AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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INTRODUCTION

Section 2 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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Background

In 1983, Warren (a biologist) and Marshall (a clinician) described Helicobacter pylori (HP). At first, they named the bacterium Campylobacter pyloridis. Later, it was named Campylobacter pylori. Since then, a large number of reports have been produced on HP and its pathogenetic potential. In fact, although peptic ulcer disease is the most studied disease related to HP infection, this bacterium is seemingly involved in the pathogenesis of several extragastric diseases, such as mucosa-associated lymphoid tissue lymphomas (MALTomas), coronaritis, gastroesophageal reflux disease, iron deficiency anemia, skin disease, and rheumatological conditions. However, at present, many of these associations remain largely uncertain, and the debate to confirm or refute causality related to these associations is still open.

The association of chronic HP infection with alterations in gastric mucosal cell proliferation is recognized worldwide. In addition, HP can produce and release several bioactive factors that may directly affect the stomach's parietal cells, which produce hydrochloric acid, and enterochromaffinlike (ECL) cells (ie, G cells and D cells), which produce gastrin and somatostatin, respectively. Evidence suggests that HP inhibits D cells and stimulates G cells. HP has some control mechanisms able to switch the transcription of different genes on or off when needed.

A strong association has been reported between HP infection and gastric lymphoma and adenocarcinoma of the body and antrum of the stomach. Some cofactors may play a key role in determining such diseases. Currently, whether HP eradication can decrease the risk of cancer remains unknown.

HP infection occurs more frequently in developing countries than in industrialized countries. HP strains differ in their potential to cause diseases. Although anyone can develop a microscopic gastritis, only a minority of infected persons develop ulcers or other diseases.

In the last 12 years, some Helicobacter-like organisms (HLOs) have been detected by specific polymerase chain reaction tests. The first of these HLOs was described in ferrets and is called Helicobacter mustelae. More recently, Helicobacter hepaticus has been described in Syrian hamsters. These HLOs are useful for researching HP infection modalities.

Pathophysiology

The most common route of HP infection is either oral-to-oral (stomach contents are transmitted from mouth to mouth) or fecal-to-oral (from stool to mouth) contact. Parents and siblings seem to play a primary role in transmission.

In a susceptible host, HP determines chronic active gastritis that may lead, in turn, to duodenal and gastric ulcer disease, gastric cancer, and MALTomas. HP infection causes chronic active gastritis, which is characterized by a striking infiltrate of the gastric epithelium and the underlying lamina propria by neutrophils, T and B lymphocytes, macrophages, and mast cells. Mast cells, usually responsible for the immune response balance, may be important effector cells in the pathogenesis of gastritis. However, HP does not seem to invade the gastric mucosa, although evidence suggests that the mucus creates a niche wherein the germ is protected from gastric secretions.

The release of host cytokines after direct contact of HP with epithelial cells of the gastric lining could recall the inflammatory cells in the infected area. A recent study has demonstrated that gastric epithelium, when infiltrated by neutrophils and macrophages in the lamina propria, highly express 2 neutrophil chemotactic factors: gro-alpha, and interleukin-8. In addition, the interferon-gamma inducible protein–10 (IP-10) and the monokine induced by interferon-gamma (MIG), 2 selective chemotactic factors for T lymphocytes, are expressed by the endothelium and mononuclear cells of gastric mucosa in patients with HP-related gastritis. According to the same study, gro-alpha and interleukin-8 may have a central role in neutrophils trafficking from the vessels to the mucosal epithelium, while IP-10 and MIG determine T lymphocyte recruitment into the mucosa.

Another hypothesis states that HP may recall immune cells from afar because of its own molecules, such as urea or lipopolysaccharide (LPS). Outer-membrane permeability is a function mediated by LPS. Despite the presence of bacterial LPS in biologically active quantities in the gastric mucosa, the mechanisms by which it may recall the immune cells are still unknown. According to one hypothesis, HP may induce the production of autoantibodies against the host's gastric lining.

