Pediatric Helicobacter Pylori Infection 

  • Author: Mutaz I Sultan, MBChB; Chief Editor: Carmen Cuffari, MD   more...
 
Updated: Apr 7, 2010
 

Background

Helicobacter pylori (Hp) is a gram-negative bacillus responsible for one of the most common infections found in humans worldwide.[1] Warren and Marshall first cultured and identified the organism as Campylobacter pylori in 1982. By 1989, it was renamed and recognized to be associated closely with antral gastritis (gastric and duodenal ulcers in adults and children). In recognition of this crucial discovery, they were awarded the Nobel Prize for medicine in 2005. By the early-to-mid 1990s, further evidence supported a link between chronic gastritis of H pylori infection in adults and malignancy, specifically gastric lymphoma and adenocarcinoma.

Objectives of current and future research on H pylori include improving the understanding of the immunopathogenesis of gastric disease associated with H pylori infection, elucidating the modes of transmission, and improving the safety and efficacy of vaccines to prevent H pylori infection.

Helicobacter pylori infection revealed by endoscopHelicobacter pylori infection revealed by endoscopy (nodular gastropathy). Helicobacter pylori–associated peptic ulcer in theHelicobacter pylori–associated peptic ulcer in the duodenal bulb.
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Pathophysiology

H pylori organisms are spiral-shaped gram-negative bacteria that are highly motile because of multiple unipolar flagella. They are microaerophilic and potent producers of the enzyme urease. H pylori inhabits the mucus adjacent to the gastric mucosa.

Important adaptive features that enhance survival of the organism in an acidic environment include its shape and motility, its reduced oxygen requirement, its adhesion molecules that are trophic to certain gastric cells, and its urease production. Bacterial urease converts urea to ammonium and bicarbonate, neutralizing gastric acid and providing protection in the hostile, highly acidic gastric environment. Some of the lipopolysaccharide of the organism mimics the Lewis blood group antigens in structure. This molecular mimicry also helps in the continued existence of H pylori in the unfavorable gastric environment.[2]

H pylori produces suspected disease-inducing factors, including urease, vacuolating cytotoxin, catalase, and lipopolysaccharide (LPS). Urease, a potent antigen, induces increased immunoglobulin G and immunoglobulin A production. Expression of vacuolating cytotoxin, which induces inflammatory cytokines, may be associated with more pronounced inflammation and increased propensity to cause disease. Catalase helps H pylori survive in the host by preventing the formation of reactive oxygen metabolites from hydrogen peroxide. The LPS outer membrane of H pylori is a less potent inducer of the host complement cascade.

Cytotoxin-associated antigen (CagA) is probably the most important virulence factor in H pylori. Translocating the CagA protein into the gastric epithelial cells causes rearrangement of the host cytoskeleton and alters cell signaling and perturbs cell cycle control. Furthermore, CagA-positive strains are known to induce the expression of a DNA-editing enzyme, which leads to accumulation of mutations in the tumor suppressor p53.[3]

CagA in situ expression is increased in children with H pylori infection who have peptic ulcers and may play a role in the pathogenesis of peptic ulcer disease (PUD).[4]

Two Japanese groups demonstrated the important role of Peyer patches (PPs) in the development of H pylori– induced gastritis. Kiriya et al showed that Helicobacter– induced gastritis was impaired in PP-null mice.[5] Another study by Nagai et al also supports the notion that PPs are inductive sites for generating CD4 T-cell responses in the gastric mucosa.[6]

H pylori colonizes the stomach, induces inflammatory cytokines, and causes gastric inflammation. Individuals with H pylori– associated antral-predominant gastritis with increased gastric acid production are prone to PUD.[7] In contrast, H pylori pan-predominant gastritis or corpus-predominant gastritis with decreased gastric acid production are more prone to developing gastric atrophy (intestinal metaplasia and gastric adenocarcinoma).

H pylori has been associated with iron-deficiency anemia. The 2 main hypotheses that potentially explain this relation are (1) sequestration of iron due to antral H pylori infection and (2) decreased non-heme iron absorption caused by hypochlorhydria.

H pylori infection and its association with gastric malignancy have been well described in several epidemiologic studies.[8] However, the course of progression from inflammation to cancer remains unclear. One model describes the stepwise progression of H pylori infection to hypochlorhydria, chronic gastritis, atrophic gastritis, intestinal metaplasia, and gastric cancer. Increased production of the cytokine interleukin 1β has been linked to an increased risk of hypochlorhydria and gastric cancer in infected subjects.

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Epidemiology

Frequency

United States

Overall, approximately one-third of the population is infected with H pylori, increasing with age. See Age.

International

In general, the prevalence is high in developing countries and the infection is acquired at a young age. The incidence is 3-10% of the population each year in developing countries compared with 0.5% in developed countries.[9] The prevalence of H pylori infection is not only lower in industrialized countries than in developing countries, but the incidence of H pylori infection, gastric cancer, and ulcer disease are also declining. Worldwide, more than 1 billion people are estimated to be infected with H pylori. See Age.

