OBJECTIVE: Given a history of peptic ulcer is more frequent in parkinsonism, to investigate the role of Helicobacter pylori in its pathogenesis and of cross-infection in familial aggregation. METHODS: Facets of parkinsonism were quantified in 33 elderly subjects with idiopathic parkinsonism and in their 39 siblings with double the number of controls, all obeying inclusion/exclusion criteria. Specific-IgG antibody was assayed. RESULTS: Siblings, compared with controls, had brady/hypokinesia of gait (P< or =0.002), bradykinesia of hands (P = 0.01), abnormal posture (P = 0.001), rigidity (P < 0.001) and seborrhoea/seborrhoeic dermatitis (P = 0.02). Both parkinsonians and siblings differed from controls in the odds of being H. pylori seropositive [odds ratios 3.04 (95% C.I.: 1.22, 7.63) and 2.94 (1.26, 6.86) respectively, P < 0.02], seropositivity being found in 0.70 of sufferers. CONCLUSION: Familial transmission of chronic infection plus part of syndrome links Helicobacter with causality. Seropositivity not being universal throughout parkinsonism, consequent on gastric atrophy +/- sporadic antibiotic exposure, might explain less aggressive disease in older sufferers.
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Charlett et al. (2009) studied this question.
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