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Role of Chronic Infection and Inflammation in the Gastrointestinal Tract in the Etiology and Pathogenesis of Idiopathic Parkinsonism *

Background. Links between etiology/pathogenesis of neuropsychiatric disease and infection are increasingly recognized.

Aim. Proof-of-principle that infection contributes to idiopathic parkinsonism.

Methods. Randomized, double-blind, placebo-controlled efficacy study of proven Helicobacter pylori eradication on the time course of facets of parkinsonism. Intervention was 1 week's triple eradication therapy/placebos. Routine deblinding at 1 year (those still infected received open-active), with follow-up to 5 years post-eradication. Primary outcome was mean stride length at free-walking speed, sample size 56 for a difference, active vs. placebo, of 3/4 (between-subject standard deviation). Recruitment of subjects with idiopathic parkinsonism and H. pylori infection was stopped at 31, because of marked deterioration with eradication failure. Interim analysis was made in the 20 who had reached deblinding, seven of whom were receiving antiparkinsonian medication (long-t1/2, evenly spaced) which remained unchanged.

Results. Improvement in stride-length, on active (n = 9) vs. placebo (11), exceeded size of effect on which the sample size was calculated when analyzed on intention-to-treat basis (p = .02), and on protocol analysis of six weekly assessments, including (p = .02) and excluding (p = .05) those on antiparkinsonian medication. Active eradication (blind or open) failed in 4/20, in whom B-lymphocyte count was lower. Their mean time course was: for stride-length, −243 (95% CI −427, −60) vs. 45 (−10, 100) mm/year in the remainder (p = .001); for the ratio, torque to extend to flex relaxed arm, 349 (146, 718) vs. 58 (27, 96)%/ year (p < .001); and for independently rated, visual-analog scale of stance–walk videos (worst–best per individual ≡ 0–100 mm), −64 vs. −3 mm from anterior and −50 vs. 11 lateral (p = .004 and .02).

Conclusions. Interim analysis points to a direct or surrogate (not necessarily unique) role of a particular infection in the pathogenesis of parkinsonism. With eradication failure, bolus release of antigen from killed bacteria could aggravate an effect of ongoing infection.

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As with any procedure, there could be pain or other substantial risks involved. These concerns should be discussed with your health care provider prior to any treatment so that you have proper informed consent and understand that there are no guarantees to healing.

THE INFORMATION IN THIS WEBSITE IS OFFERED FOR GENERAL EDUCATIONAL PURPOSES ONLY AND DOES NOT IMPLY OR GIVE MEDICAL ADVICE. No Doctor/Patient relationship shall be deemed to have arisen simply by reading the information contained on these pages, and you should consult with your personal physician/care giver regarding your medical treatment before undergoing any sort of treatment or therapy.

Published on 11-24-2008
Authors: Inguar T. Bjarnason †, Andre Charlett § , R. John Dobbs *†, Sylvia M. Dobbs *†, Mohammad A.A. Ibrahim ‡ , Robert W. Kerwin * , Robert F. Mahler ¶ , Norman L. Oxlade *††, Dale W. Peterson ††, J. Malcolm Plant * , Ashley B. Price ** and Clive Weller *
Source: Helicobacter Volume 10 Issue 4, Pages 276 - 287