Helicobacter pylori  and extragastric diseases: A review

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Abstract

Helicobacter pylori ( H. pylori) infection is very common and affects approximately half of the world population. It causes gastric diseases, but some authors have reported an association of H. pylori infection with other systemic manifestations beginning in 1994. The list of potential effects of H. pylori outside the stomach includes a number of extragastric manifestations and we focused on neurological, dermatological, hematologic, ocular, cardiovascular, metabolic, allergic, and hepatobiliary diseases. This review discusses these important reported manifestations that are not related to the gastrointestinal tract.

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Most cited references 195

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Inflammation in atherosclerosis: from pathophysiology to practice.

Peter Libby, Paul M Ridker, Göran K Hansson (2009)

Until recently, most envisaged atherosclerosis as a bland arterial collection of cholesterol, complicated by smooth muscle cell accumulation. According to that concept, endothelial denuding injury led to platelet aggregation and release of platelet factors which would trigger the proliferation of smooth muscle cells in the arterial intima. These cells would then elaborate an extracellular matrix that would entrap lipoproteins, forming the nidus of the atherosclerotic plaque. Beyond the vascular smooth muscle cells long recognized in atherosclerotic lesions, subsequent investigations identified immune cells and mediators at work in atheromata, implicating inflammation in this disease. Multiple independent pathways of evidence now pinpoint inflammation as a key regulatory process that links multiple risk factors for atherosclerosis and its complications with altered arterial biology. Knowledge has burgeoned regarding the operation of both innate and adaptive arms of immunity in atherogenesis, their interplay, and the balance of stimulatory and inhibitory pathways that regulate their participation in atheroma formation and complication. This revolution in our thinking about the pathophysiology of atherosclerosis has now begun to provide clinical insight and practical tools that may aid patient management. This review provides an update of the role of inflammation in atherogenesis and highlights how translation of these advances in basic science promises to change clinical practice.

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B J Marshall, J R Warren (1984)

Biopsy specimens were taken from intact areas of antral mucosa in 100 consecutive consenting patients presenting for gastroscopy. Spiral or curved bacilli were demonstrated in specimens from 58 patients. Bacilli cultured from 11 of these biopsies were gram-negative, flagellate, and microaerophilic and appeared to be a new species related to the genus Campylobacter. The bacteria were present in almost all patients with active chronic gastritis, duodenal ulcer, or gastric ulcer and thus may be an important factor in the aetiology of these diseases.

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IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance.

A Budavari, G Hotamisligil, George Spiegelman … (1996)

Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. An inhibitory form of IRS-1 was observed in muscle and fat tissues from obese rats. These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling.

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Author and article information

Contributors

Antonietta Gerarda Gravina

Rocco Maurizio Zagari

Cristiana De Musis

Lorenzo Romano

Carmelina Loguercio

Marco Romano

Journal

Journal ID (nlm-ta): World J Gastroenterol

Journal ID (iso-abbrev): World J. Gastroenterol

Journal ID (publisher-id): WJG

Title: World Journal of Gastroenterology

Publisher: Baishideng Publishing Group Inc

ISSN (Print): 1007-9327

ISSN (Electronic): 2219-2840

Publication date (Print): 7 August 2018

Publication date (Electronic): 7 August 2018

Volume: 24

Issue: 29

Pages: 3204-3221

Affiliations

Dipartimento di “Medicina di Precisione”, UOC Epatogastroenterologia, Università della Campania “Luigi Vanvitelli”, Napoli 80131, Italy

Dipertimento Di Scienze Mediche e Chirurgiche, Università di Bologna, Bologna 40138, Italy

Dipartimento di “Medicina di Precisione”, UOC Epatogastroenterologia, Università della Campania “Luigi Vanvitelli”, Napoli 80131, Italy

Dipartimento di “Medicina di Precisione”, UOC Epatogastroenterologia, Università della Campania “Luigi Vanvitelli”, Napoli 80131, Italy. marco.romano@ 123456unicampania.it

Author notes

Author contributions: Gravina AG designed and wrote the manuscript; Zagari RM, Romano M and Loguercio C designed and revised the manuscript; De Musis C and Romano L contributed to the literature search. All authors equally contributed to this paper with the conception and design of the study, literature review and analysis, drafting and critical revision and editing, and final approval of the final version.

Correspondence to: Marco Romano, MD, PhD, Full Professor, Dipartimento di “Medicina di Precisione”, UOC Epatogastroenterologia, Università degli Studi della Campania “Luigi Vanvitelli”, Via Pansini, 5, Napoli 80131, Italy. marco.romano@ 123456unicampania.it

Telephone: +39-335-6768097

Article

Other ID: jWJG.v24.i29.pg3204

DOI: 10.3748/wjg.v24.i29.3204

PMC ID: 6079286

PubMed ID: 30090002

SO-VID: 1fa0a07b-8e1c-4b2b-9c8d-f3e88937b8c4

License:

This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

History

Date received : 9 April 2018

Date revision received : 19 May 2018

Date accepted : 27 June 2018

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Helicobacter pylori and extragastric diseases: A review

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Abstract

Related collections

When did Helicobacter first colonise humans?

Most cited references 195

Inflammation in atherosclerosis: from pathophysiology to practice.

Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration.

IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance.

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