出版商:W.B. Saunders    

年代:1983

数据来源: WILEY

摘要:

AbstractPrimary sclerosing cholangitis (PSC) is a syndrome of unknown etiology characterized by an association with inflammatory bowel disease in 50% or more cases. Since altered immunity, including circulating immune complexes, has been implicated in the pathogenesis of inflammatory bowel disease, we postulated that humoral immune mechanisms might also be important in the development of PSC. Therefore, as an initial step in testing this hypothesis, we examined sera of patients with PSC for the presence of circulating immune complexes by two independent methods: Clq binding and Raji cell assays. Twenty‐four patients with PSC, 16 of whom had coexisting chronic ulcerative colitis, were prospectively selected by predefined biochemical, histologic, and radiographic criteria. Sixteen patients with inflammatory bowel disease and normal liver tests as well as six patients with extrahepatic biliary obstruction served as disease controls. Sera were positive for circulating immune complexes by at least one method in 80% (16/20) of patients with PSC; 70% (14/ 20) were positive by the Raji cell assay, 58% (14/24) by the Clq binding assay, and 45% (9/20) by both methods. Levels of circulating immune complexes by each assay were higher in sera from patients with PSC than in sera from healthy controls or patients with inflammatory bowel disease alone (p<0.01). There were no differences in the levels of circulating immune complexes or in the frequency of positive tests in PSC patients with or without associated inflammatory bowel disease. In addition, there was no difference between the Raji cell binding of sera from six patients with extrahepatic biliary obstruction and six healthy controls tested concurrently. These data are consistent with the hypothesis that immunologic mechanisms may be important in the pathogenesis of PS

ISSN:0270-9139    

DOI:10.1002/hep.1840030203

出版商:W.B. Saunders    

年代:1983

数据来源: WILEY

摘要:

AbstractHepatocytes isolated from 101 biopsies were examined for membrane‐bound IgG. The sera of the patients were tested for anti‐liver‐specific lipoprotein by radioimmunoassay and for liver membrane autoantibody (by indirect immunofluorescence on isolated rabbit hepatocytes. The seven patients with normal liver or minor nonspecific alterations were negative for membrane IgG and serum antibodies. Membrane IgG with granular distribution was found in 41 patients [21 hepatitis B virus‐related chronic active hepatitis (CAH), 3 cryptogenic CAH, 3 chronic persistent hepatitis, 6 prolonged viral hepatitis, 1 alcoholic cirrhosis, and 6 primary biliary cirrhosis]. Membrane IgG with linear fluorescence pattern was detected in 12 cases (4 autoimmune CAH, 3 HBsAg‐positive CAH, 2 alcoholic cirrhosis, 1 anti‐HBc positive CAH, 1 cryptogenic CAH, and 1 prolonged viral hepatitis). A strong association between granular IgG and serum HBsAg was found. Nuclear localization of IgG was found in 34 patients and correlated with the positivity of granular membrane IgG.The highest prevalence of anti‐liver‐specific lipoprotein was found in primary biliary cirrhosis and autoimmune CAH cases which were also positive for liver membrane autoantibody. No relationship was found between the presence of membrane IgG and circulating liver‐specific autoantibodies.Membrane IgG and anti‐liver‐specific lipoprotein correlated with the presence of moderate and severe portal inflammatory infiltration but not with piecemeal necrosis or transaminase levels. Eleven of the twelve patients with linear membrane IgG presented chronic active liver disease with moderate to severe signs of liver damage.Therefore, it is suggested that, while granular membrane IgGs are related to hepatitis B virus, antigenic expression on the hepatocyte surface and/or the presence of immune complexes, linear membrane IgG could play a role in the immunopathogenesis of liver cell damage particularly in “autoimmune” cases which present high percentages of positive cells live

ISSN:0270-9139    

DOI:10.1002/hep.1840030204

出版商:W.B. Saunders    

年代:1983

数据来源: WILEY

摘要:

AbstractA sensitive and specific radioimmunoassay for human ligandin has been developed and used to study ligandin release into the serum in acute and chronic hepatitis. Serum ligandin concentrations were elevated in 67 of 68 cases of acute viral hepatitis. Ligandin levels frequently returned to normal within the first 2 weeks of illness. The rapid disappearance of ligandin preceded the return to normal of serum SGOT. In chronic active hepatitis, serum ligandin levels correlated significantly (p< 0.01) with histologic severity of disease. This correlation was not seen with SGOT. Serum ligandin may be useful in monitoring progress and the need for therapy in chronic active hepatitis.