The LPS of HP shows certain blood group antigens such as Le^b, Le^x, Le^y, and H-type I. Such antigens are thought to represent important virulence factors involved in the adhesive process of the germ. Le^b constitutes an adhesin, and differences exist in the Le compositions of adherent and nonadherent bacteria. This, perhaps, accounts for a relationship between adhesion and Le expression. In addition, any Le antigen shows phase variation leading to the spontaneous and random switching on and off of the expression of these antigens. For example, the H-type I antigen seems to be the result of a reversible singular nucleotidic deletion/insertion in a tract of a glycosyl transferase gene. The LPS of the HP also seems to influence tumoral proliferation of ECL cells, stimulating the intracellular polyamine biosynthesis pathway and ornithine decarboxylase activity by the activation of a CD14 receptor on the ECL cell.

In 1997, Tomb and coworkers completely sequenced the HP genome, and some differences were found in gene encoding factors that are likely to interact with the host, such as surface proteins. Two of the most important genes of HP are VACA and CAGA. The VACA gene codes for the Vac-A cytotoxin, a vacuolizating toxin. Most HP strains (60%), by unexplained causes, do not produce this protein. The CAGA gene codes for the Cag-A protein, which seems to stimulate the production of chemotactic factors for the neutrophils by the gastric epithelium of the host. A certain portion of HP strains (40%), by unexplained causes, does not produce this protein.

After the exposure to CAGA-positive HP strains, an increase has been reported in catalase, glutathione peroxidase, and superoxide dismutase activity. This increase is associated with fewer DNA adducts and reduced susceptibility of the gastric cells to the irreversible injuries from reactive oxygen species (ROS) compared with exposure to CAGA-negative HP strains. Such alterations of the ROS scavenging enzymes may partly account for the increased risk of gastric cancer in individuals with HP infection.

A relationship among CAGA/Cag-A, VACA alleles, and the Le subtype of HP strains has been reported, as has a link between these and the redox status of the gastric mucosa. For example, HP is able to induce apoptosis in epithelial cells and T lymphocytes. The CAGA-positive strains of HP seem to be able to increase FASL expression in T lymphocytes (up-regulation of FASL on such cells is redox-sensitive), which facilitates a selective killing of the T lymphocytes. This molecular mechanism may have a key role in the persistence of CAGA-positive strains.

In addition, HP up-regulates caspases 3, 6, 8, and 9. Caspases 3 and 9 in epithelial cells are fundamental in inducing apoptosis. The expression of some bacterial genes is acid-regulated, as reported for the FILA gene (responsible for the HP motility) that codes for a sigma factor required for transcription of the flagellin gene FLAA. Flagella and urease are very important for the colonization of the gastric mucosa by the bacterium.

Frequency

United States

The frequency of HP infection may be linked to race. White persons account for 29% of cases, and Hispanic persons account for 60% of cases.

International

HP is a ubiquitous organism. At least half of all people are infected, but an exact determination is not available, mostly because exact data are not available from developing countries. HP may be detected in approximately 90% of individuals with peptic ulcer disease; however, less than 15% of infected persons may have this disease.

Mortality/Morbidity

The mortality rate related to HP infection is not precisely known, but it seems to be minimal (ie, approximately 2-4% of all infected people). Mortality is due to the complications of the infection, such as gastric ulcer perforation or MALTomas of the GI tract. Otherwise, the morbidity of HP infection can be very high.

Race

The pathogenetic role of HP may differ depending on geography and race. White persons are infected with HP less frequently than persons of other racial groups. The prevalence rate is approximately 20% in white persons, 54% in African American persons, and 60% in Hispanic persons.

Sex

No sex predilection is known; however, females have a higher incidence of reinfection (5-8%) than males.

Age

HP infection may be acquired at any age. According to some epidemiologic studies, this infection is acquired most frequently during childhood. Children and females have a higher incidence of reinfection (5-8%) than adult males.

CLINICAL

Section 3 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

In the authors' opinion, no significant differences in the presence and frequency of symptoms, such as nausea, vomiting, pain, heartburn, or diarrhea, occur in patients who are infected with HP and patients who are not. No definite evidence demonstrates a clear relationship between the symptoms of the HP-associated gastritis and abdominal pain or dyspeptic symptoms from other conditions. Of patients, 30-35% have no symptoms.

• Adults and children differ in immune response to HP infection. This is probably due to a physiologic lower density of neutrophils and T lymphocytes during childhood, especially in children younger than 8 years.
• Although HP infection is not significantly related to recurrent abdominal pain, weekly pain is reported more often in children who are infected with HP compared with children who are not infected.

Physical

No specific clinical signs have been described in patients with HP infection.

• Patients may feel dyspepsia or abdominal discomfort, such as during gastritis or with epigastric pain (eg, duodenal ulcers).
• In some cases, patients may feel hungry in the morning and may have halitosis.

Causes

• HP infection causes atrophic and even metaplastic changes in the stomach.
• The bacterial adhesion appears to result in tyrosin phosphorylation and is specific for gastric cells.
• The adhesion of HP to the gastric cells causes a direct decrease in mucosal levels of glutathione, a fundamental molecule in the maintenance of the cellular redox status and in the molecular regulation of host immune responses. However, the LPS of HP may induce the production of autoantibodies that are able to worsen atrophy in the corpus mucosa and cause a concomitant increase in parietal cell antibodies. Such events are accompanied by a decrease in anti-HP immunoglobulin titers. This process leads to a scenario of severe atrophy without bacterial colonization combined with high levels of autoantibodies against gastric parietal cells.
• A number of reports show the close association between HP infection and low-grade gastric MALTomas.

DIFFERENTIALS

Section 4 of 11  

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• Follow-up
• Miscellaneous
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WORKUP

Section 5 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• HP fecal antigen test
• • This is a novel rapid test based on monoclonal antibody immunochromatography of stool samples. It has been reported to be very specific (98%) and sensitive (94%).
  • The results are positive in the initial stages of infection and can be used to detect eradication after treatment.
  • Although the HP fecal antigen test is an interesting tool, information about the cost of the test is pending.
• Carbon 13 urea breath test
• • The carbon 13 urea breath test (UBT) is based on the detection of the products created when urea is split by the organism.
  • Patients are asked to drink urea (usually with a beverage) labeled with a carbon isotope (carbon 13 or carbon 14). After a certain duration, the concentration of the labeled carbon is measured in the breath. The concentration is high only when urease is present in the stomach. Because the human stomach does not produce urease, such a reaction is possible only with HP infection.
  • The breath test is expensive but is becoming increasingly more available.
  • Other problems include false-negative results due to infection with coccoid forms of HP that do not produce as much urease or intake of antibiotics, bismuth, histamine 2 (H2) blockers, or proton pump inhibitors.
• HP serology
• • The serology test has a high (>90%) specificity and sensitivity. It is currently based on the quantitation of immunoglobulin G antibodies against HP by the means of an enzyme-linked immunosorbent assay.
  • It is useful for detecting a newly infected patient, but it is not a good test for follow-up of treated patients because the results do not indicate present infection with HP. The antibody titer may remain elevated for a long time after HP eradication. The number of false-positive results is age-related and increases with age.
• Antibiogram
• • In geographic areas with a high resistance rate against metronidazole and clarithromycin, culture for antibiotic susceptibility testing (antibiogram) seems to be useful.
  • Alternatively, metronidazole and clarithromycin should not be recommended as first-line drugs in such areas.

Imaging Studies

• Imaging studies are not helpful in the diagnosis of HP infection. Otherwise, they may be useful in patients with complicated disease (eg, ulcer disease, gastric cancer, MALToma).

Other Tests

• Esophagogastroduodenoscopy
• • An esophagogastroduodenoscopy (EGD) is often necessary in patients with symptoms of peptic ulcer disease in order to view the condition of the mucosal lining of the stomach and duodenum and to obtain biopsy specimens from the gastric antrum.
  • An echography associated with an EGD is mandatory in patients with biopsy results that are positive for gastric MALTomas in order to allow a more precise staging of the disease.
• Peptic ulcer disease and gastric cancer may manifest with the same symptoms, and the only way to differentiate them is to view the lesion and perform a histologic examination on biopsy specimens.

Procedures

• Patients with new peptic ulcer disease should have a UBT, they should be tested for antibody titers, or they may require an investigation for stool antigens.
• In patients with prior peptic ulcer disease, an EGD with biopsy and histological studies may be performed. Also, a UBT is helpful in these patients.

Histologic Findings

HP is a gram-negative bacterium. It produces urease, has a spirallike conformation, and is microaerophilic and motile because of the flagella. Flagella and urease are very important for its colonization of the gastric mucosa. Urease neutralizes gastric acidity, converting the gastric urea to ammonium ions, and flagella help the bacterium pass from the acidic gastric lumen into the mucus of the stomach. Two of the most important genes of HP are VACA and CAGA. The VACA gene codes the Vac-A cytotoxin, a vacuolizating toxin, and the CAGA gene codes for Cag-A protein, which seems to stimulate the production of chemotactic factors for the neutrophils by the gastric epithelium of the host.

Biopsy specimens from EGD, stained with Giemsa stain, usually demonstrate a variable number of HP organisms adhering to the gastric epithelium, both coating the gastric wall and lining the gastric glands. The mucous film appears decreased. A large inflammatory infiltrate is present, with lymphocytes, neutrophils, and a variable number of mast cells that seem to play an important role in the pathogenesis of the gastric injury of persons infected with HP. Other stains are Genta, Warthin-Starry silver, and the classic hematoxylin and eosin. A rapid urease test may demonstrate the presence of the HP in the gastric mucosa via histochemistry results. Bacterial culture is very difficult. It is not used for diagnosis; it is used for experimental purposes only.

Staging

Although a staging system for the HP infection does not exist, some steps of the disease are well described. The first step is chronic gastritis, followed after a time by the second step, atrophic gastritis. The third step is intestinal metaplasia, which may evolve into dysplasia. The last step in this process is gastric adenocarcinoma. This process is very slow and may stop at any step because gastric cancers undoubtedly require several other factors to develop, not only an HP infection. As reported above, ultrasound and EGD should be considered in patients with gastric MALTomas in order to allow a more precise staging of the disease.

TREATMENT

Section 6 of 11  

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Medical Care

Only treat patients who have a test result positive for HP infection. Carefully educate patients regarding the importance of completing the prescription and about the potential adverse effects of the medication. Importantly, consider possible antibiotic resistance when selecting the treatment regimen.

• The US Food and Drug Administration has approved some regimens, which are now accepted internationally, for the treatment of HP infection in patients with peptic ulcer disease, both gastric and duodenal.
• • These regimens are also known as triple therapies and have reported cure rates from 85-90%.
  • Administer triple therapies for 10-14 days. The treatment regimens are omeprazole, amoxicillin, and clarithromycin (OAC) for 10 days; bismuth subsalicylate, metronidazole, and tetracycline (BMT) for 14 days; and lansoprazole, amoxicillin, and clarithromycin (LAC), which has been approved for either 10 or 14 days of treatment.
  • Macrolide resistance in patients with HP infection is an important problem. Although the molecular mechanisms of nitroimidazole resistance are very complex and still unclear, resistance has been shown to be due to a single point mutation (usually in the RDXA gene, although other genes may be involved, eg, FRDXA) in 1 of 4 positions of the bacterial 23S rDNA. Such mutations also determine cross-resistance to other macrolides.
  • An emerging and increasing problem in many Western countries is the fact that some HP strains in children are resistant to the antibiotic clarithromycin. The causes are not known.
• All the eradication treatments have a high incidence of certain adverse effects (eg, nausea, metallic taste). If skin rash, vomiting, or diarrhea occurs, discontinue treatment.
• The links between HP and nonulcer dyspepsia are debated; however, some patients with nonulcer dyspepsia benefit from eradication. Patients with symptoms have a higher eradication rate than patients with nonulcer dyspepsia disease. Eradication of HP in patients without peptic ulcer disease has resolved the dyspepsia in a few cases.
• See also American College of Gastroenterology Issues Guidelines for Treatment of Helicobacter pylori Infection.

Surgical Care

Surgery is not required for patients with HP infection, but it may be considered in patients with severe complications, such as cancer.

Diet

Usually, no dietary restrictions are needed.

Activity

No limitations of physical activity are needed if patients do not have complications.

MEDICATION

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The goals of pharmacotherapy are to eradicate the microorganism, to prevent complications, and to reduce morbidity. Triple therapies are used. Worldwide, accepted treatment regimens are BMT, LAC, and OAC. BMT regimen is based on the administration of bismuth subsalicylate, metronidazole, and tetracycline. Add an H2-receptor antagonist for an additional 4 wk. LAC regimen is based on the administration of lansoprazole, amoxicillin, and clarithromycin. OAC regimen is based on the administration of omeprazole, amoxicillin, and clarithromycin.

Drug Category: Antidiarrheals

The approved antidiarrheal for this infection is bismuth subsalicylate. It has both antisecretory and antimicrobial activity.

Drug Category: Antibiotics

Use agents known to be effective against HP.

Drug Name	Tetracycline (Sumycin)
Description	Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s).
Adult Dose	500 mg PO qid
Pediatric Dose	<8 years: Not recommended >8 years: Not established
Contraindications	Documented hypersensitivity; severe hepatic dysfunction
Interactions	Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy; can increase hypoprothrombinemic effects of anticoagulants; cholestyramine and colestipol have been shown to reduce tetracycline absorption
Pregnancy	D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions	Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; also may increase photosensitizing effects of aminolevulinic acid, methoxsalen, and vitamin A analogs; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last half of pregnancy through 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines

Drug Name	Clarithromycin (Biaxin)
Description	Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Adult Dose	500 mg PO q12h
Pediatric Dose	<20 months: Not recommended >20 months: Not established
Contraindications	Documented hypersensitivity; coadministration with pimozide or cisapride
Interactions	Toxicity increases with coadministration of fluconazole and pimozide; effects decrease and adverse GI effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, and HMG CoA-reductase inhibitors; serious cardiac arrhythmias may occur with coadministration of cisapride; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents; may decrease efficacy of oral contraceptives
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Coadministration with ranitidine or bismuth citrate not recommended with CrCl <25 mL/min; administer half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies

Drug Name	Amoxicillin (Amoxil, Trimox)
Description	Inhibits final stage of bacterial cell wall synthesis due to binding to specific PBPs on inner part of bacterial wall, leading to bacterial lysis.
Adult Dose	1 g PO bid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	Reduces efficacy of oral contraceptives; concomitant administration can reduce bioavailability of amoxicillin
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Adjust dose in renal impairment; high incidence of drug-related rashes reported in infants and patients with leukemias, viral infections, and allergies or atopic conditions

Drug Category: Proton pump inhibitors

Bind to proton pump of parietal cell, inhibiting secretion of hydrogen ions into gastric lumen. Relieve pain and heal peptic ulcers more rapidly than H2 antagonists.

Drug Name	Omeprazole (Prilosec)
Description	Decreases gastric acid secretion by inhibiting parietal cell H+/K+-ATP pump.
Adult Dose	20 mg PO bid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	May decrease effects of ketoconazole, itraconazole, iron salts, and ampicillin; may increase theophylline clearance; may affect absorption of cyanocobalamin
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Bioavailability may increase in elderly; not recommended during breastfeeding

Drug Category: H2 receptor blockers

Reversible competitive blockers of histamine at H2 receptors, particularly those in gastric parietal cells, wherein they inhibit acid secretion. H2 antagonists are highly selective, do not affect the H1 receptors, and are not anticholinergic agents. Proton pump inhibitors are usually preferred.

Drug Name	Famotidine (Pepcid)
Description	Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Adult Dose	40 mg/d PO bid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	May decrease effects of ketoconazole and itraconazole
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	If changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment

FOLLOW-UP

Section 8 of 11  

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Further Outpatient Care

• Consider performing a UBT 4-12 weeks after the end of treatment.
• EGD with biopsy and a urease test also may be useful, but, importantly, remember that this test does have a significant rate of false-negative results.

Deterrence/Prevention

• Risk is increased for patients who have an HP infection and whose first-degree relatives have a history of gastric cancer, even if they are asymptomatic.
• Persons emigrating from geographic areas with a high incidence of gastric cancer have an increased risk.
• Consider any patient with precancerous lesions of the stomach (ie, intestinal metaplasia) for treatment of HP.

Complications

• Gastric adenocarcinoma is the most severe consequence of an HP infection.
• Gastric MALToma may be treated with HP eradication therapy and has a better prognosis than gastric adenocarcinoma.
• • A significant difference exists between the therapeutic response of MALTomas restricted to the mucosa and other, more infiltrating lesions.
  • The only predictive factor for disease regression seems to be the absence of nodal involvement.
• HP infection is associated with squamous cell esophageal cancer.
• HP may play an important role in idiopathic thrombocytopenic purpura. This is due to anti-CagA antibodies that cross-react with platelet antigens.
• According to some reports, HP eradication may cause peptic esophagitis, probably due to a protective action of the bacteria on the cardia area.

Prognosis

• Prognosis is usually excellent, even in patients with complications such as gastric MALToma. However, the prognosis becomes poor for patients who develop squamous cell esophageal cancer or gastric carcinoma.
• The rate of reinfection is very low (1-2%); however, children and females have a higher incidence of reinfection (5-8%).

Patient Education

• Educate patients with a high risk for gastric cancer about clinical control methods and, if HP-positive, to begin eradication therapy. However, patients must be educated about the adverse effects of the therapy in order to impress upon them the importance of compliance with the full regimen in order to prevent antibiotic resistance and relapse.
• For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center and Heartburn/GERD/Reflux Center. Also, see eMedicine's patient education articles Gastritis, Peptic Ulcers, Heartburn, Understanding Heartburn/GERD Medications, and Abdominal Pain in Adults.

MISCELLANEOUS

Section 9 of 11  

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Medical/Legal Pitfalls

• Consider performing an EGD before prescribing a treatment for peptic ulcer disease. Peptic ulcer disease and gastric cancer may manifest with the same symptoms, and a correct diagnosis is mandatory to avoid legal claims. Also consider that in a small number of cases (2%), peptic ulcer disease and gastric carcinoma, even ulcerated, may coexist.

Special Concerns

• If HP infection occurs during pregnancy, delay the treatment until after delivery because of the adverse teratogenous effects of some drugs used in the therapeutic protocols for HP eradication. In addition, delaying a new pregnancy for at least 1 month after the end of treatment may be advisable.

MULTIMEDIA

Section 10 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
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Media file 1:  An antral gland of the stomach with a large Giemsa-stained colony of Helicobacter pylori in the lumen (arrow) at 250X power. Courtesy of Pantaleo Bufo, University of Foggia, Italy.
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Media type:  Photo

Media file 2:  Helicobacter pylori infection. Lamina propria of the stomach is shown with 2 mast cells overlapping each other. Note the upper part the degranulating process with the release of granules of inflammation mediators (Giemsa staining, 250X). Courtesy of Pantaleo Bufo, University of Foggia, Italy.
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Media type:  Photo

Media file 3:  Helicobacter pylori infection. A transverse section of the gastric lamina propria is shown. In the lower part, an antral gland of the stomach is present with some Helicobacter pylori in the lumen (red-blue arrow). In the upper part, a mast cell (yellow arrow) is present (Giemsa staining, 250X). Courtesy of Pantaleo Bufo, University of Foggia, Italy.
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Media type:  Photo

Media file 4:  An antral gland of the stomach is shown with a large colony of Helicobacter pylori in the lumen (Giemsa staining, 425X). Courtesy of Pantaleo Bufo, University of Foggia, Italy.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
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• Differentials
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• Follow-up
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• El-Omar EM, Carrington M, Chow WH, McColl KE, Bream JH, Young HA. Interleukin-1 polymorphisms associated with increased risk of gastric cancer. Nature. Mar 23 2000;404(6776):398-402. [Medline].
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Article Last Updated: Oct 17, 2007