Korean J Pediatr Gastroenterol Nutr.  2011 Dec;14(Suppl 1):S1-S8. 10.5223/kjpgn.2011.14.Suppl1.S1.

Helicobacter pylori Infection and Extraintestinal Manifestations in Children

• Park JS
• Seo JH
• Youn HS
• Kang HL
• Baik SC
• Lee WK
• Cho MJ
• Rhee KH

• KMID: 1451143
• DOI: http://doi.org/10.5223/kjpgn.2011.14.Suppl1.S1

Abstract

Helicobacter pylori (H. pylori) may be one of the most common pathogen in gastrointestinal tract. Although several recent articles have reported a decline in the prevalence of H. pylori infection in both children and adults over the last several years, H. pylori infection usually occurs early in life and persists for a long time. The role of H. pylori in some digestive diseases, such as gastritis, ulcer and gastric cancer has been well established. And the possible role of H. pylori as a trigger for some extraintestinal diseases in children and adults has been considered in the last year. H. pylori infection might be associated with refractory iron deficiency anemia, idiopathic thrombocytopenic purpura, growth retardation and obesity etc, directly or indirectly. Most of the studies are classified as epidemiological, clinical researches about effects on extraintestinal manifestations after eradication, or case reports. This review describes the possibility of association with several extraintestinal diseases and H. pylori infection and their possible mechanisms based on reported studies in the world and our several studies, even though there are still many conflicting results about that.

Keyword

Helicobacter pylori; Extraintestinal; Manifestation

MeSH Terms

Adult
Anemia, Iron-Deficiency
Child
Gastritis
Gastrointestinal Tract
Helicobacter
Helicobacter pylori
Humans
Obesity
Prevalence
Purpura, Thrombocytopenic, Idiopathic
Stomach Neoplasms
Ulcer

Figure

• 

  Fig. 1 Schematic representation of the substances released by the immune system following gastric colonization by Helicobacter pylori2). TNF: tumor necrosis factor, PAF: platelet activating factor, LT: leukotriene, PG: prostaglandin, IL: interleukin, INF: interferon.

• 

  Fig. 2 Possible physiopathologic mechanism of the anemia7). Lf: lactoferrin, Tf: transferring, R: outer membrane receptor.

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