Leukocyte-subset counts in idiopathic parkinsonism provide clues to a pathogenic pathway involving small intestinal bacterial overgrowth. A surveillance study

Table 3 Summary of evidence that H. pylori infection and small intestinal bacterial overgrowth drive facets of parkinsonism

Gastrointestinal disorder	Evidence	Outcome
H. pylori infection	Double-blind, placebo-controlled, randomised efficacy study of eradication.	Differential effects with improvement in hypokinesia and worsening rigidity over year post-eradication and subsequent (2-year) plateau. Overall: net improvement[5].
	Surveillance	(i) Detrimental effect of Helicobacter positivity on hypo- and bradykinesia (adjusted for natural-killer count) [Results: Cellular associations with clinical measurements].
	Surveillance	(ii) Improvement in hypokinesia followed Helicobacter- eradication, but not antimicrobials given for other indications (i.e. indication specific)[73].
Small intestinal bacterial overgrowth	Surveillance	(i) Same three leukocyte subset associated with hydrogen-breath-test positivity and facets (biological gradient of rigidity on natural killer and T-helper counts; brady/hypokinesia on natural killer; tremor on neutrophil) [Results: Cellular association with breath-hydrogen & Cellular associations with clinical measurements].
		(ii) Increased rigidity followed antimicrobials for indications other than Helicobacter (i.e. not indication-specific), suggesting alteration in intestinal microbiota as a player[73].

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