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  • 1
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    Online Resource
    IP-10 Correlates with Hepatitis C Viral Load, Hepatic Inflammation and Fibrosis and Predicts Hepatitis C Virus Relapse or Non-Response in HIV–HCV Coinfection
    SAGE Publications ; 2008
    In:  Antiviral Therapy Vol. 13, No. 8 ( 2008-11), p. 969-976
    Details
    In: Antiviral Therapy, SAGE Publications, Vol. 13, No. 8 ( 2008-11), p. 969-976
    Abstract: Interferon (IFN)-γ inducible protein 10 (IP-10) is increased in hepatitis C virus (HCV) monoinfection, correlates with hepatic inflammation and predicts non-response (NR) to antiviral therapy. We aimed to clarify the role of IP-10 in HIV-HCV coinfection. Methods Serum IP-10 levels of 30 HIV-HCV- coinfected patients treated with pegylated (PEG)-IFN-α2a (180 μg/week) and ribavirin (800-1,200 mg/day) were measured at baseline and 24 h after first IFN dose. The predictive value of IP-10 was compared with established markers of treatment outcome by applying a multivariate logistic regression model. Results Patients with NR (476 ±156 pg/ml) or virological relapse (508 ±298 pg/ml) had significantly higher baseline IP-10 levels compared with patients who had a sustained virological response (SVR; 293 ±97 pg/ml, P=0.001). The IFN-induced increase of IP-10 was significantly stronger in patients with an SVR ( P=0.017). IP-10 levels were associated with HCV viral load, alanine aminotransferase (ALT) levels, hepatic inflammatory activity and fibrosis stage. Advanced fibrosis, high HCV viral load, hepatovenous pressure gradient and pretreatment IP-10 〉 400 pg/ml predicted NR to antiviral therapy. In the multivariate analysis, IP-10 was identified as the strongest baseline predictor of SVR with a specificity and sensitivity of 83.4% and 92.9%, respectively. Conclusions Pretreatment IP-10 levels correlated with HCV viral load, ALT levels, hepatic inflammation and fibrosis. An IP-10 cutoff level of 400 pg/ml might serve as a useful predictive marker for anti-HCV therapy in HIV–HCV-coinfected patients because it could discriminate patients with expected NR or HCV relapse after therapy from patients with an SVR before starting antiviral treatment.
    Type of Medium: Online Resource
    ISSN: 1359-6535 , 2040-2058
    URL: Article
    DOI: 10.1177/135965350801300815
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2008
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  • 2
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    Review: Hepatocellular carcinoma: the place of new medical therapies
    SAGE Publications ; 2010
    In:  Therapeutic Advances in Gastroenterology Vol. 3, No. 4 ( 2010-07), p. 259-267
    Details
    In: Therapeutic Advances in Gastroenterology, SAGE Publications, Vol. 3, No. 4 ( 2010-07), p. 259-267
    Abstract: Medical therapies have entered center stage in the treatment of hepatocellular carcinoma (HCC) little more than a year after the positive results of a large phase III trial of sorafenib showed a clear survival benefit with sorafenib, a targeted agent, in this setting. Even though this marks a breakthrough in the treatment of HCC, the narrow patient profile necessary for the study to be successful has generated a number of questions regarding the efficacy of this approach in other clinical settings. New studies aiming to define the role of sorafenib from in the adjuvant setting, through patients with more advanced liver disease, all the way to combination treatments of HCC have been initiated. The success of one targeted drug has stimulated enormously the efforts of competitors to develop additional and better drugs, either in a first-line or a second-line setting. These are exciting times for the treatment of HCC, both for physicians and patients. In the years to come we will see an extension of treatment options in different clinical situations in patients with HCC, and survival will be improved in many stages of the disease, except for the most advanced. The rapid increase in knowledge about the molecular mechanisms underlying the development and progression of HCC will lead to a more tailored approach to treatment depending on the molecular characteristics of the tumor and the disease stage.
