Towards defining a rigidity-associated pathogenic pathway in idiopathic parkinsonism.
Helicobacter pylori eradication has a differential effect on the facets of idiopathic parkinsonism (IP): brady/hypokinesia improves, but rigidity worsens. Small intestinal bacterial overgrowth is common in IP and has been described as a sequel to Helicobacter eradication. The hyperhomocysteinaemia of IP is, in part, explained by serum vitamin B(12), but the concentration is not explained by Helicobacter status. Moreover, Helicobacter-associated gastric atrophy is uncommon in IP. However, overgrowth both increases B(12) utilization and provides a source of inflammation to drive homocysteine production. It is not a bystander event in IP: clouds of lysosomes are seen in duodenal enterocytes. Its candidature for causality of a rigidity-associated pathway is circumstantial: there are biological gradients of rigidity on natural killer and T-helper blood counts, both being higher with hydrogen breath test positivity for overgrowth.
Institute of Pharmaceutical Sciences, King's College London, London, UK.
R John
RJ
Dobbs
André
A
Charlett
Sylvia M
SM
Dobbs
Clive
C
Weller
Owens
O
Iguodala
Cori
C
Smee
James
J
Bowthorpe
David
D
Taylor
Ingvar T
IT
Bjarnason
D016481:Helicobacter Infections / Q000150:complications* / Q000453:epidemiology; D016480:Helicobacter pylori; D006801:Humans; D020138:Hyperhomocysteinemia / Q000209:etiology; D007694:Killer Cells, Natural / Q000473:pathology; D009127:Muscle Rigidity / Q000209:etiology* / Q000382:microbiology; D010300:Parkinson Disease / Q000453:epidemiology / Q000209:etiology* / Q000382:microbiology*; D006377:T-Lymphocytes, Helper-Inducer / Q000473:pathology