Impact of Helicobacter pylori‐related metabolic syndrome with hyperhomocysteinemia on extragastric pathologies.

Specifically, cognitively normal elderly persons with high A have hyperhomocysteinemia, thinner temporal lobe, and lesser daily memory.14 Our own results indicate that active I Hp i -I could be involved in the pathophysiology of mild cognitive impairment (MCI), a prodromal phase highly predictive of consequent AD development, via induction of chronic atrophic gastritis-hyperhomocysteinemia-AD sequence.15 Hyperhomocysteinemia seems to be an active player involved in the neuropathophysiology of MCI-AD sequence by inducing A and tau pathologies with synaptic dysfunction, neuroinflammation and memory deterioration, thereby suggesting a novel therapeutic option for the treatment of people bearing this risk factor.16 In this regard, beyond hyperhomocysteinemia, additional I Hp i -related MetS parameters contribute to MCI-AD sequence.4 Comparable data may also introduce in isolate clinical syndrome (CIS)-multiple sclerosis (MS) sequence.17,18 Our own data indicate that active I Hp i -I, beyond MS,17 is also frequent with CIS, the prodromal phase of consequent MS development, accompanied by hyperhomocysteinemia, and I Hp i eradication may delay CIS progression to MS development.18 Active I Hp i -I is also associated with primary open-angle glaucoma, which has been called "ocular AD" and pseudoexfoliative glaucoma in some populations studied.19,20 Moreover, I Hp i eradication seems to improve glaucoma parameters, thereby signifying a potential casual relation between I Hp i -I and glaucoma. Cardio-cerebrovascular disease and Helicobacter pylori -related metabolic syndrome: we consider eradication therapy as a potential cardio-cerebrovascular prevention strategy. [Extracted from the article]