Trial reportHelicobacter2010
Differential effect of Helicobacter pylori eradication on time-trends in brady/hypokinesia and rigidity in idiopathic parkinsonism.
Trial report in Helicobacter, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 73 citations in OpenAlex.
- Non-International journal of molecular sciences · 2024Pooled it
- Helicobacter pylori eradication for Parkinson's disease.The Cochrane database of systematic reviews · 2011Pooled it
- Pharmacomicrobiomics: a new field contributing to optimizing drug therapy in Parkinson's disease.Gut microbes · 2025Review
- Interplay of constipation, intestinal barrier dysfunction and fungal exposome in aetiopathogenesis of Parkinson's disease: hypothesis with supportive data.The Biochemical journal · 2025Article
- The microbiota-gut-brain axis in mental and neurodegenerative disorders: opportunities for prevention and intervention.Frontiers in aging neuroscience · 2025Review
- The Role of the Gastrointestinal Microbiota in Parkinson's Disease.Biomolecules · 2024Review
- Exploring Fecal Microbiota Transplantation for Modulating Inflammation in Parkinson's Disease: A Review of Inflammatory Markers and Potential Effects.International journal of molecular sciences · 2024Review
- Causal associations betweenFrontiers in immunology · 2024Article
- A review of studies on gut microbiota and levodopa metabolism.Frontiers in neurology · 2023Review
- Therapies for Parkinson's disease and the gut microbiome: evidence for bidirectional connection.Frontiers in aging neuroscience · 2023Review
- The gut-brain axis and Parkinson disease: clinical and pathogenetic relevance.Annals of medicine · 2021Review
- Gut brain axis: an insight into microbiota role in Parkinson's disease.Metabolic brain disease · 2021Review
- Article
- [The role of the gut microbiome in idiopathic Parkinson's disease].Der Nervenarzt · 2020Review
- Role ofJournal of clinical medicine · 2020Review
- Review
- Targeting Microbiota: What Do We Know about It at Present?Medicina (Kaunas, Lithuania) · 2019Review
- Altered Gut Microbiome and Intestinal Pathology in Parkinson's Disease.Journal of movement disorders · 2019Article
- Infectious Etiologies of Parkinsonism: Pathomechanisms and Clinical Implications.Frontiers in neurology · 2019Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe examine the effect of eradicating Helicobacter in idiopathic parkinsonism (IP). Marked deterioration, where eradication-therapy failed, prompted an interim report in the first 20 probands to reach de-blinding. The null-hypothesis, "eradication has no effect on principal outcome, mean stride length at free-walking speed," was rejected. We report on study completion in all 30 who had commenced post-treatment assessments.
methodsThis is a randomized, placebo-controlled, parallel-group efficacy study of eradicating biopsy-proven (culture and/or organism on histopathology) Helicobacter pylori infection on the time course of facets of IP, in probands taking no, or stable long-t(1/2), anti-parkinsonian medication. Persistent infection at de-blinding (scheduled 1-year post-treatment) led to open active eradication-treatment.
resultsStride length improved (73 (95% CI 14-131) mm/year, p = .01) in favor of "successful" blinded active over placebo, irrespective of anti-parkinsonian medication, and despite worsening upper limb flexor rigidity (237 (57-416) Nm x 10(-3)/year, p = .01). This differential effect was echoed following open active, post-placebo. Gait did not deteriorate in year 2 and 3 post-eradication. Anti-nuclear antibody was present in all four proven (two by molecular microbiology only) eradication failures. In the remainder, it marked poorer response during the year after eradication therapy, possibly indicating residual "low-density" infection. We illustrate the importance of eradicating low-density infection, detected only by molecular microbiology, in a proband not receiving anti-parkinsonian medication. Stride length improved (424 (379-468) mm for 15 months post-eradication, p = .001), correction of deficit continuing to 3.4 years. Flexor rigidity increased before hydrogen-breath-test positivity for small intestinal bacterial overgrowth (208 (28-388) Nm x 10(-3), p = .02), increased further during (171 (67-274), p = .001) (15-31 months), and decreased (136 (6-267), p = .04) after restoration of negativity (32-41 months).
conclusionHelicobacter is an arbiter of progression, independent of infection-load.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.