External validation of the Dat'AIDS score: A risk score for predicting 5-year overall mortality in people living with HIV aged 60 years or older.

OBJECTIVE To perform an external validation of the Dat'AIDS score for predicting 5-year overall mortality among people with HIV (PWH) aged 60 years or older. METHODS This was a multi-centre prospective cohort study at all sites participating in the Swiss HIV Cohort Study (SHCS). We calculated the Dat'AIDS score in PWH aged 60 years or older at their first visit between 1 January 2015 and 1 January 2020. People living with HIV-2 and those whose Dat'AIDS score could not be calculated were excluded. Patients were followed until 1 January 2020. The primary endpoint was all-cause mortality. Vital status was collected throughout the study period. We obtained population and score descriptive statistics and assessed the score's discrimination and calibration. RESULTS We included 2205 participants (82% male) of median [interquartile range (IQR)] age 62.0 (60.3-67.0) years, mostly with viraemia <50 copies/mL (92.7%). Median follow-up time was 15.9 years and median (IQR) CD4 cell count at enrolment was 586 (420-782) cells/μL. In all, 152 deaths were recorded during a total follow-up period of 7147 patient-years. The median (IQR) observed Dat'AIDS score was 3 (0-8). Discriminative capacities were good as the C-statistic was 0.73 (95% CI: 0.69-0.77) and consistent across all subgroups. Comparison of observed and expected survival probabilities showed good calibration. CONCLUSIONS External validation of the Dat'AIDS score in patients aged 60 years or older showed that it could be a useful tool not only for research purposes, but also to identify older patients at a higher mortality risk and to tailor the most appropriate interventions

External validation of the Dat'AIDS score: A risk score for predicting 5-year overall mortality in people living with HIV aged 60 years or older

OBJECTIVE: To perform an external validation of the Dat'AIDS score for predicting 5-year overall mortality among people with HIV (PWH) aged 60 years or older. METHODS: This was a multi-centre prospective cohort study at all sites participating in the Swiss HIV Cohort Study (SHCS). We calculated the Dat'AIDS score in PWH aged 60 years or older at their first visit between 1 January 2015 and 1 January 2020. People living with HIV-2 and those whose Dat'AIDS score could not be calculated were excluded. Patients were followed until 1 January 2020. The primary endpoint was all-cause mortality. Vital status was collected throughout the study period. We obtained population and score descriptive statistics and assessed the score's discrimination and calibration. RESULTS: We included 2205 participants (82% male) of median [interquartile range (IQR)] age 62.0 (60.3-67.0) years, mostly with viraemia <50 copies/mL (92.7%). Median follow-up time was 15.9 years and median (IQR) CD4 cell count at enrolment was 586 (420-782) cells/μL. In all, 152 deaths were recorded during a total follow-up period of 7147 patient-years. The median (IQR) observed Dat'AIDS score was 3 (0-8). Discriminative capacities were good as the C-statistic was 0.73 (95% CI: 0.69-0.77) and consistent across all subgroups. Comparison of observed and expected survival probabilities showed good calibration. CONCLUSIONS: External validation of the Dat'AIDS score in patients aged 60 years or older showed that it could be a useful tool not only for research purposes, but also to identify older patients at a higher mortality risk and to tailor the most appropriate interventions