Mortality/Morbidity

Most children infected with H pylori are asymptomatic. Antral gastritis is the most common manifestation in children. Duodenal and gastric ulcers may be associated with H pylori gastritis in adults but is uncommon in children. The risk of gastric cancers, including non-Hodgkin lymphoma (eg, mucosa-associated lymphoid tissue [MALT]) and adenocarcinoma, is increased in adults.

The relationship between H pylori gastritis and recurrent abdominal pain (RAP) is controversial. The incidence of H pylori gastritis in patients with RAP is not significantly higher than the incidence of H pylori infection in the general population. Although some studies demonstrate an improvement in symptoms in children with RAP and H pylori gastritis after eradication therapy for H pylori, data from a recent double-blind controlled trial did not confirm that finding.[10] The heterogenicity of their definition of RAP and the varying study methodologies may have led to different results and conclusions. The medical positional statement of the North American Society of Pediatric Gastroenterology, Hepatology, and Nutrition regarding H pylori infection in children also found no convincing data to support the routine testing of children with RAP for H pylori.[11]

A meta-analysis reviewed published evidence for an association between H pylori infection and GI symptoms in children and found no association between RAP and H pylori infection and found conflicting evidence for an association between epigastric pain and H pylori infection.[12]

Some studies suggest that H pylori protects human subjects from developing gastroesophageal reflux disease, whereas others postulate a causative association between them. A meta-analysis of studies in adults found no association between H pylori eradication and development of new cases of gastroesophageal reflux disease in the population of dyspeptic patients.[13]

One pediatric retrospective study revealed a significantly higher prevalence of reflux esophagitis in children with H pylori infection.[14]

H pylori infection has also been associated with extraintestinal manifestations, such as short stature, immune thrombocytopenic purpura, and migraine with varying level of evidence.

Race

The prevalence is increased in black, Hispanic, Asian, and Native American populations.

Sex

Infection rates are similar in males and females.

Age

In developed countries, less than 10% of children younger than 12 years are infected; however, seropositivity increases with age at a rate of 0.3-1% per year. Studies of seropositivity in adults in developed countries revealed prevalences of 30-50%. In the United States, the estimated prevalence is 20% for people younger than 30 years and 50% for those older than 60 years. In developing countries, the prevalence rates are much higher. The serological prevalence rates of H pylori were 15% and 46% in Gambian children younger than 20 months and age 40-60 months, respectively.[15]

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Contributor Information and Disclosures
Author

Mutaz I Sultan, MBChB  Instructor and Fellow, Department of Pediatrics, Division of Gastroenterology and Nutrition, Medical College of Wisconsin, Children's Hospital

Mutaz I Sultan, MBChB is a member of the following medical societies: American Gastroenterological Association and North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Nothing to disclose.

Coauthor(s)

B UK Li, MD  Professor of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, Director, Pediatric Fellowships and Gastroenterology Fellowship, Medical Director, Functional Gastrointestinal Disorders and Cyclic Vomiting Program, Medical College of Wisconsin; Attending Gastroenterologist, Children's Hospital of Wisconsin

B UK Li, MD is a member of the following medical societies: Alpha Omega Alpha, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Maria Triantafyllopoulou Greene, MD  Assistant Professor of Pediatrics, Northwestern University Feinberg School of Medicine; Attending Physician, Division of Gastroenterology, Hepatology, and Nutrition, Children's Memorial Hospital

Maria Triantafyllopoulou Greene, MD is a member of the following medical societies: American Gastroenterological Association and North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Nothing to disclose.

Specialty Editor Board

Hisham Nazer, MB, BCh, FRCP, DCh, DTM&H  Professor of Pediatrics, Consultant in Pediatric Gastroenterology, Hepatology and Clinical Nutrition, Bushnaq Medical Centre, University of Jordan

Hisham Nazer, MB, BCh, FRCP, DCh, DTM&H is a member of the following medical societies: Royal College of Paediatrics and Child Health, Royal College of Physicians, Royal College of Surgeons in Ireland, Royal College of Surgeons of Edinburgh, and Royal Society of Tropical Medicine and Hygiene

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Stefano Guandalini, MD  Director, University of Chicago Celiac Disease Program, Section Chief of Gastroenterology, Hepatology and Nutrition; Professor, Department of Pediatrics, University of Chicago Comer Children's Hospital

Stefano Guandalini, MD is a member of the following medical societies: American Gastroenterological Association, European Society for Paediatric Gastroenterology, Hepatology & Nutrition, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Steven M Schwarz, MD, FAAP, FACN, AGAF  Professor of Pediatrics, Children's Hospital at Downstate, SUNY-Downstate Medical Center

Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research

Disclosure: Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor; Johnson & Johnson, Inc. Grant/research funds Independent contractor

Chief Editor

Carmen Cuffari, MD  Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine

Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

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Helicobacter pylori infection revealed by endoscopy (nodular gastropathy).
Helicobacter pylori–associated peptic ulcer in the duodenal bulb.
 
 
 
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