Mortality for liver disease in patients with HIV infection: a cohort study.
ABSTRACT 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.
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ABSTRACT: Interferon and ribavirin combination therapy for chronic hepatitis C induces a low response rate in human immunodeficiency virus (HIV) infected patients. To assess the impact of intensification of interferon administration and of the addition of amantadine on the efficacy and safety of standard anti-hepatitis C virus (HCV) treatment in HIV-infected patients. Multicentre, prospective, open-label, randomized, phase III clinical trial. Eighty co-infected patients were randomized to receive ribavirin 800-1,000 mg/day in combination with, group A: interferon alpha 2a 3MIU thrice weekly; group B: IFN alpha 2a 3MIU daily, plus amantadine 200 mg/day; treatment duration was 24-48 weeks according to HCV genotype. Forty-one patients were randomized in group A and 39 in group B. Intention-to-treat analysis showed a sustained virological response, defined as HCV-RNA negativization, 6 months after stopping treatment in 22% of patients from group A and 13% from group B (P>0.05). The lack of a 2-log drop in HCV-RNA levels after 12 weeks of treatment showed a 100% predictive value of lack of sustained response. Amantadine addition and interferon intensification do not improve the low efficacy of combination of interferon alfa plus ribavirin in HIV/HCV co-infected patients. Patients with no early virologic response did not have any probability of sustained response.Journal of Hepatology 09/2004; 41(2):312-8. DOI:10.1016/j.jhep.2004.04.016 · 10.40 Impact Factor
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ABSTRACT: Chronic infection with either hepatitis B (HBV) or hepatitis C virus (HCV) is frequently present in patients seropositive for human immunodeficiency virus (HIV) because of shared routes of transmission. With the advent of highly active antiretroviral therapy (HAART) regimens capable of controlling HIV replication and dramatically prolonging the survival of HIV-infected patients, the impact of co-morbid infections such as HBV and HCV has come into focus. Several studies have monitored HBV or HCV viral loads following initiation of HAART, with disparate results. The effects of HAART on hepatitis B and C plasma viral loads (n = 9 and 32, respectively) and on liver enzyme levels were studied in a large cohort of prospectively studied subjects with advanced stage HIV disease. Comparing the mean pre- and post-HAART levels, there was an estimated increase of (a) 1.40 log(10) from 4.83 to 6.24 log(10) for HBV plasma viral load (P = 0.07), (b) 0.74 log(10) from 6.38 to 7.12 log(10) for HCV plasma viral load (P = 0.001), and (c) 19.4 U/L from 37.4 to 56.8 U/L for serum alanine aminotransferase (P < 0.001). While the number of subjects co-infected with HIV and HBV was limited, these data collected in a population of advanced stage HIV-infected patients raises questions regarding the interactions of these viruses with each other and the host immune system and has implications regarding the order in which antiviral therapies are initiated.Antiviral Research 08/2004; 63(2):123-31. DOI:10.1016/j.antiviral.2004.03.006 · 3.43 Impact Factor
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ABSTRACT: Objective: Recent studies suggest all-cause mortality in HIV mono-infected patients approaches that of the general population. We aimed to compare participants in the Canadian Co-infection Cohort to the general population to determine if co-infected patients have had similar improvements in mortality. Design: Prospective multicentre cohort study. Methods: Between 2003 and 2013, deaths were captured using specific case reports and through linkage to provincial vital statistics for participants lost to follow-up. Standardized mortality ratios (SMRs) were calculated using age, sex and province-specific mortality rates from the Canadian Human Mortality Database, 2009, and compared across behavioural and clinical characteristics of participants at their most recent visit. Results: Among the 1150 patients, we observed 133 deaths over 3351 person-years (4.0 per 100 person-years, 95% confidence interval 3.3, 4.6). SMRs (95% confidence interval) were: 12.1(10.1, 14.2) overall; 9.3 (7.5, 11.1) for men and 19.4 (12.7, 26.2) for women. CD4_ cell counts below 200 cells/mu l [25.5 (17.7, 33.3)], active injection drug use [19.9 (13.9, 25.9)] and smoking [14.9 (12.1, 17.7)] were strongly associated with excess mortality. Lowest SMRs were seen for those who had spontaneous [4.5 (-0.6, 9.5)] or treatment-induced clearance of hepatitis C virus (HCV) infection [5.1 (1.3, 8.8)]. Conversely, high SMRs were seen with advanced liver disease [17.0 (11.7, 22.3)]. In no category did SMRs approach mortality seen in the general Canadian population. Conclusions: HIV-HCV co-infected persons remain at markedly increased risk for death despite antiretroviral therapy. Interventions targeting modifiable risk factors such as substance use, smoking, adherence to antiretrovirals and timely provision of HCV therapy could substantially reduce death rates. (C) 2014 Wolters Kluwer Health vertical bar Lippincott Williams & WilkinsAIDS (London, England) 08/2014; 28(13):1957-65. DOI:10.1097/QAD.0000000000000377 · 6.56 Impact Factor