    Type of Medium: Online Resource
    ISSN: 1756-2848 , 1756-2848
    URL: Article
    DOI: 10.1177/1756283X10362278
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2010
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  • 3
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    Online Resource
    A Prospective Evaluation of Pulmonary, Systemic and Hepatic Haemodynamics in HIV–HCV-Coinfected Patients before and after Antiviral Therapy with Pegylated Interferon and Ribavirin
    SAGE Publications ; 2012
    In:  Antiviral Therapy Vol. 17, No. 7 ( 2012-10), p. 1327-1334
    Details
    In: Antiviral Therapy, SAGE Publications, Vol. 17, No. 7 ( 2012-10), p. 1327-1334
    Abstract: Patients coinfected with HIV and HCV are at risk for developing portal hypertension (PHT), hyper-dynamic circulation and pulmonary arterial hypertension (PAH). Data on the influence of antiviral therapy with pegylated interferon-α (PEG-IFN-α) and ribavirin (RBV) are limited. Methods Haemodynamic parameters, including hepatic venous pressure gradient (HVPG), pulmonary arterial pressure (PAP mean ), cardiac output (CO) and systemic vascular resistance (SysVR), were prospectively evaluated before and after PEG-IFN-α+RBV therapy in 80 HIV–HCV-coinfected patients. Results Baseline evaluation showed a mean HVPG of 4.7 mmHg, CO of 6.15 l/min and PAP mean of 14.8 mmHg. PHT was present in 26% of patients, hyperdynamic circulation in 5% and PAH in 4%. Patients with advanced fibrosis (METAVIR stage F3/F4; n=32) had significantly higher CO ( P=0.008), lower SysVR ( P=0.035), higher PAP mean ( P=0.018) and higher pulmonary vascular resistance ( P=0.022) than patients with stage F0–F2 fibrosis ( n=48). Both hyperdynamic circulation and PAH were significantly associated with liver stiffness, fibrosis stage and portal pressure; a non-significant trend was found for CD4 + T-cell counts and HIV RNA levels. No significant changes in PAP mean , CO and SysVR were observed after PEG-IFN-α+RBV treatment, although a significant decrease in HVPG was noted in patients with HCV eradication ( P=0.013). Conclusions The overall prevalence of hyperdynamic circulation and PAH in HIV–HCV coinfection is low. Advanced fibrosis, increased liver stiffness, elevated portal pressure and probably CD4 + T-cell count and HIV viraemia represent risk factors for hyperdynamic circulation and PAH. PHT is present in 26% of HIV–HCV-coinfected patients evaluated for antiviral therapy. Successful HCV eradication significantly decreases HVPG.
    Type of Medium: Online Resource
    ISSN: 1359-6535 , 2040-2058
    URL: Article
    DOI: 10.3851/IMP2349
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2012
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  • 4
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    Daclatasvir plus Sofosbuvir, with or without Ribavirin, in Real-World Patients with HIV–HCV Coinfection and Advanced Liver Disease
    SAGE Publications ; 2017
    In:  Antiviral Therapy Vol. 22, No. 3 ( 2017-04), p. 225-236
    Details
    In: Antiviral Therapy, SAGE Publications, Vol. 22, No. 3 ( 2017-04), p. 225-236
    Abstract: HIV–HCV-coinfected patients respond just as well to modern direct-acting antiviral HCV therapy as HCV-monoinfected patients. However, clinical data for all-oral HCV treatments are sparse in HIV–HCV-coinfected patients with an advanced stage of liver cirrhosis. Methods A subanalysis of efficacy and safety for a daclatasvir (DCV) and sofosbuvir (SOF) regimen, with or without ribavirin (RBV), was undertaken in HIV–HCV-coinfected patients with advanced liver disease and no other treatment options enrolled into a European DCV compassionate use programme. Results Fifty five HIV–HCV (mostly genotypes 1, 3, 4) coinfected patients were treated with DCV+SOF with ( n=16) or without RBV ( n=39), mostly for 24 weeks. Patients were predominantly (95%) cirrhotic (50% were Child–Pugh class B or C) and were receiving a wide range of antiretrovirals; 40% were injection drug users and 25% were receiving oral opioid substitution. Sustained virological response at post-treatment week 12 (SVR12) by modified intention-to-treat analysis ( n=52) was 92% overall (95% CI 81.5, 97.9), and was similar with (94% [95% CI 69.8, 99.8]) or without RBV (92% [95% CI 77.5, 98.2] ). Only one patient relapsed (Child–Pugh class B). The overall SVR12 rate after excluding non-virologi-cal failures ( n=49) was 98% (95% CI 89.1, 99.9). Four patients discontinued treatment for adverse events and one died during treatment (not treatment-related). No patient lost opioid maintenance or required a change of antiretrovirals due to drug–drug interactions. Conclusions DCV+SOF, with or without RBV, showed high SVR12 rates and was well tolerated in this real-world cohort of HIV–HCV-coinfected patients with very advanced liver disease. ClinicalTrials.gov ID NCT02097966 (Study AI444-237).
