Prise en charge de la toxoplasmose cérébrale chez le patient infecté par le VIH en Martinique (intérêt de l'association triméthoprim-sulfaméthoxazole)

La toxoplasmose est une infection bénigne et le plus souvent inapparente chez la personne immunocompétente, mais elle peut être très grave voire mortelle chez l'immunodéprimé, notamment chez le patient infecté par le VIH. En 2004, la prévalence de l'infection par le VIH reste importante dans les départements français d'Amérique, et la toxoplasmose cérébrale est la première infection opportuniste en Martinique. Le traitement de référence de la toxoplasmose cérébrale est l'association pyriméthamine-sulfadiazine. La tolérance à ce traitement est médiocre, obligeant à de fréquents arrêts de traitement. Depuis 1993, au CHU de Fort-de-France, l'association triméthoprim-sulfaméthoxazole a été utilisée en première ligne de traitement de la toxoplasmose cérébrale. Nous avons mené une étude rétrospective d'août 1993 à décembre 2003 pour évaluer l'efficacité et la tolérance de cette association dans le traitement d'attaque de la toxoplasmose cérébrale. Avec une efficacité de 77,1 % en intention de traiter et 11,5 % d'arrêts de traitement pour effets indésirables, l'association triméthoprim-sulfaméthoxazole paraît être une alternative valable au traitement de référence, avec comme avantages la disponibilité d'une voie intraveineuse, un nombre réduit de comprimés et un faible coûtFORT-DE-FRANCE-CHRU-BU (972332102) / SudocBESANCON-BU Médecine pharmacie (250562102) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Real-Life Impact on Lipid Profile of a Switch from Tenofovir Disoproxil Fumarate to Tenofovir Alafenamide in HIV-Infected Patients

International audienceTenofovir disoproxil fumarate is a prodrug of tenofovir diphosphate that exposes patients to renal toxicity over the long term. Tenofovir alafenamide, a new prodrug, now makes it possible to reduce toxicity, but at the cost of an alteration in lipid profile. There is currently no recommendation for follow-up of lipid profile when switching from tenofovir disoproxil fumarate to tenofovir alafenamide. Objective: Our study aimed to evaluate the effects on renal function and lipid profile of a switch from tenofovir disoproxil fumarate to tenofovir alafenamide, and the consequences for patient management. Methods: Demographic, clinical and biological data was recorded from a retrospective clinical cohort study in real-life, including patients who switched from tenofovir disoproxil fumarate to tenofovir alafenamide. A descriptive analysis of the study population, with comparison of biological parameters using the paired Student t test for paired data was performed. Results: From January 2016 to January 2019, a total of 103 patients were included. There was no significant difference in renal function before vs after the switch in therapy (p=0.29 for creatinine, p=0.30 for phosphoremia). We observed a change in lipid profile, with a significant increase in total cholesterol (p=0.0006), HDL cholesterol (p=0.0055) and triglycerides (p=0.0242). Four patients received lipid-lowering therapy after switching. Conclusion: In patients who switch from tenofovir disoproxil fumarate to tenofovir alafenamide, lipid profile is altered, and may require initiation of lipid-lowering therapy. It seems necessary to monitor lipid parameters after this switch, despite the absence of an official recommendation

A highly virulent variant of HIV-1 circulating in the Netherlands

We discovered a highly virulent variant of subtype-B HIV-1 in the Netherlands. One hundred nine individuals with this variant had a 0.54 to 0.74 log10 increase (i.e., a ~3.5-fold to 5.5-fold increase) in viral load compared with, and exhibited CD4 cell decline twice as fast as, 6604 individuals with other subtype-B strains. Without treatment, advanced HIV-CD4 cell counts below 350 cells per cubic millimeter, with long-term clinical consequences-is expected to be reached, on average, 9 months after diagnosis for individuals in their thirties with this variant. Age, sex, suspected mode of transmission, and place of birth for the aforementioned 109 individuals were typical for HIV-positive people in the Netherlands, which suggests that the increased virulence is attributable to the viral strain. Genetic sequence analysis suggests that this variant arose in the 1990s from de novo mutation, not recombination, with increased transmissibility and an unfamiliar molecular mechanism of virulence