PLoS One

Compared to the general population, HIV-infected patients are at higher risk of developing non-AIDS-defining cancers. Chronic HCV infection has also been associated with a higher risk than that of the general population of developing cancers other than hepatocarcinoma. Evaluation of the impact of HCV-related factors on non-AIDS-defining and non HCV-liver (NANL) related cancers among HIV/HCV co-infected patients are scarce. The aim of this study was to identify the impact of HIV/HCV clinical characteristics on NANL related cancers in a large cohort of HIV/HCV-coinfected patients followed from 2005 to 2017. Cox proportional hazards models with delayed entry were used to estimate factors associated with NANL related cancer. Among 1391 patients followed for a median of 5 years, 60 patients developed NANL related cancers, yielding an incidence rate of 8.9 per 1000 person-years (95% CI, [6.6-11.1]). By final multivariable analysis, after adjustment for sex, tobacco or alcohol consumption, baseline CD4 cell count and HCV sustained viral response (SVR), age and a longer duration since HIV diagnosis were independently associated with a higher risk of NANL related cancer (aHR for each additional year 1.10, 95% CI 1.06-1.14, p<0.0001 and 1.06, 95% CI 1.01-1.11, p = 0.02, respectively). Duration of HCV infection, cirrhosis, HCV viral load, genotype and SVR were not associated with the occurrence of NANL related cancer. Among HIV/HCV-coinfected patients, age and the duration of HIV infection were the only characteristics found to be associated with the occurrence of NANL related cancer. In contrast, no association was observed with any HCV-related variables

The French national prospective cohort of patients co-infected with HIV and HCV (ANRS CO13 HEPAVIH): Early findings, 2006-2010

<p>Abstract</p> <p>Background</p> <p>In France, it is estimated that 24% of HIV-infected patients are also infected with HCV. Longitudinal studies addressing clinical and public health questions related to HIV-HCV co-infection (HIV-HCV clinical progression and its determinants including genetic dimension, patients' experience with these two diseases and their treatments) are limited. The ANRS CO 13 HEPAVIH cohort was set up to explore these critical questions.</p> <p>To describe the cohort aims and organization, monitoring and data collection procedures, baseline characteristics, as well as follow-up findings to date.</p> <p>Methods</p> <p>Inclusion criteria in the cohort were: age > 18 years, HIV-1 infection, chronic hepatitis C virus (HCV) infection or sustained response to HCV treatment. A standardized medical questionnaire collecting socio-demographic, clinical, biological, therapeutic, histological, ultrasound and endoscopic data is administered at enrolment, then every six months for cirrhotic patients or yearly for non-cirrhotic patients. Also, a self-administered questionnaire documenting socio-behavioral data and adherence to HIV and/or HCV treatments is administered at enrolment and yearly thereafter.</p> <p>Results</p> <p>A total of 1,175 patients were included from January 2006 to December 2008. Their median age at enrolment was 45 years and 70.2% were male. The median CD4 cell count was 442 (IQR: 304-633) cells/μl and HIV RNA plasma viral load was undetectable in 68.8%. Most participants (71.6%) were on HAART. Among the 1,048 HIV-HCV chronically co-infected patients, HCV genotype 1 was predominant (56%) and cirrhosis was present in 25%. As of January, 2010, after a median follow-up of 16.7 months (IQR: 11.3-25.3), 13 new cases of decompensated cirrhosis, nine hepatocellular carcinomas and 20 HCV-related deaths were reported, resulting in a cumulative HCV-related severe event rate of 1.9/100 person-years (95% CI: 1.3-2.5). The rate of HCV-related severe events was higher in cirrhotic patients and those with a low CD4 cells count, but did not differ according to sex, age, alcohol consumption, CDC clinical stage or HCV status.</p> <p>Conclusion</p> <p>The ANRS CO 13 HEPAVIH is a nation-wide cohort using a large network of HIV treatment, infectious diseases and internal medicine clinics in France, and thus is highly representative of the French population living with these two viruses and in care.</p

