Role of Chronic Infection and Inflammation in the Gastrointestinal Tract in the Etiology and Pathogenesis of Idiopathic Parkinsonism. Part 1: Eradication of Helicobacter in the Cachexia of Idiopathic Parkinsonism

摘要: Background.  Links between etiology/pathogenesis of neuropsychiatric disease and infection are increasingly recognized. Aim.  Proof-of-principle that contributes to idiopathic parkinsonism. Methods.  Randomized, double-blind, placebo-controlled efficacy study proven Helicobacter pylori eradication on the time course facets parkinsonism. Intervention was 1 week's triple therapy/placebos. Routine deblinding at 1 year (those still infected received open-active), with follow-up 5 years post-eradication. Primary outcome mean stride length free-walking speed, sample size 56 for a difference, active vs. placebo, 3/4 (between-subject standard deviation). Recruitment subjects parkinsonism H. pylori stopped 31, because marked deterioration failure. Interim analysis made in 20 who had reached deblinding, seven whom were receiving antiparkinsonian medication (long-t1/2, evenly spaced) which remained unchanged. Results.  Improvement stride-length, (n = 9) placebo (11), exceeded effect calculated when analyzed intention-to-treat basis (p = .02), protocol six weekly assessments, including (p = .02) excluding (p = .05) those medication. Active (blind or open) failed 4/20, B-lymphocyte count lower. Their was: −243 (95% CI −427, −60) 45 (−10, 100) mm/year remainder (p = .001); ratio, torque extend flex relaxed arm, 349 (146, 718) 58 (27, 96)%/ year (p < .001); independently rated, visual-analog scale stance–walk videos (worst–best per individual ≡ 0–100 mm), −64 −3 mm from anterior −50 11 lateral (p = .004 .02). Conclusions.  points direct surrogate (not necessarily unique) role particular pathogenesis With failure, bolus release antigen killed bacteria could aggravate an ongoing infection.