摘要:

ABSTRACT—Pre‐S1and pre‐S2encoded antigens of hepatitis B virus were localized in liver tissue using monoclonal antibodies. They were found to be exclusively expressed in the cytoplasm of liver cells. Cell bound pre‐S1encoded protein was often detected in patients with chronic liver disease and viremia. Only a small number of the HBsAg positive cells also contained pre‐S1antigen. There was no correlation with nuclear HBcAg. Livers of non‐viremic HBsAg carriers contained many HBsAg expressing liver cells, that were frequently also positive for pre‐S2encoded protein but contained no detectable pre‐S1encoded protein at all. It remains open whether cell bound pre‐S2containing proteins of middle size have a significance for pathogenesis, as they are present in individuals with chronic liver disease as well as in healthy HBsAg carriers, and may be associated with both increased and normal liver enzymes. Cell bound pre‐S1antigen with viremia may, however, be involved in the maintenance of viremi

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1987.tb00352.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

ABSTRACT—To aid in evaluating the functional significance of various domains of the hepatocyte plasma membrane, we have developed monoclonal antibodies that react with three different antigens on the surface of rat hepatocytes. One antigen is present on the sinusoidal‐lateral plasma membrane but is absent from the bile canalicular membrane. On the basis of apparent molecular weight and ability to bind a desialylated glycoprotein, this antigen may be the asialoglycoprotein receptor. It was also identified immunocytochemically on the sinusoidal‐lateral plasma membrane of human hepatocytes. The second antigen is present only on the bile canalicular membrane, whereas the third is present on the entire cell surface of rat hepatocytes. Our monoclonal antibodies may be useful in investigations of the sorting mechanisms of hepatocyte membrane proteins and the pathogenesis of certain liver dis

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1987.tb00353.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

ABSTRACT—The interrelationship among expression patterns of hepatitis B surface and core antigens (HBsAg and HBcAg) in the liver, hepatitis B virus (HBV) DNA in sera, HBeAg/anti‐HBe status and histological features was examined in 189 liver specimens and 106 sera from Japanese patients with chronic HBV infection, utilizing immunoperoxidase methods and a spot hybridization technique. HBsAg and HBcAg were distributed uniformly among the lobules in 8 viral carriers with “normal” liver (NVC) and 30 patients with persistent hepatitis (PH) seropositive for HBeAg. This uniform staining pattern was quite distinct from the non‐uniform and irregular patterns in 137 patients with chronic active hepatitis (CAH) associated with or not associated with cirrhosis. HBcAg was often found to be stained strongly in the cytoplasm as well as in the nucleus of hepatocytes in HBeAg‐positive CAH, in contrast to NVC/PH, in which cytoplasmic HBcAg was very weak. Serum HBV DNA was detected in all 22 cases with HBeAg‐positive NVC/PH, 41 of 46 (89.1%) cases with HBeAg‐positive CAH, 6 of 23 (26.1%) cases with anti‐HBe‐positive CAH and none of 3 cases with anti‐HBe‐positive NVC/PH. The level of serum HBV DNA and staining of HBcAg were in decreasing order in these groups. While the presence of serum HBV DNA and HBcAg staining was always associated with HBeAg seropositivity in NVC/PH, this was not always found in CAH. Moreover, necroinflammatory activity in the liver did not always parallel viral replication in CAH. These findings seem to confirm that NVC/PH and CAH have different biologic processes; viral replication is always concordant in the former, but is sometimes discordant in the latter with HBeAg/anti‐HBe status. The immunologic response of the host seems to suppress and distort replication of the virus to a varying degree among patients and areas of the same liver in CAH differently to that in NVC/PH. The different life cycle of the virus, including integration of viral DNA into the cellular genome, may subsequently result in discordant states of var

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1987.tb00354.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

ABSTRACT—Liver biopsies from 34 patients with morbid obesity, performed before and 5–9 months after jejunoileal bypass, were studied. The patients were divided into four groups according to preoperative findings: A: no or slight steatosis (15 patients), B: moderate‐severe steatosis (6), C: steatohepatitis (steatosis+lobular lymphocytic inflammation) (8), D: steatofibrosis (steatosis+pericellular fibrosis) (5). In Group A, 12 patients showed postoperative progression to either moderate/severe steatosis, steatohepatitis, or steatofibrosis. In Group B, all patients progressed to steatohepatitis or steatofibrosis, and one developed septate fibrosis. All patients in Group C progressed to steatofibrosis, and 5 developed septate fibrosis or cirrhosis. In Group D, 3 developed bridging fibrosis. Mallory bodies appeared postoperatively in 11 patients (32%), all of whom preoperatively had either severe steatosis, steatohepatitis, or steatofibrosis. Only patients with postoperative pericellular fibrosis and Mallory bodies developed deranged architecture: 6 septate/bridging fibrosis, and 3 cirrhosis. Five patients, all with deranged architecture, developed reversible liver insufficiency. Progressive liver injury after jejunoileal bypass appears to reflect aggravation of a preexisting liver lesion. The sequence of events: increasing steatosis, lobular lymphocytic inflammation, pericellular fibrosis, Mallory bodies, and deranged architecture is similar to that of the alcoholic liver lesion, indicating common pathogenetic mecha

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1987.tb00355.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

