CNA110329: a prospective epidemiological study to determine the prevalence of HLA-B*5701 in HIV-1 infected individuals in five European countries
In: Journal of the International AIDS Society, Volume 11, Issue Suppl 1, p. P155
ISSN: 1758-2652
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In: Journal of the International AIDS Society, Volume 11, Issue Suppl 1, p. P155
ISSN: 1758-2652
In: Journal of the International AIDS Society, Volume 15, Issue S4, p. 1-2
ISSN: 1758-2652
An outbreak of HIV was detected amongst Finnish injecting‐drug users (IDUs) in 1998. The outbreak was caused by CRF01‐AE virus [1]. A comprehensive care programme including infectious diseases, addiction medicine, low threshold methadone program, needle exchange, accommodation and other social services started in December 2000. Funding was provided by municipalities. We have described earlier how the outbreak became geographically and socially restricted [2]. The data of newly diagnosed HIV infections in the hospital district of Helsinki and Uusimaa (Helsinki region) amongst IDUs and HIV‐1 subtypes were obtained from the Finnish national HIV registry. The Helsinki University Central Hospital (HUCH) registry was used to obtain the number of IDUs in HIV care, on antiretroviral therapy (ART), and plasma HIV‐1 RNA (VL) amongst IDUs. The HUCH registry also includes IDUs diagnosed with HIV infection in other Finnish regions, but currently living in Helsinki region. The highest number (n=65) of newly diagnosed HIV infections among IDUs in Helsinki region was observed in 1999 (Figure 1). Between 1998 and 2011, 249 IDUs were diagnosed with HIV infection. From 1998 to 2004 the subtype was CRF01‐AE in 187 (92%) cases, other subtypes in 5 (2%) cases and not subtyped in 11 (5%) cases. From 2005 to 2011 the subtype was CRF01‐AE in 25 (54%) cases, other subtypes in 15 (33%) cases and not subtyped in 6 (13%) cases. In 2011 there were 4 IDUs diagnosed with HIV, one of them with CRF01‐AE. In the Helsinki region out of 183 HIV‐infected IDUs in 2005, 100 (55%) had VL<50 copies/ml and out of 167 HIV‐infected IDUs in 2011, 133 (80%) had VL<50 copies/ml in 2011. We propose that from 2005 the low HIV‐1 RNA in plasma of IDUs has contributed to the low incidence of HIV among IDUs in Helsinki region. However, the incidence of HIV started to decline before the decline of VL in the cohort (Figure 1). This suggests that other factors besides ART may have decreased the risk of HIV infection among IDUs before ART coverage of the cohort became considerable. Other subtypes of HIV circulated among IDUs in the Helsinki region during the observation period, which emphasises the necessity of health promoting services (e.g. needle exchange) to be available to all IDUs.image
Publisher's version (útgefin grein) ; Objectives There are currently few data on the long‐term risk of cancer and death in individuals taking raltegravir (RAL). The aim of this analysis was to evaluate whether there is evidence for an association. Methods The EuroSIDA cohort was divided into three groups: those starting RAL‐based combination antiretroviral therapy (cART) on or after 21 December 2007 (RAL); a historical cohort (HIST) of individuals adding a new antiretroviral (ARV) drug (not RAL) to their cART between 1 January 2005 and 20 December 2007, and a concurrent cohort (CONC) of individuals adding a new ARV drug (not RAL) to their cART on or after 21 December 2007. Baseline characteristics were compared using logistic regression. The incidences of newly diagnosed malignancies and death were compared using Poisson regression. Results The RAL cohort included 1470 individuals [with 4058 person‐years of follow‐up (PYFU)] compared with 3787 (4472 PYFU) and 4467 (10 691 PYFU) in the HIST and CONC cohorts, respectively. The prevalence of non‐AIDS‐related malignancies prior to baseline tended to be higher in the RAL cohort vs. the HIST cohort [adjusted odds ratio (aOR) 1.31; 95% confidence interval (CI) 0.95–1.80] and vs. the CONC cohort (aOR 1.89; 95% CI 1.37–2.61). In intention‐to‐treat (ITT) analysis (events: RAL, 50; HIST, 45; CONC, 127), the incidence of all new malignancies was 1.11 (95% CI 0.84–1.46) per 100 PYFU in the RAL cohort vs. 1.20 (95% CI 0.90–1.61) and 0.83 (95% CI 0.70–0.99) in the HIST and CONC cohorts, respectively. After adjustment, there was no evidence for a difference in the risk of malignancies [adjusted rate ratio (RR) 0.73; 95% CI 0.47–1.14 for RALvs. HIST; RR 0.95; 95% CI 0.65–1.39 for RALvs. CONC] or mortality (adjusted RR 0.87; 95% CI 0.53–1.43 for RALvs. HIST; RR 1.14; 95% CI 0.76–1.72 for RALvs. CONC). Conclusions We found no evidence for an oncogenic risk or poorer survival associated with using RAL compared with control groups. ; EuroSIDA was supported by the European Union's Seventh Framework Programme for research, technological development and demonstration under EuroCoord grant agreement no. 260694. Current support includes unrestricted grants from Bristol‐Myers Squibb, Gilead, GlaxoSmithKline LLC, Janssen R&D, Merck and Co. Inc. and Pfizer Inc. The participation of centres from Switzerland was supported by The Swiss National Science Foundation (Grant 108787). The study is also supported by a grant (grant number DNRF126) from the Danish National Research Foundation. ; Peer Reviewed
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