23 research outputs found

    Role of Self-Stigma in Pathways from HIV-Related Stigma to Quality of Life among People Living with HIV

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    Funding Information: This study was supported by Viiv Healthcare, Gilead, and Aidsfonds (research Grant Number AF-P.42601). The funders had no role in decisions regarding the study design, data analysis, or publication. Acknowledgments We extend our gratitude to all PLHIV who completed the survey. We further thank the HIV specialist nurses and doctors at OLVG hospital for their effort in recruiting patients to complete the surveys.Peer reviewedPublisher PD

    UvA-DARE (Digital Academic Repository) BMC Infectious Diseases A fatal pseudo-tumour: disseminated basidiobolomycosis

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    General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Abstract Background: Basidiobolomycosis is a rare disease caused by the fungus Basidiobolus ranarum, member of the class Zygomycetes, order Entomophthorales, found worldwide. Usually basidiobolomycosis is a subcutaneous infection but rarely gastrointestinal manifestations have been described; 13 adults and 10 children and a few retroperitoneal or pulmonary cases. In gastrointestinal basidiobolomycosis the colon is most frequently involved, usually presenting with subacute mild abdominal pain. In contrast to children only very few described adult patients had hepatic masses. Definitive diagnosis requires culture, serological testing can be helpful. The fungal morphology and the Splendore-Hoeppli phenomenon are characteristic histological features. There are no prominent risk factors. Usually surgery and prolonged antifungal therapy are required

    Protective effect of hepatitis B virus-active antiretroviral therapy against primary hepatitis B virus infection

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    Current guidelines advise to vaccinate every hepatitis B virus (HBV)-susceptible HIV patient against HBV until sufficient antibody titers have been reached. However, in this era of combination antiretroviral therapy (cART), acute HBV infection rarely occurs in patients who lack this immune protection. We analyzed whether HBV-active cART (lamivudine, emtricitabine, tenofovir) might work as a preexposure prophylaxis (PrEP) to explain this effect. From our HIV cohort at the Onze Lieve Vrouwe Gasthuis hospital (N=2942), patients were selected retrospectively for negative HBV serology (HBsAg, anti-HBs and anti-HBc-negative) at cohort entry. Men who have sex with men (MSM) with a second HBV serology available were included for analysis. The incidence of anti-HBc conversion was determined and correlated with the use of HBV-active drugs. Kaplan-Meier curves and log-rank tests were used to compare HBV-free survival for MSM. In total, 33 HBV infections occurred in 381 eligible MSM over a median follow-up of 2470 days (interquartile range 1146-3871.5). The incident rate per 100 patient-years of follow-up was 1.10 overall, but differed strongly dependent on the use of HBV-active drugs: 2.85/100 patient-years of follow-up in the absence of HBV-active drugs, 1.36 when only lamivudine was used, and 0.14 in the presence of tenofovir. Furthermore, HBV-free survival rate was significantly higher when HBV-active cART was used, in particular when this HBV-active cART contained tenofovir (log-rank P <0.001). Our findings demonstrate that HBV-active cART protects against the occurrence of de-novo HBV infection, most strongly when tenofovir is use

    The effect of switching protease inhibitors to raltegravir on endothelial function, in HIV-infected patients

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    Objective: Lipid management is one of the cornerstones of cardiovascular risk reduction. Treatment of HIV infection with protease inhibitors (PIs) may cause dyslipidaemia, whilst the integrase inhibitor raltegravir (RAL) has a relatively favorable effect on plasma lipids. We examined the effect of switching from PIs to RAL on endothelial function, and its effect on immunological and inflammatory parameters. Methods: We performed a 16-week open-label prospective crossover study: 8 weeks intervention (switch PIs to RAL) and 8 weeks control (unchanged cART regimen). Flow-mediated dilatation (FMD), inflammatory plasma, and cellular markers of immune activation were measured at weeks 0, 8, and 16. Results: Study participants (n = 22) with a median age of 50 years (IQR 42–60) and known HIV infection of 6.5 years (IQR 5.0–17.3) were on stable cART with undetectable HIV viral loads. After 8 weeks of RAL therapy, a reduction in FMD of −0.81% was seen, compared to +0.54% control (pairwise, p = 0.051), while fasting total cholesterol (−17% versus +10%; p < 0.001), LDL cholesterol (−21% versus −3%; p = 0.026), and triglycerides (−41% versus +18%; p = 0.001) significantly decreased during RAL therapy compared to the control. Furthermore, a relation between the change in percentage of B-1 cells and the change in FMD was found (ÎČ 0.40, 95%CI 0.16; 0.64, p = 0.005) during treatment with RAL. Finally, during RAL therapy, 27% of the patients experienced an increased ALT rise. Conclusions: We present an overall negative study, where switching from PIs to RAL slightly reduced the endothelial function while decreasing plasma lipids, thus possibly decreasing the CVD risk in the long term. A transient elevation of ALT was seen upon switch to RAL

    No advantage of quadruple- or triple-class antiretroviral therapy as initial treatment in patients with very high viraemia

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    We assessed whether quadruple or triple-class therapy for the initial treatment of HIV-1 infection provides a virological benefit over standard triple therapy in patients with very high plasma viraemia. The assessment was made based on a national observational HIV cohort in the Netherlands. Inclusion criteria were age ≄18 years, treatment-naive, plasma viral load (pVL) ≄500,000 copies/ml and initiation of quadruple or triple therapy between 2001 and 2011. Time to viral suppression, defined as pVL <50 copies/ml, was compared between the two groups using Kaplan-Meier plots and multivariate Cox regression analysis. A total of 675 patients were included: 125 (19%) initiated quadruple and 550 (81%) triple therapy. Median pVL was 5.9 (IQR 5.8-6.1) log(10) copies/ml in both groups (P=0.49). 22 (18%) patients on quadruple and 63 (12%) on triple therapy interrupted the treatment regimen because of drug-related toxicity (P=0.06). Median time to viral suppression was 5.8 (IQR 4.6-7.9) and 6.0 (4.0-9.4) months in the patients on quadruple and triple therapy, respectively (log-rank, P=0.42). In the adjusted Cox analysis, quadruple therapy was not associated with time to viral suppression (HR 1.07 [95% CI 0.86, 1.33], P=0.53). Similar results were seen when comparing triple- versus dual-class therapy (n=72 versus n=601, respectively). Initial quadruple- or triple-class therapy was equally effective as standard triple therapy in the suppression of HIV-1 in treatment-naive patients with very high viraemia and did not result in faster pVL decreases, but did expose patients to additional toxicit

    Characteristics and culture results of patients who had BSI.

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    <p><i>Abbreviations: A. baumannii =  Acinetobacter baumannii, E. cloacae =  Enterobacter cloacae, E. faecalis =  Enterococcus faecalis, K. pneumoniae =  Klebsiella pneumoniae, MRSA = Methicillin-resistant Staphylococcus aureus, MSSA = Methicillin-susceptible Staphylococcus aureus, P. mirabilis = Proteus mirabilis, S. aureus = Staphylococcus aureus, S. epidermidis = Staphylococcus epidermidis,</i></p><p>SJS =  Stevens Johnson syndrome; TEN =  toxic epidermal necrolysis; TB =  tuberculosis.</p
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