PARTICULARITES DE L'INFECTION VHC ET DE LA THERAPEUTIQUE ANTI-VHC CHEZ LES PATIENTS CO-INFECTES VIH/VHC

With the introduction of highly active antiretroviral therapy in 1996, liver disease has emerged as an important cause of morbidity and mortality in HIV/HCV-coinfected patients. In 2000, RIBAVIC HC02 trial, a randomized controlled trial (the ANRS HC02 RIBAVIC study) comparing pegylated interferon alfa-2b plus ribavirin vith conventional interferon alfa-2b plus ribavirin was conducted. In order to describe the effect of interferon plus ribavirin-based therapies on the incidence of long-term clinical outcomes in HIV/HCV-coinfected patients, a prospective cohort study was performed from the patients included in the ANRS HC02 RIBAVIC trial in 2001. The RIBAVIC trial and the cohort contribute to show these results : - HCV viral load kinetics could differ according to the choice of HAART regimen. - the prevalence (61%) and risk factors for steatosis are similar to that observed in HCV-monoinfected patients. None of the characteristics of HIV infection, including antiretroviral therapy, is independently associated with steatosis. - the rate of sustained virological response is lower in HIV/HCV-coinfected patients (27%) than in HCV-monoinfected patients - the rate of non response (HCV RNA decline of less than 2 logs at 12 weeks of peginterferon and ribavirin combination therapy) is high, ranging from 29% to 33% (14% in HCV-monoinfected patients). The potential loss of ribavirin efficacy on HCV during concomitant use of NRTIs, such abacavir, is suspected. - the best positive and negative predictive values of sustained virological response (SVR) were respectively obtained with an undetectable HCV RNA at W4 (97%) and with more than a 2 log10 decrease at W12 (99%). The HCV viral load decrease at week 2 and week 4 was significantly slower in relapsing patients than in patients with sustained virological response. - During anti-HCV therapy, 1- severe anemia occurred in 15.9% of patients and was significantly higher in patients receiving zidovudine-based HAART ; 2- severe weight loss (> 10% of baseline weight) is frequent (28%) and could be one of the first clinical sign of a mitochondrial toxicity; 3- markers of advanced liver fibrosis and not neutropenia are predictors of increased susceptibility to bacterial infections 4- concomitant treatment with didanosine and interferon-2b or peg-interferon-2b plus ribavirin is associated with an increase risk of symptomatic mitochondrial toxicity, hepatic decompensation and fibrosis worsening.En 1998, le traitement de la co-infection VHC rarement discuté avant l'ère des HAART, compte tenu d'une réponse médiocre à la monothérapie par IFNα et d'un pronostic de vie lié au VIH estimé en moyenne à 10 ans, fût reconsidéré. C'est ainsi que débuta en 2000, l'essai RIBAVIC HC02, essai randomisé et multicentrique comparant l'association de la ribavirine 800 mg/j à l'Interféron 3 MUI x3/semaine ou au PEG-α-2b Interféron 1,5 μg/kg/semaine pendant 48 semaines. Une cohorte des patients inclus dans l'essai RIBAVIC (cohorte RIBAVIC EP10) débuta en 2001 pour évaluer le devenir à long terme de ces patients. L'essai RIBAVIC et la cohorte RIBAVIC ont apporté les enseignements suivants : - la cinétique de la charge virale VHC peut différer selon la nature du traitement antirétroviral. - la prévalence et les facteurs de risque de la stéatose sont similaires à ceux observés dans la population mono-infectée VHC - le taux de réponse virologique soutenue est inférieur chez les patients co-infectés (27%) comparé aux patients mono-infectés VHC (50%) - le taux de non réponse virologique (diminution de la charge virale VHC inférieure à 2 log à S12) sous traitement par pegIFN plus ribavirine est plus élevé (33%) comparé aux patients monoinfectés VHC (14%). L'interaction entre la ribavirine et l'abacavir pourrait être un facteur de risque. - l'indétectabilité de l'ARN VHC dès S4 est prédictive de la réponse à long terme (valeur prédictive positive 97%) et la décroissance de la charge virale VHC est significativement plus lente chez les patients rechuteurs comparée aux patients répondeurs long terme à S2 et à S4 - Au cours du traitement anti-VHC :1- le risque d'anémie est élevé et majoré par la coprescription de zidovudine et de ribavirine ; 2- l'amaigrissement est fréquent et sévère et peut être révélateur d'une toxicité mitochondriale ; 3- le risque bactérien n'est pas lié au taux des polynucléaires neutrophiles mais à la fibrose hépatique ; 4- le risque de toxicité mitochondriale, d'aggravation de la fibrose et de décompensation hépatique est majoré par l'interaction entre la didanosine et la ribavirine - une réponse virologique soutenue est associée à un bénéfice histologique et clinique

