BACKGROUND/AIMSWe aimed to study the relationship between HBcAg in liver tissue, histological and biochemical activity and serum HBV-DNA levels among HBeAg-negative patients.METHODOLOGY49 biopsy specimens taken from 16 females and 29 males were studied. Immunostaining for HBcAg was performed with commercially available kits (Dako). Serum HBV-DNA was detected by the hybridization method, in case of negative hybridization, repeated by PCR.RESULTSHBcAg was found in 16 biopsy specimens (32.6%) (group I)--in 10 cases in hepatocytes nuclei and cytoplasm, in 5 in the nuclei and in one case in cytoplasm only. 15 out of 16 patients were serum HBV-DNA positive. Seven patients showed chronic liver disease of moderate or severe activity with HBcAg expression both in the nuclei and cytoplasm. Group II consisted of 33 patients who were HBcAg-negative. In 7 patients HBV-DNA was not found by hybridization or by PCR. In eleven patients ALT and AST activity exceeded 1.5x the ULN. ALT and AST differed significantly between group II and I.CONCLUSIONSIn our opinion immunohistochemical examination is an essential part of classification to antiviral treatment. HBcAg immunostaining should be performed in every HBeAg-negative patient to exclude reasons for aminotransferase elevation other than HBV infection.
Background/aims: Lipopolysaccharide (LPS) induces liver injury which is associated with upregulated endothelin (ET)-1 production. The aim of this study was to investigate the effects of tezosentan, a nonselective ETA and ETB receptor antagonist, in LPS challenged rats with cirrhosis.Methods: Rats with cirrhosis received LPS and then tezosentan or placebo one hour later. Four hours after LPS administration, rats were killed to measure serum transaminase activity and plasma tumour necrosis factor alpha (TNF-alpha) levels. Hepatic inducible nitric oxide synthase (iNOS), myeloperoxidase (MPO), a marker of neutrophil infiltration, and cyclooxygenase (COX)-2 expression were also measured.Results: LPS administration significantly decreased arterial pressure and significantly increased plasma endothelin levels. Following LPS and tezosentan administration, serum aspartate aminotransferase and alanine aminotransferase activities were similar to those in the control group while they were increased by more than 700% with LPS alone. Plasma TNF-alpha levels were significantly lower in rats receiving LPS and tezosentan (182 (38) pg/ml) compared with those receiving LPS alone (821 (212) pg/ml). Tezosentan significantly decreased hepatic MPO activity and hepatic neutrophils but had no effect on LPS induced iNOS or COX-2. Survival rate was significantly higher in rats receiving LPS plus tezosentan (80%) than in rats receiving LPS alone (50%).Conclusion: In LPS challenged cirrhotic rats, tezosentan administration prevents LPS induced liver injury by decreasing intrahepatic neutrophil infiltration. In addition, tezosentan increases survival in these rats.
In cirrhosis, lipopolysaccharide (LPS, a product of Gram-negative bacteria) in the blood may cause septic shock. LPS-elicited induction of arterial inducible nitric oxide synthase (iNOS) results in nitric oxide (NO)-induced vasodilation, which causes arterial hypotension and hyporeactivity to alpha(1)-adrenergic constrictors. In vitro studies have suggested that vasopressin inhibits iNOS expression in cultured vascular smooth muscle cells exposed to LPS. Thus, the aim of this study was to investigate the effects of terlipressin administration (a vasopressin analog) on in vivo LPS-induced aortic iNOS in rats with cirrhosis. LPS (1 mg/kg, intravenously) was administered followed by the intravenous administration of terlipressin (0.05 mg/kg, intravenously) or placebo 1 hour later. Arterial pressure was measured, and contractions to phenylephrine (an alpha(1)-adrenoceptor agonist), iNOS activity, and iNOS expressions (mRNA and protein) were investigated in isolated aortas. LPS-induced arterial hypotension and aortic hyporeactivity to phenylephrine were abolished in rats that received terlipressin. LPS-induced aortic iNOS activity and expression were suppressed in terlipressin-treated rats. In conclusion, in LPS-challenged rats with cirrhosis, terlipressin administration inhibits in vivo LPS-induced aortic iNOS expression. Terlipressin administration may be a novel approach for the treatment of arterial hypotension and hyporeactivity to alpha(1)-adrenergic constrictors in patients with cirrhosis and septic shock.
