Clinical findings and anti-neuronal antibodies in @entity66 with XXXX .

@entity1 @entity66 @entity16 @entity1897 @entity7025 @entity302 @entity6447 @entity3918 @entity2414 @entity15
BACKGROUND: Little is known about the clinical and immunological features of @entity66 @entity1 with @entity16 . In a large series of adult @entity66 @entity1 , we investigated the prevalence of @entity16 and anti-neuronal antibodies, along with the clinical course. METHODS: @entity16 were investigated in 160 consecutive @entity1 (120 F, 40 M) with biopsy-proven @entity66 . Anti-neuronal antibodies to central/enteric nervous systems were investigated in all neurological @entity1 , 20 unaffected ones and 20 controls. RESULTS: Thirteen (8%) @entity1 had @entity16 , including @entity302 (n = 3), @entity2414 (n = 3), @entity6447 (n = 2), @entity1897 (n = 2), @entity15 (n = 1), @entity7025 (n = 1) and @entity3918 (n = 1). No significant demographic or clinical differences (gastrointestinal or other gluten-related signs) were found between @entity1 with and without neurological involvement. In all but 2 of the 13 cases, the @entity16 preceded @entity66 . @entity16 improved or disappeared in 7 @entity1 who started a gluten-free diet within 6 months after neurological onset, and in none of 4 @entity1 who began later. Prevalence of central nervous system anti-neuronal antibodies was significantly higher in neurological (61%) than in other @entity1 (5%) (P = 0.0007) or controls (0%) (P = 0.00001). CONCLUSIONS: @entity66 can sometimes present in the guise of a @entity16 , which may greatly improve when a gluten-free diet is started promptly. Therefore, the possible presence of @entity66 needs to be carefully considered in @entity1 with @entity6447 , @entity302 , @entity2414 or @entity1897 .
