Abstract

Pierantozzi et al.1 did not consider that the Helicobacter pylori infections might have been the result of a systemic metabolic abnormality that was the primary cause of the Parkinson disease (PD) and gut dysfunction as in peptic ulceration.2 H pylori requires a microaerophilic environment and optimally a much higher pco2 than that found in the lumen of the gut of healthy subjects in which to thrive in vitro. A common cause of an abnormally elevated gastric intraluminal pco2 in ambulatory patients is chronic mesenteric ischemia but this may only be present during metabolic stress because of metabolic compensation.3 A chronically reduced intramucosal pH, often associated with an elevated pco2, might be the product not only of mesenteric artery disease but also of mitochondrial toxins including translocating gut endotoxin and the cytokines it releases. An abnormally low intramucosal pH appears to be an …

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