Letters| July 28 2000 HBV and HCV Infections in Relation to the Chosen Genetic Features in Hemodialyzed Patients Subject Area: Nephrology Waldemar Urbanowicz; Waldemar Urbanowicz Department of Infectious Diseases, Pomeranian Medical School, Szczecin, Poland Search for other works by this author on: This Site PubMed Google Scholar Marta Wawrzynowicz-Syczewska; Marta Wawrzynowicz-Syczewska Department of Infectious Diseases, Pomeranian Medical School, Szczecin, Poland Search for other works by this author on: This Site PubMed Google Scholar Anna Boroń-Kaczmarska Anna Boroń-Kaczmarska Department of Infectious Diseases, Pomeranian Medical School, Szczecin, Poland Search for other works by this author on: This Site PubMed Google Scholar Nephron (2000) 85 (4): 357. https://doi.org/10.1159/000045689 Article history Published Online: July 28 2000 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Waldemar Urbanowicz, Marta Wawrzynowicz-Syczewska, Anna Boroń-Kaczmarska; HBV and HCV Infections in Relation to the Chosen Genetic Features in Hemodialyzed Patients. Nephron 1 August 2000; 85 (4): 357. https://doi.org/10.1159/000045689 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsNephron Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 2000Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.
Dialysed patients constitute one of the most important risk groups for viral hepatitis infection. That is why different forms of prophylaxis are undertaken to diminish the number of infections. The aim of our study was to determine the efficacy of vaccination against HBV infection among dialysed patients who may be regarded as immunocompromised subjects. There were 104 patients in the dialysis programme enrolled to the study. The full serology of HBV infection was done at the beginning. We determined also anti-HCV status. 20 patients (19.2%) were HBsAg-positive. 53 patients HBsAg-negative and anti-HBs-negative were subjected to vaccination. Engerix-B was the vaccine used and the scheme was the following: 0, 1, 2 and 6 months with each dose doubled (40 mcg). The shortest time of observation was 4 months. Good response to HBV vaccine is achieved in those dialysed patients who had been infected in the past but lost anti-HBs (anti-HBc-positive). The vaccine works as a "reminder" in this group. Anti-HBc-negative patients respond rather poorly to HBV vaccine and that protection may be incomplete ("low responders"-maximal antibody level below 100 IU/l). In 8 vaccinated patients anti-HBc total negative with anti-HBs level below 10 IU/l (non-responders) we observed acute B hepatitis during or shortly after vaccination. These infections were mostly subclinical. We did not observe significant difference of age, sex and HCV infection between responders and non-responders.
The aim of the study was the clinical and epidemiological evaluation of HBV and HCV infections among 96 patients with chronic renal failure entering dialysis programme, 31 patients with insulin-dependent diabetes and among staff members of Dialysis Unit (29 persons) and Department of Infectious Diseases (54 persons). In the group of haemodialyzed patients we have performed immuno-serological examinations every three months in the period of 18 months. During our study we have not observed any new seroconversion to anti-HCV. Among 66 HBsAg-negative patients 7 (10.6%) of them became HBsAg- and HBeAg-positive despite of active vaccination.
A case of chronic type B hepatitis with HBsAg persisting for 15 years and its clearance as well as HBeAg-->HBeAb seroconversion and histological improvement after acute HCV superinfection is described. Possible mechanisms of suppressive effects of acute HCV superinfection on the established HBV infection is discussed.