ISSN:0270-9139    

DOI:10.1002/hep.1840030205

出版商:W.B. Saunders    

年代:1983

数据来源: WILEY

摘要:

AbstractQualitative and quantitative changes in glutathione S‐transferase (GSH‐T) were studied in human hepatocellular carcinoma. GSH‐T specific activity (/imoles per min per mg protein) was variably reduced in hepatocellular carcinoma. Similar changes were seen in “cationic” GSH‐T (ligandin) concentration determined by radioimmunoassay. Immunohistochemical studies with antihuman liver ligandin suggest that positive staining was more frequently found in well‐differentiated tumors.The relative activities of “cationic,” “neutral,” and “anionic” transferases were estimated after separation by isoelectric focusing. Tumor “cationic” transferase (pI ± 7.5) activity ranged from virtually absent to near normal values. “Neutral” (pI 6 to 6.5) and “anionic” (pI< 5.4) species were present more often in tumors than in normal liver. In two cases, normal liver tissue and tumor were obtained from the same patient. In one, only quantitative differences were present, while in the other “cationic” and “neutral” GSH‐Ts were present in the normal liver tissue while both “cationic” and “anionic” species were found in the tumor. Our studies indicate that qualitative as well as quantitative

ISSN:0270-9139    

DOI:10.1002/hep.1840030206

出版商:W.B. Saunders    

年代:1983

数据来源: WILEY

摘要:

AbstractA method was developed to extract quantitatively the bilirubins from bile, urine, serum, stool, and preparations from liver with a chloroform‐ethanol mixture at pH 1.8 in the presence of ascorbic acid and NaCl. Extracted pigment was submitted to thin‐layer chromatography, and the separated bilirubins were either immediately eluted and determined spectrophotometrically or individually converted to ethyl anthranilate azo derivatives for thin‐layer chromatographic analysis of each isolated pigment band. Bilirubins in duodenal bile of eight healthy adults comprised 1.5 ± 1.3% unconjugated bilirubin‐IXα, 69 ± 6% bilirubin diglucuronide, and 16 ± 4% bilirubin monoglucuronides. Mixed diconjugates containing one glucuronosyl moiety and either one xylosyl or one glucosyl group amounted to 10 ± 3%. Most samples (6 of 8) contained trace amounts (0.6 ± 0.6%) of unconjugated bilirubin‐IXβ, in agreement with nearly exclusive cleavage of heme at the α‐meso position. The composition of the bilirubins in bile was normal in 6 patients with cholesterol gallstones, 4 with chronic hepatitis, and 3 with hemolysis. In duodenal bile of individuals with Gilbert's syndrome (n = 10), the concentration of bttirubin conjugates was comparable to that in healthy adults, but the proportion of bilirubin diglucuronides (52 ± 8%) was decreased. The concentration of unconjugated bilirubin‐IXα showed a fair positive correlation with that of bilirubin monoglucuronide and was increased in half of the patients

ISSN:0270-9139    

DOI:10.1002/hep.1840030207

出版商:W.B. Saunders    

年代:1983

数据来源: WILEY

摘要:

