Short Statement of the First European Consensus Conference on the Treatment of Chronic Hepatitis B and C in HIV Co-infected Patients

Centre Hospitalier Universitaire Saint-Pierre, Bruxelles, Brussels Capital, Belgium
Journal of Hepatology (Impact Factor: 10.4). 06/2005; 42(5):615-24. DOI: 10.1016/j.jhep.2005.03.003
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Available from: Ola Weiland, Aug 11, 2015
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    • "Finally, the rate of relapses for similar treatment regimens is higher in co-infected than in monoinfected individuals [73]. For all these reasons, older guidelines recommended that duration of treatment in co-infected patients when possible should be 48 weeks regardless HCV genotype [74]. As in HCV-monoinfected individuals with slow virological response [75] [76], extended periods of treatment may improve SVR rates in co-infected patients [18]. "
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    ABSTRACT: Co-infection with either HIV or HBV in chronic hepatitis C patients is common, since all these viruses share transmission routes and geographical distribution. Interaction between these viruses generally amplifies liver damage, increasing the risk of developing end-stage liver disease and hepatocellular carcinoma. HIV-HCV co-infection is associated with poorer response to antiviral therapy. New antivirals against HCV are eagerly awaited for this population. HBV-HCV dual infections are less common. The principles guiding indication of therapy in monoinfected patients should be followed considering which virus replicates in persons with serological markers of dual HBV-HCV infection. Although there is growing evidence supporting the use of direct acting antivirals (DAA) in dually infected patients with active HCV replication, prospective trials should be conducted to demonstrate their benefit, assessing carefully the rate and clinical consequences of HBV rebounds.
    Best practice & research. Clinical gastroenterology 08/2012; 26(4):517-30. DOI:10.1016/j.bpg.2012.09.007 · 3.28 Impact Factor
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    • "As HIV-1 and other pathogens share some or all transmission routes, the occurrence of co-infections is frequent . Among all those infected with HIV in the world, it is estimated that approximately 10% are co-infected with HBV and approximately 15% with HCV (Alberti et al. 2005, Soriano et al. 2006). It has been suggested that HIV-1/HCV co-infection of pregnant women increases the rate of mother-child transmission of HCV to their infants (Polis et al. 2007). "
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    ABSTRACT: Human immunodeficiency virus type 1 (HIV-positive) pregnant women require specific prophylactic and therapeutic approaches. The efficacy of established approaches is further challenged by co-infection with other sexually transmitted diseases (STDs). The objective of this study was to determine the prevalence of co-infections in pregnant women infected with different HIV-1 subtypes and to relate these findings, together with additional demographic and clinical parameters, to maternal and infant outcomes. Blood samples from pregnant women were collected and tested for syphilis, hepatitis B virus (HBV) and hepatitis C virus (HCV). Human papillomavirus (HPV) diagnosis was evaluated by the presence of alterations in the cervical epithelium detected through a cytopathological exam. Medical charts provided patient data for the mothers and children. Statistical analyses were conducted with STATA 9.0. We found a prevalence of 10.8% for HCV, 2.3% for chronic HBV, 3.1% for syphilis and 40.8% for HPV. Of those co-infected with HPV, 52.9% presented high-grade intraepithelial lesions or in situ carcinoma. Prematurity, birth weight, Apgar 1' and 5' and Capurro scores were similar between co-infected and non-co-infected women. The presence of other STDs did not impact maternal and concept outcomes. More than half of the patients presenting cervical cytology abnormalities suggestive of HPV had high-grade squamous intraepithelial lesions or cervical cancer, evidencing an alarming rate of these lesions.
    Memórias do Instituto Oswaldo Cruz 03/2012; 107(2):205-10. DOI:10.1590/S0074-02762012000200009 · 1.57 Impact Factor
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    • "Nevertheless, as shown in our previous EPIB 2003 and 2005 surveys [7] [8], the management in a real-life setting often differs from the recommended one. Moreover, the guidelines on the management of chronic hepatitis B in these patients have evolved since 2005 [6] [9]. Since many anti-HBV drugs have become available quite recently, the mid and long-term impact of HBV therapy in HIV positive patients remains to be established, as highlighted by the increasing number of recent publications dealing with this topic. "
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    ABSTRACT: To compare the management and the virological and serological efficacy of treatments for chronic hepatitis B (CHB) in HIV positive and negative patients. Two hundred and forty-six HIV positive and 205 HIV negative consecutive patients with past or present CHB, seen in October 2008 in participating departments, were included in a multicenter study. All the data were retrospectively collected from the first visit to October 2008 through a standardized questionnaire. Compared to HIV negative patients, HIV positive patients more often presented positive HBeAg (46.4% vs. 32.8%, p=0.01), HBV genotype A (54.8% vs. 17.1%, p<0.0001), co-infection with HCV (12.4% vs. 5.9%, p=0.0002) or HDV (12.6% vs. 2.9%, p=0.04). HIV positive patients were more often on HBV therapy (92.7% vs. 57.1%, p<0.0001), leading to undetectable serum HBV DNA levels (71.0% vs. 44.1%, p<0.0001). In HIV positive patients, multivariate analysis showed that older age, lower initial HBV DNA levels, and longer time on HBV therapy significantly correlated with undetectable HBV DNA. No difference in efficacy was observed between tenofovir used alone or in combination. HBsAg (but not HBe) loss was more often observed in HIV positive patients, sometimes followed by HBsAg re-appearance after withdrawal of HBV treatment. Excluding the 37 HBV-HCV-co-infected patients, the last clinical presentation and liver fibrosis scores were similar in HIV positive and negative patients. The assessment of CHB and the efficacy of HBV therapy have improved in HIV positive patients. HIV infection did not have a negative impact on the likelihood of HBV therapeutic success.
    Journal of Hepatology 12/2010; 53(6):1006-12. DOI:10.1016/j.jhep.2010.04.041 · 10.40 Impact Factor
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