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 23 November 2017

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Gastrointestinal infection and idiopathic Parkinsonism

Categorization the presence or absence of Helicobacter infection, is a useful therapeutic tool in idiopathic parkinsonism, and interim analysis points to a role of a particular infection in the pathogenesis, reports two studies in the latest issue of Helicobacter.

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Neuronal damage in idiopathic parkinsonism may be in response to ubiquitous occult infection.

Since peptic ulceration is prodromal, Helicobacter is a prime candidate.

Dr John Dobbs and colleagues considered the candidature of Helicobacter in parkinsonism with cachexia.

The researchers explored the relationship between being underweight and inflammatory products in 124 subjects with idiopathic parkinsonism and 195 controls.

The team presented case-series evidence of efficacy of H pylori eradication, in parkinsonism advanced to the stage of cachexia for the first part of their study.

The team also obtained proof-of-principle that infection contributes to idiopathic parkinsonism.

An association of a low body mass index with circulating interleukin-6 that was specific to parkinsonism
Helicobacter

For the second part of the researcher's investigation, the team conducted a randomized, double-blind, placebo-controlled efficacy study.

The researchers considered proven Helicobacter pylori eradication on the time course of facets of parkinsonism.

Intervention was 1 week's triple eradication therapy versus placebos.

For Study 1, the team found an association of a low body mass index with circulating interleukin-6 that was specific to parkinsonism.

Marked reversibility in both cachexia and disability of idiopathic parkinsonism followed Helicobacter heilmannii eradication in 1 case.

The team noted that, H pylori eradication in another case presented with postprandial bloating, and persistent nausea.

The researchers found that, following eradication, radioisotope gastric-emptying returned towards normal, and upper abdominal symptoms regressed.

Reversibility of their cachexia contrasts with the outcome of anti-Helicobacter therapy, where eradication failed in 1 case, and in non-Helicobacter gastritis in 3 cases.

The researchers noted that in Study 1, anti-parkinsonian medication remained constant.

Intestinal absorption and barrier function were normal in all.

In the second study, the team noted active vs placebo improvements in stride-length.

The improvement exceeded size of effect on which the sample size was calculated when analyzed on intention-to-treat basis.

The researchers also observed an improvement on protocol analysis of 6 weekly assessments, including and excluding those on antiparkinsonian medication.

Active eradication failed in 4 out of 20 patient , in whom B-lymphocyte count was lower.

Dr Dobbs' team concludes, “Categorization, according to presence or absence of Helicobacter infection, was a useful therapeutic tool in late idiopathic parkinsonism.”

“In the second study, interim analysis points to a direct or surrogate 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.”

Helicobacter 2005: 10(4): 267
11 August 2005

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