Baisse de l'acuité visuelle chez une patiente traitée par corticoïdes pour maladie de Horton : choriorétinopathie séreuse centrale iatrogène

International audienceIntroduction : Visual complications of temporal arteritis are frequent and serious. Their risk prompts glucocorticoid therapy, but this treatment may also cause ophthalmologic troubles.Exegesis : A sudden and isolated monocular visual blur, occurring in a 66 years old woman after 4 month of glucocorticoid treatment for temporal arteritis, revealed a case of iatrogenic central serous chorioretinopathy. The diagnosis of this disease is established by fluorescein angiography and its functional prognosis is excellent. Tapering the doses of glucocorticoids, as fast as the underlying disease allows, hastens visual recovery.Conclusion : When the treatment of temporal arteritis is commenced for more than a month, new visual complications are rare. Central serous chorioretinopathy induced by glucocorticoids belongs to the diagnoses that should be evoked in this case, especially if there is no clinical manifestation of arteritis and no inflammatory markers.Introduction : Les complications visuelles de la maladie de Horton sont fréquentes et graves. Leur risque justifie l'instauration rapide d'une corticothérapie, mais ce traitement peut lui aussi induire des problèmes ophtalmologiques.Exégèse : Un flou visuel monoculaire brutal et isolé, survenant chez une patiente de 66 ans sous corticoïdes depuis quatre mois pour une maladie de Horton, révélait un cas de choriorétinopathie séreuse centrale iatrogène. Le diagnostic de cette maladie est porté par l'angiographie rétinienne à la fluorescéine et le pronostic visuel est excellent. La décroissance des corticoïdes, aussi rapide que la maladie de fond le permet, accélère la récupération fonctionnelle.Conclusion : Lorsque le traitement de la maladie de Horton est débuté depuis plus d'un mois, la survenue d'une nouvelle complication visuelle est rare. La choriorétinopathie séreuse centrale secondaire aux corticoïdes figure parmi les diagnostics à évoquer dans ce cadre, surtout en l'absence de manifestation clinique d'artérite et de syndrome inflammatoire

Resistance to trimethoprim/sulfamethoxazole and Tropheryma whipplei

Whipple's disease (WD) is a chronic infection caused by Tropheryma whipplei. A 1-year treatment of oral trimethoprim/sulfamethoxazole (SXT) is commonly used. Advances in the culture of T. whipplei have allowed for full genome sequencing and antibiotic susceptibility testing, which has demonstrated resistance of T. whipplei to trimethoprim. Several mutations in the folP gene that encodes dihydropteroate synthase, the target of sulphonamides, has been reported for one patient with clinically acquired resistance to SXT. Here we report three new patients who experienced clinically acquired resistance to SXT during treatment and one patient with biological failure. Sixty-two folP sequences from DNA samples of 59 WD patients were also obtained. Among the detected amino acid changes, two positions (N4S and S234F) significantly predicted secondary sulfamethoxazole failure (four of five). We suggest that these mutations should be detected at the time of WD diagnosis by sequencing folP in order to avoid sulfamethoxazole monotherapy