C Infections (c + infections)

Distribution by Scientific Domains


Selected Abstracts


Adiponectin levels among patients with chronic hepatitis B and C infections and in response to IFN-, therapy

LIVER INTERNATIONAL, Issue 4 2005
Jin-Ying Lu
Abstract: Aims: The study was designed to survey the change of adiponectin levels before and after interferon-, (IFN-,) therapy in patients with chronic hepatitis B and C infections. Methods: Twenty-one biopsy-proved patients with chronic hepatitis B (10 cases) and hepatitis C (11 cases) were given IFN-, for a total of 24 weeks. Fasting plasma glucose, insulin and adiponectin levels were obtained before and 12 weeks after completion of IFN-, therapy. Insulin suppression test was conducted before and within 1 week after IFN-, therapy. Results: The change of adiponectin levels differed significantly between responders (eight cases) and non-responders (13 cases) to IFN-, treatment (,4.8±2.2 vs. 0.5±1.0 ,g/ml, P=0.03). After adjusting for age, gender and change in body mass index, the study found the change of adiponectin levels still significantly related to the response to IFN-, (P=0.04). When hepatitis B virus (HBV) and hepatitis C virus (HCV)-infected patients were separately analyzed, the adiponectin levels reported a trend to decrease in HCV responders (11.9±3.2 vs. 10.8±3.0 ,g/ml, P=0.02, n=4) and HBV responders (17.7±4.1 vs. 9.2±1.0 ,g/ml, P=0.10, n=4). In addition, a significant decrease of steady-state plasma glucose in insulin suppression test was noted in responders (13.6±1.8,11.7±1.2 mmol/l, P=0.03), but not in non-responders (12.3±1.1,11.0±1.0 mmol/l, P=0.20), after IFN-, therapy. Conclusions: IFN-, resulted in a decrease of serum adiponectin levels but an improvement of insulin resistance in responders to the treatment. The result contradicts previous concept of the relationship between insulin resistance and adiponectin levels. Whether and how the augmented immune response, which was supposed to result from the disappearance or the profound down-regulation of the virus or viral antigens in responders to IFN-, treatment, contributes to the lowering of adiponectin levels needs to be further investigated. [source]


Antituberculosis drugs and hepatotoxicity

RESPIROLOGY, Issue 6 2006
Wing Wai YEW
Abstract: Isoniazid, pyrazinamide and rifampicin have hepatotoxic potential, and can lead to such reactions during antituberculosis chemotherapy. Most of the hepatotoxic reactions are dose-related; some are, however, caused by drug hypersensitivity. The immunogenetics of antituberculosis drug-induced hepatotoxicity, especially inclusive of acetylaor phenotype polymorphism, have been increasingly unravelled. Other principal clinical risk factors for hepatotoxicity are old age, malnutrition, alcoholism, HIV infection, as well as chronic hepatitis B and C infections. Drug-induced hepatic dysfunction usually occurs within the initial few weeks of the intensive phase of antituberculosis chemotherapy. Vigilant clinical (including patient education on symptoms of hepatitis) and biochemical monitoring are mandatory to improve the outcomes of patients with drug-induced hepatotoxicity during antituberculosis chemotherapy. Some fluoroquinolones like ofloxacin/levofloxacin may have a role in constituting non-hepatotoxic drug regimens for management of tuberculosis (TB) in the presence of hepatic dysfunction. Isoniazid administration is currently the standard therapy for latent TB infection. Rifamycins like rifampicin or rifapentine, alone or in combination with isoniazid, may also be considered as alternatives, pending accumulation of further clinical data. During treatment of latent TB infection, regular follow up is essential to ensure adherence to therapy and facilitate clinical monitoring for hepatic dysfunction. Monitoring of liver chemistry is also required for those patients at risk of drug-induced hepatotoxicity. [source]


Mode of splenectomy and immunogenicity of meningococcal vaccination in patients with hereditary spherocytosis,

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 4 2008
G. A. Stoehr
Background: Splenectomy predisposes patients to invasive disease from pneumococci, meningococci, and Haemophilus influenzae; immunization is mandatory. However, data on the impact of the splenectomy on vaccine immunogenicity are scarce. Methods: A total of 41 children with hereditary spherocytosis (aged 5·8,14·4 years) had complete (16) or near-total (25) splenectomy. All received one dose of monovalent meningococcal C conjugate vaccine (MCV-C) and, 2 months later, a tetravalent meningococcal polysaccharide vaccine (MPV-ACWY). Serum bactericidal activity and antibodies against serogroups A and C were determined before and after they received MCV-C, and 4 weeks after they received MPV-ACWY. Results: Before vaccination, only four of the 16 children who had a complete splenectomy were protected against serogroup A, compared with 15 of the 25 who had near-total splenectomy (P < 0·050), with the latter responding to immunization with significantly higher serogroup A serum bactericidal activity: geometric mean (95 per cent confidence interval) 1625.5 (49.9 to 3201.1) versus 980.6 (2.00 to 6204.1) (P < 0·050). All patients achieved putative protective serum bactericidal activity titres (at least 8) against serogroup C. Conclusion: Near-total splenectomy provides a favourable immunological basis for natural and vaccine-induced protection against meningococcal serogroup A and C infections. Sequential meningococcal vaccination is immunogenic in patients splenectomized for hereditary spherocytosis. Copyright © 2007 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source]