Journal
JOURNAL OF PARKINSONS DISEASE
Volume 11, Issue 1, Pages 61-69Publisher
IOS PRESS
DOI: 10.3233/JPD-202298
Keywords
Parkinson's disease; inflammation; microbiome; levodopa; pharmacodynamics
Categories
Funding
- Parkinsonfonden
- Neuroforbundet
- Uppsala University
- ALF 2019
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Certain studies have shown a 1.6-fold higher prevalence of Helicobacter pylori in Parkinson's disease patients compared to control populations. The eradication of Helicobacter pylori can lead to an improved response to levodopa therapy in Parkinson's disease, likely due to increased bioavailability of the drug. Patients with both Helicobacter pylori infection and Parkinson's disease on levodopa therapy tend to have worse motor control than those without the infection.
Background: Infection with Helicobacter pylori seems overrepresented in Parkinson's disease. Clinical observations suggest a suboptimal treatment effect of levodopa in Helicobacter positive patients. Objective: Describe and explain the connection between a Helicobacter pylori infection of the upper gut and changes in pharmacokinetics of oral levodopa treatment in Parkinson's disease. Methods: PubMed, Google Scholar, and Cross Reference search was done using the key words and combined searches: Bioavailability, drug metabolism, dyskinesia, Helicobacter, L-dopa, levodopa, motor control, pharmacodynamics, pharmacokinetics, prevalence, unified Parkinson's disease rating scale. Results: The prevalence of Helicobacter pylori in Parkinson's disease patients is reported to be about 1.6-fold higher than in a control population in some studies. Helicobacter has therefore been assumed to be linked to Parkinson's disease, but the mechanism is unclear. As regards symptoms and treatment, patients with Parkinson's disease on levodopa therapy and with Helicobacter pylori infection display worse motor control than those without Helicobacter infection. Eradication of the infection improves levodopa response in Parkinson's disease, likely as a consequence of an increased oral pre-systemic bioavailability of levodopa, likely to be explained by reduced Helicobacter-dependent levodopa consumption in the stomach. In addition, small intestinal bacterial overgrowth may also have an impact on the therapeutic setting for levodopa treatment but is less well established. Conclusion: Eradication of Helicobacter pylori improves levodopa bioavailability resulting in improved motor control. Eradication of Helicobacter should be considered in patients with poor symptomatic control and considerable motor fluctuations.
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