<i>Helicobacter pylori</i> induced cognitive dysfunction might be associated with falls and fractures in cirrhosis
Authors: Jannis Kountouras, Christos Zavos, Georgia Deretzi, Elizabeth Vardaka, Marina Boziki, Emmanouel Gavalas, George Kouklakis, Panagiotis Katsinelos, Ioannis Venizelos, Christina Nikolaidou, Stergios A. Polyzos, Evaggelia Giartza-Taxidou
Journal: Hepatology (2012)

In their prospective series, Soriano et al.1 concluded that cognitive dysfunction (CD) is a factor associated with falls in patients with cirrhosis, and further studies are warranted to address the mechanisms implicated in this predisposition and to design preventive strategies. Apart from CD causes that can be the result of multiple issues, including the etiology of cirrhosis, mentioned by the authors,1 Helicobacter pylori infection (Hp-I) appears to be a common denominator associated with CD-related falls and fractures and liver cirrhosis.2-4 In this respect, we reported that Hp-I is frequently detected in neurodegenerative diseases including CD and Alzheimer's disease (AD) and Hp eradication may positively influence AD manifestations at 2- and 5-year clinical endpoints,2 thereby supporting a role for this common infection in the pathobiology of the disease. Others also found that AD patients infected by Hp tended to be more cognitively impaired, and patients with dementia have a higher risk of falls and fractures3; Hp-I may also be responsible for osteoporosis. Moreover, hepatitis B (HBV) and C (HCV) are among the commonest causes of liver cirrhosis worldwide4, 5 and Hp-I is strongly associated with HBV- and HCV-related cirrhosis in Europe (Italy); Hp-I is more common in cirrhosis patients with hepatic encephalopathy (HE) than in those without,5 and HE is not a fully reversible condition. Summarizing the aforementioned data, Hp may be involved in the pathophysiology of cirrhosis-related CD by several mechanisms,4 such as the release of proinflammatory and vasoactive substances, involved through blood-brain barrier (BBB) disruption, in a number of vascular disorders including AD, which can lead to long-term neurologic deficits; promoting platelet-leukocyte aggregation proposed to play pathophysiologic roles in AD and liver fibrosis; producing reactive oxygen metabolites involved in the AD pathophysiology and complications of cirrhosis; or influencing the apoptotic process, an important form of cell death in AD and cirrhosis. Finally, activated monocytes (possibly infected with Hp due to defective autophagy resulting in Hp replication in autophagic vesicles) might also enter the brain due to BBB disruption contributing to cirrhosis-related CD development associated with falls and fractures.3 Jannis Kountouras M.D., Ph.D.*, Christos Zavos M.D., Ph.D.*, Georgia Deretzi M.D., Ph.D.*, Elizabeth Vardaka Ph.D.*, Marina Boziki M.D.*, Emmanouel Gavalas M.D.*, George Kouklakis M.D., Ph.D.*, Panagiotis Katsinelos M.D., Ph.D.*, Ioannis Venizelos M.D., Ph.D.*, Christina Nikolaidou M.D.*, Stergios A. Polyzos M.D., Ph.D.*, Evaggelia Giartza-Taxidou M.D., Ph.D.*, * Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece.