Deretzi, Georgia

Doulberis, Michael

Katsinelos, Panagiotis

Kazakos, Evangelos

Koffas, Apostolos

Kountouras, Jannis

Liatsos, Christos

Papaefthymiou, Apostolis

Polyzos, Stergios A

Srivastava, David S

English

Polyzos, Stergios A.

Srivastava, David S.

Bern Open Repository and Information System (BORIS)

Letter: Helicobacter pylori in proton pump inhibitor-associated biliary disease

ZORA

Zurich Open Repository andArchiveUniversity of ZurichMain LibraryStrickhofstrasse 39CH-8057 Zurichwww.zora.uzh.chYear: 2020Letter: Helicobacter pylori in proton pump inhibitor-associated biliarydiseasePapaefthymiou, Apostolis ; Doulberis, Michael ; Polyzos, Stergios A ; Katsinelos, Panagiotis ; Liatsos,Christos ; Koffas, Apostolos ; Kazakos, Evangelos ; Deretzi, Georgia ; Srivastava, David S ; Kountouras,JannisDOI: https://doi.org/10.1111/apt.15608Posted at the Zurich Open Repository and Archive, University of ZurichZORA URL: https://doi.org/10.5167/uzh-187557Journal ArticleAccepted VersionOriginally published at:Papaefthymiou, Apostolis; Doulberis, Michael; Polyzos, Stergios A; Katsinelos, Panagiotis; Liatsos, Chris-tos; Koffas, Apostolos; Kazakos, Evangelos; Deretzi, Georgia; Srivastava, David S; Kountouras, Jannis(2020). Letter: Helicobacter pylori in proton pump inhibitor-associated biliary disease. AlimentaryPharmacology Therapeutics, 51(2):313-314.DOI: https://doi.org/10.1111/apt.15608Letter: Helicobacter pylori in proton pump inhibitor-associated biliary disease   Apostolis Papaefthymiou1 Michael Doulberis2,3 Stergios A. Polyzos3,4 Panagiotis Katsinelos3 Christos Liatsos1 Apostolos Koffas5 Evangelos Kazakos3 Georgia Deretzi3, David S. Srivastava6 and Jannis Kountouras3  1Department of Gastroenterology, 401 General Military Hospital of Athens, Athens, Greece  2Department of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland  3Department of Internal Medicine, Second Medical Clinic, Ippokration Hospital, Aristotle University of Thessaloniki, Thessaloniki, Macedonia, Greece  4First Department of Pharmacology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Macedonia, Greece  5Department of Gastroenterology, Faculty of Medicine, School of Health Sciences, University of Thessaly, Larissa, Greece  6Department of Emergency Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland  Email: jannis@auth.gr; ancoratus2010@gmail.com EDITORS,  Min et al,1 in their cohort study, proposed the role of proton pump inhibitors (PPI) as a risk factor of cholangitis, especially during the period of their use. This observational result could include unrecog- nized confounders, one of which to consider being the overlap be- tween Helicobacter pylori infection (Hp-I) and the conditions treated using a PPI; dyspepsia, peptic ulcer disease and, at least in some pop- ulations, gastro-oesophageal reflux disease—Barrett’s oesophagus— oesophageal cancer sequence are associated with Hp-I and represent the most frequent indications for PPI prescription.2 Moreover Hp-I is involved in PPI-related disorders discussed by the authors.1-3  The impact of Hp-I with biliary tree diseases has been described. Bile stasis has primarily been connected with hepatobiliary Hp con- tamination, thus leading to a threefold risk of chronic lithiasis and cholecystitis, triggered by a perpetual inflammation of the gallblad- der.4,5 In this respect, our data indicated Hp presence in gallbladder tissue in 19.33% of patients who were submitted to cholecystec- tomy due to lithiasis,6 while chronic biliary Hp-I has been identified in 75% of patients with gallbladder cancer.7  The proposed routes of contamination, although unproved, in- clude ascending migration through the sphincter of Oddi and hae- matogenous spread to the liver and then excretion into bile. In this respect, the potential influx of activated monocytes infected with Hp (due to defective autophagy) from the circulation into the gall- bladder might relate to gallbladder-related pathologies (“Trojan horse” pathway); biliary excretion of Hp invaded macrophages might trigger proinflammatory cytokine release, oxidative stress and inflammation, thus promoting gallstone formation and its  complications (cholecystitis/cholangitis/pancreatitis). Additionally, biliary Hp-I could provoke an imbalance of apoptotic cellular pro- cesses and contribute to biliary carcinogenesis. In vitro data support this, indicating that Hp promotes cell proliferation and suppresses apoptosis of human intrahepatic biliary epithelial cells by increasing reactive oxygen species release.8 Finally, the authors suggested as a possible pathogenetic mechanism of PPI-related cholangitis, the imbalance between the normal small intestine microbiota and the bacterial overgrowth due to gastric acid suppression.1 Nevertheless, Hp-I seems to cause more significant alterations in gut microbiota than PPI use, thus contributing to biofilm formation.9  Hp-I has also been associated with a plethora of extragastric conditions, such as cardiovascular and neurodegenerative diseases, glaucoma, gastrointestinal tract oncogenesis, non-alcoholic fatty liver disease and hepatic encephalopathy.10 Therefore, it seems rea- sonable to consider adjusting for the presence of Hp-I as a potential cofounder in PPI-related disorders, as it is perhaps potentially rele- vant to a wide range of conditions necessitating their use.  ACKNOWLEDGEMENT  Declaration of personal interests: None. FUNDING INFORMATION  None.  LINKED CONTENT  This article is linked to Min et al paper. To view this article, visit https://doi.org/10.1111/apt.15466.  REFERENCES  1. Min YW, Kang D, Shin J-Y, et al. Use of proton pump inhibitors and the risk of cholangitis: a nationwide cohort study. Aliment Pharmacol Ther. 2019;50:760-768.  2. Kountouras J, Doulberis M, Papaefthymiou A, et al. A perspec- tive on risk factors for esophageal adenocarcinoma: emphasis on Helicobacter pylori infection. Ann N Y Acad Sci. 2019;1452:12-17.  3. Kountouras J, Boziki M, Polyzos SA, et al. The emerging role of Helicobacter pylori-induced metabolic gastrointestinal dysmotility and neurodegeneration. Curr Mol Med. 2018;17:389-404.  4. Leong RWL, Sung JJY. Helicobacter species and hepatobiliary dis- eases. Aliment Pharmacol Ther. 2002;16:1037-1045.  5. Cen L, Pan J, Zhou B, et al. Helicobacter pylori infection of the gall- bladder and the risk of chronic cholecystitis and cholelithiasis: a sys- tematic review and meta-analysis. Helicobacter. 2018;23:e12457.  6. Kountouras J, Tsiaousi E, Trigonis S, et al. Comment on “The correla- tion of Helicobacter pylori with the development of cholelithiasis and cholecystitis: the results of a prospective clinical study in Saudi Arabia”. Eur Rev Med Pharmacol Sci. 2016;20:3-4.  7. Rawla P, Sunkara T, Thandra KC, Barsouk A. Epidemiology of gall- bladder cancer. Clin Exp Hepatol. 2019;5:93-102.  8. Ma F, Yang Y, Wang J-D, Quan Z-W, Zhou D. Helicobacter pylori and 17β-estradiol induce human intrahepatic biliary epithelial cell abnormal proliferation and oxidative DNA damage. Hepatobiliary Pancreat Dis Int. 2017;16:519-527.  9. Parsons BN, Ijaz UZ, D’Amore R, et al. Comparison of the human gastric microbiota in hypochlorhydric states arising as a result of Helicobacter pylori-induced atrophic gastritis, autoimmune atrophic gastritis and proton pump inhibitor use. PLOS Pathog. 2017;13:e1006653.  10. Franceschi F, Gasbarrini A, Polyzos SA, Kountouras J. Extragastric diseases and Helicobacter pylori. Helicobacter. 2015;20:40-46.   

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