XXXX differentially affects the clinical-biological phenotypes of @entity19417 .

@entity1 @entity286 @entity1333 @entity6129 @entity2883 @entity4841 @entity19417
OBJECTIVES: To describe the clinical-biological phenotype of @entity19417 ( @entity19417 ) according to @entity286 consumption. METHODS: We conducted a descriptive study to describe that phenotype at diagnosis according to @entity286 use. @entity19417 @entity1 entered in the @entity1333 Study Group database with data on smoking habits were analysed. The clinical-biological phenotypes at diagnosis were compared according to current @entity286 use (current smokers) or not (including previous and never smokers). RESULTS: @entity19417 diagnoses were: @entity2883 with @entity2883 (GPA) for 583 (50%), eosinophilic @entity2883 with @entity2883 (EGPA) for 326 (28%) and @entity6129 ( @entity6129 ) for 256 (22%). Among them, 973 @entity1 (84%) never smoked, 116 (10%) were previous smokers and only 76 (6%) were current smokers. Current smokers were younger age (p=0.01), male gender (p=0.004), less frequently EGPA (p=0.017) and @entity6129 (p=0.036), and had less frequent kidney involvement (p=0.10). Among GPA @entity1 , current smokers, compared to non-current smokers, were younger age (p=0.02), male gender (p=0.08), more frequent skin involvement (p=0.03) and less frequent ENT involvement (p=0.06). Among EGPA @entity1 , current smokers, compared to non-current smokers, were also younger (p=0.028) and had less frequent constitutional symptoms (p=0.02), @entity4841 (p=0.04), renal involvement (p=0.025) and MPO-ANCA (p=0.02). Finally, analysis of @entity6129 @entity1 was impossible because only 6 (2%) were current smokers. CONCLUSIONS: These results suggest that @entity286 use could differentially affect GPA and EGPA clinical-biological phenotypes, and support the role of environmental exposures in @entity19417 development and its phenotype.