    Type of Medium: Online Resource
    ISSN: 1359-6535 , 2040-2058
    URL: Article
    DOI: 10.3851/IMP3108
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2017
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  • 5
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    Online Resource
    Considerable Under-Treatment of Chronic HCV Infection in HIV Patients despite Acceptable Sustained Virological Response Rates in a Real-Life Setting
    SAGE Publications ; 2011
    In:  Antiviral Therapy Vol. 16, No. 6 ( 2011-08), p. 815-824
    Details
    In: Antiviral Therapy, SAGE Publications, Vol. 16, No. 6 ( 2011-08), p. 815-824
    Abstract: According to guidelines, treatment of HCV infection should be considered a priority in HIV–HCV-coinfected patients. Methods This multicentre study includes HIV–HCV-coinfected patients diagnosed since 2001 in 14 participating centres in Austria and Germany. Demographic and virological data were recorded. Factors associated with non-initiation of HCV treatment were identified. Results Among 9,524 HIV patients screened, 1,033 HIV– HCV-coinfected patients were identified (male/female: 760/273; age: 43 ±9 years; weight: 71 ±12 kg; CD4 + T-cell nadir: 255 ±189 cells/μl; HCV RNA: 3.79x10 6 IU/ml; HIV RNA: 65x10 3 copies/ml). HCV genotype (GT) was predominantly GT-1 (62%). A total of 416 (40%) patients received HCV treatment, whereas 617 (60%) patients remained untreated. The main reasons for deferral of HCV treatment were patient refusal (20%), adherence/compliance (18%), active intravenous drug abuse (14%) and advanced immunodeficiency/AIDS (9%). Patients starting HCV treatment had significantly lower fibrosis stage (F2 versus F4; P 〈 0.0001), higher CD4 + T-cell count (530 cells/|il versus 430 cells/|il; P 〈 0.0001), lower HIV RNA levels (18x10 3 copies/ml versus 47x10 3 copies/ml; P=0.0008) and higher alanine aminotransferase (ALT; 113 IU/ml versus 75 IU/ml; P 〈 0.0001) than patients without initiation of HCV treatment. Age, HCV GTs, HCV RNA, haemoglobin levels, platelet count and white blood cell count were similar in patients receiving and in patients not receiving antiviral therapy. Multivariate analysis identified ALT levels ( P 〈 0.0001) and CD4 + T-cell count ( P 〈 0.0001) as independent predictors of treatment uptake. The overall sustained virological response (SVR) was 41% (155/416), with GT-1 and non-GT1 patients achieving SVR rates of 29% and 48%, respectively. Conclusions This large cohort study provides evidence for considerable under-treatment of chronic HCV infection in HIV patients. Despite acceptable treatment success in this real-life setting, HCV remains untreated in the majority of patients and often owing to potentially modifable reasons.
