We undertook this study to assess the association between the various potential causes of liver disease in HIV-seropositive patients and mortality due to liver failure. Three hundred and eight in-hospital deaths were observed from 1987 to December 1995 in a prospectively followed cohort of 1894 HIV-seropositive patients. For each study subject, clinical data were evaluated to assess whether liver failure had substantially contributed to mortality. A case control study nested in the cohort was then performed, which compared demographic and clinical variables observed at enrollment and during follow-up between patients who died for liver disease as the main or concurrent cause of death (cases) and those who died as a result of illness related to AIDS or other causes (controls). Among 308 in-hospital deaths, liver failure was found the cause of death in 35 patients (12%); in 16 cases, it was the primary cause and in 19 cases it was concurrent. Multivariate analysis showed that in-hospital liver-disease-related mortality was independently associated with hepatitis B surface antigen reactivity (odds ratio [OR], 9; 95% confidence interval [CI], 3.8-21.7) and history of alcohol abuse (OR, 2.3; 95% CI, 1-5.2). Prevention and treatment of hepatitis B virus infection and alcohol intake are management priorities in HIV-seropositive patients.
"In the HAART era, HAC in HIV-infected patients has been associated with increased mortality (Braithwaite et al., 2007; Di Martino et al., 2001; Galai et al., 2005; Hooshyar et al., 2007; Lewden et al., 2005; Puoti et al., 2000; Rosenthal et al., 2003, 2007), mostly from liver diseases (Di Martino et al., 2001; Lewden et al., 2005; Puoti et al., 2000; Rosenthal et al., 2007) and particularly in women (Hessol et al., 2007). Recent heroin and cocaine use as well as homelessness, have also been identified as major determinants of early mortality in *Corresponding author. "
[Show abstract][Hide abstract] ABSTRACT: Alcohol abuse affects secondary prevention and disease progression in HIV-infected patients, and adherence and response to treatment in those chronically treated. The objective of this study was to estimate the prevalence of harmful alcohol consumption (HAC) using various indicators and identify which groups of patients may require specific targeted interventions for HAC risk reduction. A cross-sectional survey, based on a random sample representative of people living with HIV/AIDS (PLWHA) was carried out in 102 French hospital departments delivering HIV care. As alcohol abuse is particularly detrimental to patients receiving highly active antiretroviral therapy (HAART), we focused only on those individuals receiving HAART with complete alcohol assessment (CAGE, AUDIT-C, regular binge drinking, N=2340). Collected information included medical and socio-demographic data, HIV risk behaviors, adherence to treatment and substance and alcohol use, together with depression, anxiety, and experience of attempted suicide or sex work. HAC prevalence was evaluated as follows: 12% (CAGE score > or =2), 27% (AUDIT-C), and 9% (regular binge drinking). Three groups were at higher risk of HAC: men who have sex with men using stimulants, polydrug users, and to a lesser degree, ex-drug users. Innovative intervention strategies to reduce HAC and improve HIV prevention and HAART adherence in various PLWHA populations need urgent testing and implementation. Such interventions for alcohol risk reduction remain central to promoting improved HIV prevention and assuring HAART effectiveness in these populations.
AIDS Care 09/2010; 22(9):1136-45. DOI:10.1080/09540121003605039 · 1.60 Impact Factor
"Coinfection with HIV is an important issue in HCV infection because of its relatively high prevalence, higher HCV virus loads in HIV/HCV coinfected individuals and because of increased HCV-related morbidity in HIV coinfected individuals [68-70]. The higher level of IL-10 induction in PBMC from HIV-infected individuals may allow the establishment of more aggressive HCV infection, with downregulation of anti-HCV responses permitting increased HCV replication and higher HCV virus loads. "
[Show abstract][Hide abstract] ABSTRACT: Multiple immune evasion strategies by which HCV establishes chronic infection have been proposed, including manipulation of cytokine responses. Prior infection with HIV increases the likelihood of chronic HCV infection and accelerates development of HCV-related morbidity. Therefore, we investigated in vitro cytokine responses to HCV structural and non-structural proteins in peripheral blood mononuclear cells (PBMC) from uninfected, HIV-infected, HCV-infected and HIV/HCV-coinfected individuals.
Intracellular flow cytometry was used to assess IL-2, IL-10, IL-12, and IFN-gamma production by freshly isolated PBMC incubated for 16 hours with recombinant HCV core, non-structural protein 3 (NS3), and NS4 proteins. Anti-HCV cellular responses were assessed in HIV/HCV-coinfected individuals by 3H-thymidine proliferation assay. Exposure to HCV antigens increased IL-10 production by PBMC, especially in uninfected and HIV-monoinfected individuals. This IL-10 response was attenuated in chronic HCV infection even with HCV/HIV-coinfection. The cells producing IL-10 in response to HCV proteins in vitro matched a PBMC subset recently shown to constitutively produce IL-10 in vivo. This subset was found at similar frequencies in uninfected, HIV-infected, HCV-infected and HIV/HCV-coinfected individuals before exposure to HCV proteins. HCV-specific T cell proliferation was detectable in only one HIV/HCV-coinfected individual who demonstrated no HCV-induced IL-10 response.
This pattern suggests that selective induction of IL-10 in uninfected individuals and especially in HIV-monoinfected individuals plays a role in establishing chronic HCV infection and conversely, that attenuation of this response, once chronic infection is established, favours development of hepatic immunopathology.
"In patients already infected with HIV and either hepatitis B or C, the prognosis is made much worse with additional infection by other hepatotropic viruses   . Evidence from HIV-negative patients shows a rate of acute fulminant hepatitis of up to 40% when a chronic hepatitis C carrier subsequently gets hepatitis A or B   . "
[Show abstract][Hide abstract] ABSTRACT: Co-infection of HIV-positive patients with hepatitis viruses worsens the long-term prognosis and this is summative for each new infection in any individual. Vaccination against hepatitis A or B may be effective but response rates are reduced in HIV infected patients. Improvement in response can be induced through extra doses, higher doses and HAART-induced increase in the CD4 count. Hepatitis B and C may also be prevented through counselling about safer sex, particularly condom use. In intravenous drug users, harm reduction, counselling and the use of needle/syringe exchange schemes may be helpful.
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