Le syndrome de Widal en pratique clinique
Abstract
Zusammenfassung. Das Widal-Syndrom umfasst eine klinische Trias mit chroniquer Rhinosinusitis und nasalen Polypen, Asthma bronchiale und eine Unverträglichkeit auf Acetylsalicylsäure (Aspirin) und anderen nichtsteroidalen Entzündungshemmern (NSAID). Etwa 7 % der Asthmatiker und 10 % der Patienten mit chronischer Rhinosinusitis leiden darunter. Asthma und NSAID-Unverträglichkeit treten häufig mehrere Jahre nach Beginn der Rhinosinusitis auf, was zur Verzögerung der Diagnose führt. Zurzeit gibt es keine spezifischen Biomarker. Der Provokationstest mit Aspirin bleibt der Gold-Standard für die Diagnose, sollte aber wegen des Risikos eines schweren Asthmaanfalls nur durch den Spezialisten durchgeführt werden. Die Grundbehandlung beruht auf der Kombination topischer Kortikosteroide und Montelukast, sowie der Vermeidung von Hemmern der Zyklooxygenase-1. Therapierefraktäre Fälle können auf eine Desensibilisierung mit Aspirin oder neuerdings auf Biologika wie Mepolizumab ansprechen.
Abstract. Aspirin-exacerbated respiratory disease (AERD) is characterized by Samter’s triad: chronic rhinosinusitis with polyposis, asthma and sensitivity to classical non-steroidal anti-inflammatory drugs (NSAID). Approximately 7 % of asthmatics and 10 % of patients with chronic rhinosinusitis suffer from AERD. Asthma and NSAID-intolerance may appear years after ENT symptoms and often leads to a delay in diagnosis. There is no specific biomarker to date. Aspirin provocation test remains the goldstandard for diagnosis but should only be performed in specialized care, given the risk of triggering severe symptoms. The mainstay of therapy relies on combining topical corticosteroids and leukotriene-receptor antagonists and the avoidance of cyclooxygenase-1 inhibitors. Patients with refractory symptoms may respond to Aspirin desensitization or to immunobiologics such as omalizumab or mepolizumab.
Résumé. Le syndrome de Widal comprend une triade clinique avec asthme, rhinosinusite chronique et intolérance à l’acide acétylsalicylique (Aspirine) et autres anti-inflammatoires non-stéroïdiens (AINS) classiques. On estime que 7 % des asthmatiques et 10 % des patients avec rhinosinusite chronique en souffrent. L’asthme et l’hypersensibilité aux AINS apparaissent généralement plusieurs années après le début de la rhinosinusite, ce qui engendre un retard diagnostique. Il n’existe actuellement pas de biomarqueur spécifique. Le test de provocation à l’Aspirine reste le gold-standard, mais doit être effectué en milieu spécialisé. Le traitement de base consiste à associer corticostéroïdes topiques et montelukast et à éviter les inhibiteurs de la cyclooxygénase-1. Les cas réfractaires peuvent répondre à une désensibilisation à l’Aspirine ou nouvellement aux traitements biologiques comme le mepolizumab.
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