    Type of Medium: Online Resource
    ISSN: 1359-6535 , 2040-2058
    URL: Article
    DOI: 10.3851/IMP1831
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2011
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  • 6
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    Strategies for Assignment of HIV-HCV Genotype-1-Coinfected Patients to Either Dual-Therapy or Direct-Acting Antiviral Agent-Based Triple-Therapy
    SAGE Publications ; 2014
    In:  Antiviral Therapy Vol. 19, No. 4 ( 2014-05), p. 407-414
    Details
    In: Antiviral Therapy, SAGE Publications, Vol. 19, No. 4 ( 2014-05), p. 407-414
    Abstract: The aim of this study was to evaluate strategies for assignment of HIV–HCV genotype-1-coinfected patients (HIV–HCV-GT1) to either dual-therapy or direct-acting antiviral agent (DAA)-based triple-therapy. Methods A total of 148 treatment-naive HIV–HCV-GT1 who received antiviral therapy with pegylated interferon/ ribavirin were included in this multinational, retrospective analysis. Patients with rapid virological response (RVR) were treated for 48 weeks, while patients without RVR received either 48 or 72 weeks of treatment. IL28B rs12979860 (IL28B) non-C/C, advanced liver fibrosis and high HCV RNA were considered as established risk factors for treatment failure. Results A trend toward higher sustained virological response (SVR) rates in patients with IL28B C/C (65% [37/57] versus 51% [40/79] ; P=0.097) was observed. Higher SVR rates were observed in patients without advanced liver fibrosis (61% [47/77] versus 42% [22/52] ); P=0.036) and without high HCV RNA (73% [35/48] versus 49% [49/100] ; P=0.006), as well as in patients with RVR (90% [35/39] versus 45% [49/109] ; P 〈 0.001). SVR rates varied statistically significantly between the risk factors for treatment failure subgroups (86% [6/7] versus 69% [34/49] versus 48% [21/44] versus 20% [4/20] for zero, one, two and three risk factors, respectively; P 〈 0.001). In patients without RVR, higher rates of SVR were observed in those treated for 72 weeks (62% [23/37]), when compared to patients treated for 48 weeks (36% [26/72] ; P=0.01). Conclusions RVR had an excellent positive predictive value for the response to dual-therapy in HIV–HCV-GT1, emphasizing the utility of a lead-in phase for assigning these patients to dual-therapy or DAA-based triple-therapy. The use of an IL28B-guided approach was suboptimal, while a combination of established baseline predictors may provide guidance for individual treatment decisions prior to the initiation of antiviral therapy. However, the extension of treatment duration to 72 weeks in HIV–HCV-GT1 without RVR should be strongly considered if triple-therapy is not available.
    Type of Medium: Online Resource
    ISSN: 1359-6535 , 2040-2058
    URL: Article
    DOI: 10.3851/IMP2717
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2014
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  • 7
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    Online Resource
    von Willebrand Factor Antigen: A Novel On-Treatment Predictor of Response to Antiviral Therapy in Chronic Hepatitis C Genotypes 1 and 4
    SAGE Publications ; 2010
    In:  Antiviral Therapy Vol. 15, No. 6 ( 2010-08), p. 831-839
    Details
    In: Antiviral Therapy, SAGE Publications, Vol. 15, No. 6 ( 2010-08), p. 831-839
    Abstract: Levels of von Willebrand factor antigen (vWF-Ag) increase during combination antiviral therapy of chronic hepatitis C (CHC). The present study investigates the association between these changes in vWF-Ag levels and response to treatment. Methods Changes in levels of vWF-Ag on antiviral combination treatment in 184 patients with CHC genotype 1 or 4 infections were measured prospectively and effect on response was studied. Results High on-treatment levels of vWF-Ag were associated with relapse ( P 〈 0.01) and low on-treatment levels with sustained virological response (SVR). Receiver operating characteristic curve analysis showed that vWF-Ag levels of 〈 300% at week 12 of therapy have a positive predictive value (PPV) of 78% for SVR. In early virological response (EVR) patients, the PPV of vWF-Ag levels 〈 300% at week 12 was 74%. An even higher PPV of 88% in complete EVRs (undetectable HCV RNA at week 12) was observed for the same cutoff value at week 12. Conclusions On-treatment levels of vWF-Ag can be utilized as an additional predictive marker for response to antiviral therapy. This is especially relevant in EVR patients because EVR alone only has a PPV of 58–72% on SVR, which increased to 74%, when factoring in vWF-Ag levels 〈 300% at week 12, and to 88% in complete EVRs; therefore, measurement of vWF-Ag levels at week 12 is helpful. EVR patients that are above the cutoff values for vWF-Ag that make SVR very probable might profit from an extension of therapy to 72 weeks.
    Type of Medium: Online Resource
    ISSN: 1359-6535 , 2040-2058
    URL: Article
    DOI: 10.3851/IMP1654
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2010
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