AbstractTo test the hypothesis that hyperinsulinism is responsible for reduced branched‐chain amino acids in cirrhotics, plasma amino acids were sequentially determined in 8 controls and 8 matched cirrhotics during continuous i.v. insulin infusion. An artificial endocrine pancreas which infused glucose was used to sustain euglycemia. Basal plasma insulin levels were high and branched‐chain amino acids were reduced in cirrhotics. Insulin infusion raised insulin levels to 3 to 4 times basal values. During the test, the decline in branched‐chain amino acids was markedly higher in controls who had similar steady‐state insulin levels. Not only did the level of branched‐chain amino acids in controls reach the values seen in cirrhotics after 60 min, but the levels continued to fall at a significantly higher rate throughout the second hour. Glucose consumption and the ratio of glucose infused/steady‐state insulin—a measure of tissue sensitivity to insulin—were markedly reduced in cirrhotics and positively correlated with the decline in branched‐chain amino acids. In cirrhotics, insulin effects on carbohydrate and branched‐chain amino acid metabolism were reduced. Low branched‐chain amino acid levels in cirrhotics are not likely to depend on

ISSN:0270-9139    

DOI:10.1002/hep.1840030208

出版商:W.B. Saunders    

年代:1983

数据来源: WILEY

摘要:

AbstractThe intravenous administration of bacterial endotoxin to fasted rats elicited basal portal and systemic venous hyperinsulinemia and hyperglucagonemia. Enhanced pancreatic secretion of insulin and glucagon was implied by the elevated portal venous hormonal levels. Elevated insulin and glucagon levels were present at 4 hr after a 33 m̈g/100 gm intravenous endotoxin dose despite no fluctuation of the plasma glucose concentration. The role of the liver in the pancreatic hormonal response to endotoxin was investigated by infusing lipopolysaccharide slowly into the portal vein or systemic inferior vena cava. At doses of 33 and 100 m̈g per 100 gm, endotoxin administered via the systemic route stimulated significantly greater insulin and glucagon responses than did portal administration. Furthermore, rats with acute liver injury induced by partial (67%) hepatectomy, which depressed Kupffer cell phagocytosis, did respond to the 33 m̈g per 100 gm intraportal endotoxin dose with significantly greater hyperinsulinemia and hyperglucagonemia. These data suggest that hepatic Kupffer cells normally function to remove lipopolysaccharideo from the portal venous blood and that at least at low pharmacological doses the pancreatic hormonal response to endotoxin is mediated by an unknown systemic mechani

ISSN:0270-9139    

DOI:10.1002/hep.1840030209

出版商:W.B. Saunders    

年代:1983

数据来源: WILEY

摘要:

AbstractExperimental data suggest that somatostatin is metabolized by both liver and kidneys. Results in humans are conflicting. By studying a group of cirrhotic patients with surgically induced end‐to‐side portacaval shunts, basally and during a somatostatin infusion, we have been able to analyze separately the hepatic and splanchnic metabolism of this peptide. After catheterization, samples were obtained from the pulmonary artery, portal and hepatic veins. Basal pulmonary artery immunoreactive somatostatin (IRS) was significantly higher (p< 0.001) in the cirrhotic patients (96 ± 11 pg per ml) than in a sex‐ and age‐matched control group (31.4 ± 5.8 pg per ml). During the infusion of exogenous somatostatin, HiS values were higher in arterial (12,269 ± 1, 198 pg per ml) than in hepatic venous blood (7,648 ± 1,234 pg per ml), indicating hepatic extraction of the peptide; but there was also a substantial splanchnic extraction demonstrated by higher arterial (12,269 ± 1,532 pg per ml) than portal values (6,754 ± 1,040 pg per ml) of IRS.During the somatostatin infusion, at very high circulation IRS levels, the liver was able to extract 38% of the peptide. This suggests that the high basal IRS levels found in liver cirrhosis are not likely to be due to hepatic failure. Possible mechanisms may involve increased somatostatin secretion, predominance of high molecular weight moieties of IRS which may not be as effectively removed by the liver, and/or portal‐sy

ISSN:0270-9139    

DOI:10.1002/hep.1840030210

出版商:W.B. Saunders    

年代:1983

数据来源: WILEY