Particularités de l'infection VHC et de la thérapeutique anti-VHC chez les patients co-infectés VIH/VHC

En 1998, le traitement de la co-infection VHC rarement discuté avant l ère des HAART, compte tenu d une réponse médiocre à la monothérapie par IFN et d un pronostic de vie lié au VIH estimé en moyenne à 10 ans, fût reconsidéré. C est ainsi que débuta en 2000, l essai RIBAVIC HC02, essai randomisé et multicentrique comparant l association de la ribavirine 800 mg/j à l Interféron 3 MUI x3/semaine ou au PEG- -2b Interféron 1,5 g/kg/semaine pendant 48 semaines. Une cohorte des patients inclus dans l essai RIBAVIC (cohorte RIBAVIC EP10) débuta en 2001 pour évaluer le devenir à long terme de ces patients. L essai RIBAVIC et la cohorte RIBAVIC ont apporté les enseignements suivants : - la cinétique de la charge virale VHC peut différer selon la nature du traitement antirétroviral. - la prévalence et les facteurs de risque de la stéatose sont similaires à ceux observés dans la population mono-infectée VHC - le taux de réponse virologique soutenue est inférieur chez les patients co-infectés (27%) comparé aux patients mono-infectés VHC (50%) - le taux de non réponse virologique (diminution de la charge virale VHC inférieure à 2 log à S12) sous traitement par pegIFN plus ribavirine est plus élevé (33%) comparé aux patients monoinfectés VHC (14%). L interaction entre la ribavirine et l abacavir pourrait être un facteur de risque. - l indétectabilité de l ARN VHC dès S4 est prédictive de la réponse à long terme (valeur prédictive positive 97%) et la décroissance de la charge virale VHC est significativement plus lente chez les patients rechuteurs comparée aux patients répondeurs long terme à S2 et à S4 - Au cours du traitement anti-VHC :1- le risque d anémie est élevé et majoré par la co-prescription de zidovudine et de ribavirine ; 2- l amaigrissement est fréquent et sévère et peut être révélateur d une toxicité mitochondriale ; 3- le risque bactérien n est pas lié au taux des polynucléaires neutrophiles mais à la fibrose hépatique ; 4- le risque de toxicité mitochondriale, d aggravation de la fibrose et de décompensation hépatique est majoré par l interaction entre la didanosine et la ribavirine - une réponse virologique soutenue est associée à un bénéfice histologique et clinique.PARIS-BIUSJ-Thèses (751052125) / SudocPARIS-BIUSJ-Physique recherche (751052113) / SudocSudocFranceF

Pancytopénie sévère secondaire à un déficit en folates en dépit d’un dosage de folatesérythrocytaires normal

International audienceWe report the case of an alcoholic patient with severe pancytopenia with lowplasma folate level but normal erythrocyte folates and cobalamin levels. The bone marrow smear concluded to a pancytopenia due to folates and/or cobalamin deficiency. Severe pancytopenia due to acute plasma folate deficiency can be observed despite normal erythrocyte folates level which reflects the organism’s folates store.Nous rapportons un cas de pancytopénie sévère avec dosage en folates sériques isolément bas contrastant avec des folates érythrocytaires et vitamine B12 normaux, chez un patient alcoolique. Le myélogramme montrait un aspect de moelle carentielle en ces vitamines. Ce cas met en lumière la possibilité de survenue d’une pancytopénie sévère secondaire à une carence en folates, en dépit d’un dosage normal de folates érythrocytaires, qui est un indicateur des apports en folates des 3 derniers mois (durée de vie du globule rouge) et donc des réserves de l’organisme

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Poor knowledge among French travellers of the risk of acquiring multidrug-resistant bacteria during travel

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Prognostic factors associated with 30-day in-hospital mortality in coagulase-negative Staphylococcus bacteraemia: no impact of vancomycin minimum inhibitory concentration

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