ABSTRACT—Histochemical methods have invariably shown a good correlation with copper analysis by absorption spectrophotometry in the identification of canine copper storage diseases. But, in Wilson's disease (WD) in humans no such correlation exists and similar discrepancies have also been observed in copper‐loaded rats. This study attempts to quantify stainable copper in the livers of copper‐loaded rats and relate this to the hepatic copper concentrations. Male rats fed a high copper diet (1500 ppm) for 16 weeks were killed at intervals. The livers were analysed for copper and graded according to stainable copper present in paraffin sections stained with rhodanine and rubeanic acid. Initially there was a good correlation between histochemically demonstrable copper and its total concentration, but subsequently, when high liver levels of the metal were present, copper staining was very variable. This unreliability has similarities with WD, in which the higher hepatic concentrations of presymptomatic patients are difficult to detect by conventional copper stains. The variation in the binding of copper and its intracellular localisation suggested by these results may have considerable significance in the pathogenesis of copper storage dis

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1987.tb00356.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

ABSTRACT—A study was carried out to confirm the pathogenetic role of ethanol in the development of chronic active hepatitis (CAH) and to assess if previous or current superimposed hepatitis B virus (HBV) infection could be relevant to the course of alcoholic liver disease (ALD). We examined clinical and laboratory reports of 57 alcoholics with biopsy‐proven CAH. Serum and/or tissue HBV markers and the presence or absence of cirrhosis were investigated. Alcohol was the only aetiological factor present in a small group of CAH, with or without histological findings suggestive of alcoholic damage. Age, sex and survival were similar among the subgroups of CAH with and without previous or current HBV infection and among the subgroups of CAH with and without associated histological alcoholic features. Among the laboratory data, the AST/ALT ratio was higher in CAH without previous or current HBV infection. The mean age was comparable in CAH patients with and without cirrhosis, whereas the cumulative 5‐year survival was worse in CAH with cirrhosis (87% vs. 49%). These data suggest a difference in alcohol susceptibility in our sub

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1987.tb00357.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

ABSTRACT—Alcoholic liver disease (ALD) in Japan was compared clinicopathologically with the occurrence in the U.S.A. ALD found in Japan was more frequently complicated by other hepatic diseases including non‐A, non‐B chronic hepatitis than ALD found in the U.S.A. (9.9% versus 21.9%). Patients with such complications were excluded from this study. The chief complaints of the total of 51 alcoholics studied in the U.S.A. were abdominal distension or jaundice and those of 98 alcoholics studied in Japan were non‐specific: general fatigue, weakness or appetite loss. The U.S. patients exhibited more elevated levels of serum bilirubin (8.1±7.5 versus 1.9±2.4 mg/dl, mean±SD) and a higher incidence of leukocytosis (49.0% versus 5.1%). While the serum glutamic‐oxalacetic transaminase (GOT) levels were not significantly different between the two groups (146.5±116.8 versus 140.8±147.7 IU/L), the serum glutamic‐pyruvic transaminase (GPT) levels among Japanese alcoholics were higher (38.6±31.4 versus 87.4±99.1 IU/L) and in about one quarter of these patients, serum GPT was higher than serum GOT, a feature not seen in the patients in the U.S.A. Comparative histopathologic study of 337 U.S. patients and 210 Japanese patients disclosed a higher frequency of cirrhosis (46.9% versus 33.8%), the presence of Mallory bodies (58.5% versus 13.8%) and marked neutrophilic exudation (45.1% versus 6.2%). Thus, the majority of Japanese alcoholics exhibited progression of liver disease, eventually leading to cirrhosis, due to hepatocellular drop‐out and fibrosis caused by a mechanism different from alcoholic hepatitis. In addition, ALD in the U.S.A. revealed more striking extension of fibrosis. In conclusion, ALD appeared to be generally more severe clinicopathologically in the

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1987.tb00358.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

ABSTRACT—Treatment of serum precipitates with sodium thiocyanate in patients with hepatitis B virus (HBV) replication results in liberation of circulating hepatitis core antigen (HBcAg) which can be demonstrated radioimmunologically. Follow‐up investigations were performed in 80 patients with acute hepatitis B. Sera were examined for HBcAg, HBV DNA and conventional HBV markers. At the time of admission to hospital 34 of 80 (42%) patients were HBeAg positive. Twenty‐six (76%) of the 34 HBeAg positive patients were HBV DNA positive, and circulating HBcAg was detectable in 25 of 34 (73%) HBeAg positive cases. In patients with uncomplicated courses of acute hepatitis B the serological HBcAg assay and HBV DNA became negative 1 to 8 weeks before elimination of HBeAg and up to 12 weeks earlier than the sera became negative for HBsAg. Five patients (6%) showed transition to chronic hepatitis B with persistence of HBsAg, HBeAg, HBV DNA and HBcAg in serum. One patient with acute hepatitis B and development of chronic hepatitis suffered from acquired immunodeficiency syndrome and showed delayed formation of anti‐HBc. In this case uncomplexed HBcAg was demonstrable during the acute phase of hepatitis B. With the appearance of anti‐HBc HBcAg circulated in a complexed form. The data indicate that serological determinations of HBcAg and HBV DNA can serve as prognostic markers in the early phase of acute hepatitis B. The demonstration of uncomplexed HBcAg in serum of a patient with inadequate formation of anti‐HBc supports the hypothesis that circulating HBcAg is usually complexed by specific

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1987.tb00359.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1987.tb00360.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY