Development Of Peptic Ulcer Disease Research Articles

Ocular Myasthenia Gravis Treatment

M YASTHENIAGRAVIS (MG) is an autoimmunedisorder that affects the postsynapticneuromuscular junctionmembrane.Acetylcholine receptor (AChR) antibodiesare frequentlypresent, andthe numberoffunctioningpostsynapticreceptors isreduced.Muscle-specifickinaseantibodiesmaybeidentifiedinindividuals with and without AChR antibodies. Ptosis or diplopia due to ocular muscle involvement are frequently the first symptomsof thedisease. Approximately half of the patients are first seen with purely ocularMG(OMG);of these,53%develop generalizedMG(GMG)within2years ( 80% in the first year). Furthermore,aspontaneousremissionrateof 30%hasbeenreportedinpatientswith OMG during a 15-year period. Both AChRandmuscle-specifickinaseantibodies may be present in OMG. The goal of therapy for OMG and GMG is to minimize the patient’s symptoms. Another recently discussed goal is to prevent the progression of OMG to GMG. Symptomatic treatment may be as simple as observation for patients with minimal symptoms, but some patients are uncomfortable owing to diplopia or ptosis and desire a more definitive treatment. The choice of the initial medication in patients with OMG depends on each drug’s efficacy, adverse effects, contraindications, availability, and cost. Classically, the mainstay of pharmacotherapy is acetylcholinesterase inhibitors (eg, pyridostigmine bromide). However, there is evidence that pyridostigmine may not be as effective in treating purely OMG. The clinical response is variable, but approximately 50% of patients with OMG have a good response. Ptosis tends to respond better than diplopia. The most common adverse effect is diarrhea. Very large doses occasionally lead to increased weakness from cholinergic crisis. The drug should be used with caution in patients with asthma, cardiac arrhythmia, or urinary obstruction. If treatment with this agent is unsuccessful, other approaches, such as immunosuppressive agents (typically corticosteroids) or thymectomy, may be used. Prednisone is the immunosuppressive agent most frequently used in the treatment of OMG. Most patients experience relief from ptosis and diplopia within weeks of starting prednisone therapy. The typical approach is to titrate the dose up to 1.0 mg/kg per day over several weeks. Maintenance doses at this level are continued for 6 to 12 weeks and are followed by a slow taper over several months. Treatment with prednisone longer than 2 to 4 weeks can have significant morbidity. Patients require careful monitoring for development of peptic ulcer disease, diabetes mellitus, hypertension, psychosis, insomnia, myopathy, hypokalemia, hypocalcemia, osteoporosis, cataracts, glaucoma, masking of infections, and worsening MG symptoms. The failure of OMG-related ptosis and diplopia to improve after corticosteroid therapy ranges from as low as 8 of 89 patients (9%) in one study to as high as 6 of 18 (33%) in another. Somestudies suggest thatthe useofcorticosteroidsor thymectomy astheprimarytreatmentofOMGmay decrease theriskofdevelopingGMG. The firstof thesestudies summarized 32patientswhoweretreatedforOMG with prednisone for 2 months to 1 year. Only 3 of the 32 patients (9%) went on to develop GMG, a significantlylowerpercentagethanexpected fromthenaturalhistorystudiesof the disease. How long these 3 patients who progressed to GMG had symptomsbeforestartingtreatmentwasnot specified. This is critical information because patients with ocular symptoms for more than a year are less likelytodevelopGMGwhetherornot they are treated. The majority of patients who progress to GMG do so within the first year of OMG symptom onset. Two subsequent studies included patients from a myasthenia database anddidnot specifyhowlongpatients hadsymptomsbeforestartingtherapy. Therefore,patientswhohadbeen followed up for more than 2 years with onlyocularsymptomsmayhavebeen included, skewing the likelihood of progression. Amorerecent study included only patients with ocular symptoms for less than 2 years. Thirteen of 31 patients (42%) did not progress to GMG, and 10 of these patientsunderwentimmunosuppressive therapy. Two of the 10 patients receivedazathioprinesodiuminaddition to prednisone, 3 underwent prednisoneandazathioprinetherapyplusthymectomy,and3receivedimmunosupAuthor Affiliations: Neuroophthalmology Service, Wills Eye Institute (Drs Gilbert and Savino), and Department of Neurology, Thomas Jefferson University (Dr De Sousa), Philadelphia, Pennsylvania. Dr Gilbert is now with the Department of Neuro-Ophthalmology, Illinois Eye and Ear Infirmary, Chicago.

Association between promoter polymorphisms of nuclear factor-erythroid 2-related factor 2 gene and peptic ulcer diseases

Transcription factor Nrf2 regulates the expression of detoxifying and antioxidant genes. Three promoter polymorphisms of this gene have been identified. We attempted to clarify the association of these polymorphisms with the development of peptic ulcer diseases. The study was performed with 384 stocked DNAs obtained from subjects with no evidence of gastric malignancy. In all 384 DNAs, 77 and 48 were obtained from gastric and duodenal ulcer patients, respectively. By an unadjusted analysis, infection with Helicobacter pylori (H. pylori), male gender and the -686/-684 G/G carrier (OR, 2.52; 95% CI, 1.19-5.45; p=0.016) were associated with a significantly increased risk for developing gastric ulcer, whereas the -686/-684 A/G homozygote was linked to a significantly reduced risk for developing gastric ulcer (OR, 0.26; 95% CI, 0.099-0.67; p=0.0055). On the other hand, infection with H. pylori and male gender were significantly associated with the development of duodenal ulcer, whereas Nrf2 promoter polymorphisms were not. By the analysis, after adjustment for age, gender, non-steroidal anti-inflammatory drug/aspirin use and H. pylori infection status, the -686/-684 A/G homozygote was associated with a significantly reduced risk for gastric ulcer (OR, 0.25; 95% CI, 0.088-0.73; p=0.011). Our results suggest that promoter polymorphisms of the Nrf2 gene are associated with the susceptibility to gastric ulcer.

Iron Pill Gastropathy: A Case Report and Review of the Literature

Purpose: Despite the widespread use of oral iron supplements, the entity of “iron pill gastritis” has remained largely unrecognized in the Gastreonterology literature. Our patient is an 85 year-old man who presented with a several-month history of melena. Pertinent medications included daily lansoprazole 30 mg and aspirin 81 mg. He had been taking ferrous sulfate 325 mg twice daily for iron deficiency anemia for the prior 8 weeks. History included coronary artery disease, compensated congestive heart failure, and hypertension. The patient had a history of an upper gastrointestinal bleed 2 years prior to this evaluation, secondary to aspirin and celecoxib use. Upper endoscopy revealed a large esophageal ulcer, multiple duodenal ulcers, and no gastric ulcers. Testing for Helicobacter pylori was negative. Physical exam revealed stable vital signs and no orthostasis. Examination was normal except for guaiac-positive stool. Hematocrit was stable at 36%. Subsequent upper endoscopy revealed a normal esophagus and multiple sessile diminutive polyps in the gastric fundus. A non-bleeding 4 × 8 mm gastric ulcer with pigmented material was found in the gastric body. Histopathologic evaluation of gastric biopsies obtained from the ulcer revealed foveolar hyperplasia with abundant granular brown pigment, consistent with iron pill gastropathy. The patient was placed on twice daily oral lansoprazole at a dose of 30 mg, and oral iron was discontinued. A follow-up upper endoscopy performed one month later revealed no evidence of active ulceration. The patient has been maintained on lansoprazole 30 mg twice daily and aspirin 81 mg daily. He has experienced no further gastrointestinal problems. Iron injury is thought to result from a direct corrosive action on the gastrointestinal mucosa. A previous study found gastric ulcers in association with oral iron use. Histology of these biopsies showed heavy iron deposition within ulcer granulation tissue, in connective tissue, and in blood vessels of the lamina propria. Ulceration appeared to have preceded the initiation of iron therapy, suggesting that iron use exacerbated a pre-existing condition. Few clinicians are aware that oral iron has been associated with gastropathy that can lead to the development of peptic ulcer disease. Our case provides an illustration of this rare but important entity and highlights the importance of co-morbidity and concomitant use of low dose aspirin.

American College of Gastroenterology Guideline on the Management of Helicobacter pylori Infection

Helicobacter pylori (H. pylori) remains a prevalent, worldwide, chronic infection. Though the prevalence of this infection appears to be decreasing in many parts of the world, H. pylori remains an important factor linked to the development of peptic ulcer disease, gastric malignanc and dyspeptic symptoms. Whether to test for H. pylori in patients with functional dyspepsia, gastroesophageal reflux disease (GERD), patients taking nonsteroidal antiinflammatory drugs, with iron deficiency anemia, or who are at greater risk of developing gastric cancer remains controversial. H. pylori can be diagnosed by endoscopic or nonendoscopic methods. A variety of factors including the need for endoscopy, pretest probability of infection, local availability, and an understanding of the performance characteristics and cost of the individual tests influences choice of evaluation in a given patient. Testing to prove eradication should be performed in patients who receive treatment of H. pylori for peptic ulcer disease, individuals with persistent dyspeptic symptoms despite the test-and-treat strategy, those with H. pylori-associated MALT lymphoma, and individuals who have undergone resection of early gastric cancer. Recent studies suggest that eradication rates achieved by first-line treatment with a proton pump inhibitor (PPI), clarithromycin, and amoxicillin have decreased to 70-85%, in part due to increasing clarithromycin resistance. Eradication rates may also be lower with 7 versus 14-day regimens. Bismuth-containing quadruple regimens for 7-14 days are another first-line treatment option. Sequential therapy for 10 days has shown promise in Europe but requires validation in North America. The most commonly used salvage regimen in patients with persistent H. pylori is bismuth quadruple therapy. Recent data suggest that a PPI, levofloxacin, and amoxicillin for 10 days is more effective and better tolerated than bismuth quadruple therapy for persistent H. pylori infection, though this needs to be validated in the United States.

Association between Helicobacter pylori genotypes and gastric disorders in relation to the cag pathogenicity island

Helicobacter pylori is a bacterium associated with upper gastrointestinal diseases in humans. However, only a small proportion of infected people become sick. Although several studies have tried to establish an association between known virulence markers and clinical outcomes, in many cases the results have been conflicting. The aim of this study was to investigate the importance of virulence markers to predict clinical outcome in Brazil. Mixed infections by genetically unrelated strains detected by vacA genotyping were found in 18% of the patients. The cagA and cagE genes and the vacAs1 genotype were associated with the development of peptic ulcer disease (PUD). The cagAvacAs1m1 genotype was associated with PUD and duodenal ulcer (DU). Conversely, jhp947 was not associated with DU or PUD, indicating that this gene is not a universal virulence marker. These results also show that a high proportion of the patients were simultaneously infected by cag-positive and cag-negative H. pylori types. This finding suggests the existence of a dynamic equilibrium between the loss and gain of the cag pathogenicity island, probably depending on the physiologic conditions of the patient's stomach. To the best of our knowledge, this is the first study that has documented this finding in Brazil.

This Month in Gastroenterology

This Month in Gastroenterology

Epidemiology and pathophysiology of Helicobacter pylori infection in children

Helicobacter pylori is one of the commonest bacterial pathogens in human. The organism is associated with development of peptic ulcer diseases, lymphoproliferative disorders and gastric cancer. Residence in a developing country, poor socio-economic conditions and genetic predisposition are regarded as risk factors. Prevalence of infection is higher in developing countries and re-infection is higher among under five children. It is transmitted mainly through feco-oral route in developing countries and gastro-oral route in developed nations. Transmission of 'close-contact infection' depends on the degree of mixing and age-distribution between susceptible and infected individuals. Host and bacterial factors with interaction of environment contribute pathogenicity. H. pylori cytotoxin-associated geneA (cagA), vacuolating toxinA (vacA) and adherence factors to gastric epithelium have been linked to enhanced pathogenicity of the bacterium. Host genetic polymorphism of cytokines, related legends, receptors and enzymes influence H. pylori infection.

Inhibition of T-Cell Proliferation by Helicobacter pylori γ-Glutamyl Transpeptidase

Helicobacter pylori colonizes the human gastric mucosa of >50% of the world's population. Most of the patients have no overt clinical symptoms. However, the infection is invariably associated with the development of active chronic gastritis, leading in some cases to the development of peptic ulcer disease, distal gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. In contrast to most other pathogens, infection with H pylori persists lifelong, but reasons for the persistence remain obscure. CD4-positive T cells are crucial for bacterial elimination but are inhibited by H pylori. We aimed to identify the factor responsible for suppression of T-cell response and characterize this inhibitory effect on a cellular and molecular level. Using size-exclusion chromatography, sodium dodecyl sulfate/polyacrylamide gel electrophoresis, and a spectrophotometric enzyme assay, we identified the secreted gamma-glutamyl transpeptidase of H pylori (HPGGT) as the factor responsible for inhibition of T-cell proliferation. Mutagenesis of HPGGT in different H pylori strains completely abrogated this inhibitory effect. Recombinantly expressed HPGGT protein showed full antiproliferative activity. Site-directed mutagenesis and application of the GGT inhibitor acivicin revealed that inhibition of T cells depends on catalytic activity of HPGGT. Cell cycle analysis of human T cells indicated that HPGGT was necessary and sufficient to induce G(1) arrest. Reduced levels of c-Myc and phosphorylated c-Raf protein suggest the disruption of Ras-dependent signaling by HPGGT. GGT is a novel immunosuppressive factor of H pylori inhibiting T-cell proliferation by induction of a cell cycle arrest in the G(1) phase.

Significance of Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs in patients with bleeding from upper part of the gastrointestinal tract

Helicobacter pylori (H. pylori) infection and nonsteroidal anti-inflammatory drugs (NSAIDs) use are considered to be the most important risk factors having influence on the onset of bleeding gastroduodenal lesions. Whether there is an interaction between H. pylori infection and the use of NSAIDs in the development of peptic ulcer disease is still controversial. The aim of the present study was to evaluate the prevalence of NSAIDs use and H. pylori infection in patients presented with bleeding gastroduodenal lesions. During the period from January 2003 December 2003 we prospectively obtained data of all the patients (n=106) presented with signs of upper gastrointestinal bleeding. All the patients were admitted to the intensive care unit, with the endoscopy performed within 12 hours after admission. Histologic analysis was used for the detection of H. pylori infection. The NSAIDs and aspirin use data were obtained by anamnesis. The results of our study revealed that the most common sources of upper gastrointestinal bleeding were duodenal (57 patients, 53.77%) and ventricular (36 patients, 33.96%) ulcers. The majority of the examined cases were associated with both H. pylori infection and NSAIDs use. A statistically significant difference among the studied groups of patients was proven. The majority of bleeding gastroduodenal lesions were associated with the coexistance of H. pylori infection and NSAIDs use, while their independent influences were statistically less important. Eradication of H. pylori infection in patients using NSAIDs might prevent upper gastrointestinal hemorrhage and reduce peptic ulcer bleeding risk.

Helicobacter pylori cag pathogenicity island genes: clinical relevance for peptic ulcer disease development in Brazil

The purpose of this study was to verify whether the presence of any of the Helicobacter pylori cagPAI genes or segments--cagA, cagA promoter, cagE, cagM, tnpB, tnpA, cagT and the left end of the cag II (LEC) region--would be a useful marker for the risk of peptic ulcer disease development. H. pylori DNA extracted from positive urease tests of 150 peptic ulcer patients and 65 dyspeptic controls was analysed by PCR. Duodenal ulcers were present in 110, gastric ulcers in 23 and both gastric and duodenal ulcers in 17 patients. A significant association (P <0.001) was found between a conserved cagPAI and peptic ulcer disease (34 %). The positivity of the cagA gene varied according to the region of the gene that was amplified. The region near to the promoter was present in almost all of the H. pylori isolates (97.2 %). The segment from nt 1764 to 2083 and the extreme right end were frequently deleted in the isolates from the controls (P <0.01). The positivity of the promoter region of cagA and cagT, cagE, cagM and LEC showed a significant difference between the isolates from peptic ulcer patients and from the controls (P <0.01). Patients usually had moderate gastritis; however, the intensity of the active inflammation was higher in the peptic ulcer group (P <0.001). cagT, cagM, LEC and the right end terminus of the cagA-positive H. pylori isolates were associated with a 27-fold, 8-fold, 4-fold and 4-fold risk of peptic ulcer disease, respectively, and may be useful markers to identify individuals at higher risk of peptic ulcer disease development in Brazil.

Impulsivity as a predictor of newly-diagnosed peptic ulcer disease: A prospective cohort study

We examined the role of impulsivity in the development of peptic ulcer disease (PUD). The subjects were initially healthy 4636 hospital employees aged 19–62 who responded to a questionnaire on personality, health habits, mental health, and PUD in 1998 and 2000. We used multivariate logistic analyses to determine the relationship between impulsivity and newly-diagnosed PUD among those employees who did not have PUD at baseline. Impulsivity was assessed with the Karolinska Scale of Personality. High level of impulsivity was associated with increased 2-year incidence of doctor-diagnosed PUD after adjustment of age, gender, education and shift work (odds ratio = 2.42, 95% confidence interval = 1.21–4.82). Additional adjustment for the effects of smoking, alcohol consumption, BMI, physical activity, minor psychiatric morbidity and diagnosed depression and other psychiatric disease had little effect on this relationship. The present study suggests that impulsivity may be a risk factor for the development of PUD.

Primary Clarithromycin Resistance to Helicobacter pylori and Therapy Failure in Children: The Experience in West Virginia

Primary Clarithromycin Resistance to <i>Helicobacter pylori</i> and Therapy Failure in Children: The Experience in West Virginia

An enzymatic ruler modulates Lewis antigen glycosylation of Helicobacter pylori LPS during persistent infection

Helicobacter pylori persistently colonizes about half the human population and contributes to the development of peptic ulcer disease and gastric cancer. This organism has evolved means to structurally alter its surface characteristics to evade innate and adaptive immune responses. H. pylori produces LPS O-antigen units that can be posttranslationally fucosylated to generate Lewis antigens, structures also found on human epithelial cells. We demonstrate an extensive diversity of Lewis x and Lewis y expression in LPS O-antigen units, occurring over time and in different regions of the human stomach. Lewis expression patterns were correlated with the on/off status of the three fucosyltransferases (FucT), FutA, FutB, and FutC, which are regulated via slipped-strand mispairing in intragenic polyC tract regions of the corresponding genes. The alpha1,3-FucT, FutA and FutB, each contain a C-terminal heptad repeat region, consisting of a variable number of DD/NLRV/INY tandem repeats. Variations in the number of heptad repeats correlated to the sizes of O-antigen polymers to become decorated by fucose residues. Our data support a molecular ruler mechanism for how H. pylori varies its LPS fucosylation pattern, where one heptad repeat in the enzyme corresponds to one N-acetyl-beta-lactosamine unit in the O-antigen polysaccharide.

Immune responses toHelicobacter pyloricolonization: mechanisms and clinical outcomes

Helicobacter pylori colonizes the stomachs of half of the world's population and usually persists in the gastric mucosa of human hosts for decades or life. Although most H. pylori-positive people are asymptomatic, the presence of H. pylori is associated with increased risk for the development of peptic ulcer disease, gastric adenocarcinoma and gastric lymphoma. The development of a sustained gastric inflammatory and immune response to infection appears to be pivotal for the development of disease. During its long co-existence with humans, H. pylori has evolved complex strategies to maintain a mild inflammation of the gastric epithelium while limiting the extent of immune effector activity. In this review, the nature of the host immune response to H. pylori infection and the mechanism employed by the bacterium to evade them is considered. Understanding the mechanisms of colonization, persistence and virulence factors of the bacterium as well as the innate and adaptive immune responses of the host are critically important for the development of new strategies to prevent the development of H. pylori-induced gastroduodenal disease.

The Association ofHelicobacter pyloriInfection and Nonsteroidal Anti-Inflammatory Drugs in Peptic Ulcer Disease

Peptic ulcer disease (PUD) affects 10% of the world population. Helicobacter pylori infection and the use of a nonsteroidal anti-inflammatory drug (NSAID) are the principal factors associated with PUD. The aim of the present study was to evaluate a cohort of patients with PUD and determine the association between H pylori infection and NSAID use. The medical charts of patients with endoscopic diagnosis of PUD were retrospectively reviewed from September 2002 to August 2003. Patients were divided into three groups according to ulcer etiology: H pylori infection (group 1); NSAID use (group 2); and combined H pylori infection and NSAID use (group 3). One hundred two patients were evaluated: 36 men (35.3%) and 66 women (64.7%). Forty patients had H pylori infection, 43 had used NSAIDs and 15 had combined H pylori infection and NSAID use; four patients with ulcers secondary to malignancy were excluded. The frequency of women was significantly higher in group 2 (P=0.01). The mean age of patients in group 1 was significantly lower than in the other two groups (P=0.003). PUD developed earlier in group 3 than in group 2 (5.0+/-4.7 months versus 1.4+/-2.1 months, respectively, P=0.018). Thirty-two patients (32.7%) had bleeding peptic ulcer. Group 2 had a higher risk of bleeding peptic ulcer than the other two groups (P=0.001). The development of PUD was observed earlier in the combined H pylori and NSAID group than in patients with only NSAID use. This suggests a synergic effect between the two risks factors in the development of PUD.

Helicobacter pylori occurrence and transmission: A family affair?

About half of the world's population is estimated to be infected with Helicobacter pylori, a gastric bacterium that contributes to the development of peptic ulcer disease and gastric cancer. H. pylori is more prevalent in low-income areas of the world and social and economic development decreases the prevalence as reflected in comparisons both within and between countries. The infection is typically acquired in early childhood and once established commonly persists throughout life unless treated. Person-to-person transmission within the family appears to be the predominant mode of transmission, particularly from mothers to children and among siblings, indicating that intimate contact is important. The route of transmission is uncertain, but the gastro-oral, oral-oral and faecal-oral routes are likely possibilities. Hence, gastroenteritis may facilitate dissemination of the infection. The community and environment may play additional roles for H. pylori transmission in some (low-income) settings. Furthermore, host and bacterial factors may modify the probabilities of acquisition and persistence of the infection. The understanding of H. pylori occurrence and transmission is of practical importance if future study deems prevention of the infection desirable in some high-prevalence populations. The present paper reviews aspects of H. pylori occurrence and transmission with an emphasis on household factors.

CagA vacA alelles and babA2 genotypes of Helicobacter pylori associated with gastric disease in Brazilian adult patients

Helicobacter pylori is an important human pathogen that causes chronic gastritis and is associated with development of peptic ulcer disease and gastric malignancies. The vacuolating cytotoxin ( vacA), cagA gene, and babA2 gene are important virulence factor involving gastric diseases. Eighty-nine Helicobacter pylori-positive gastric biopsies were analyzed by polymerase chain reaction and Southern blotting for H. pylori detection and genotyping with primer pairs from each virulence gene. Fifty-three strains (59%) were common vacA genotype s1/m1, and only 14 (16%) were s2/m2, 12% of strains was found to have multiple infection. The cagA presence was detected in 48% (43 strains) and babA2 gene was detected in 44% of our H. pylori strains. We observed high percentage of s1/m1 strains with chronic gastritis and peptic ulcer and a significant correlation between cagA presence with the s1 allele and babA2 gene with chronic gastritis.

Effects of Helicobacter pylori on Endothelial Cell Proliferation and Chemotaxis

Background/Aim:Helicobacter pylori is associated with an increased risk of peptic ulcer disease development and recurrence. Ulcer healing is dependent upon angiogenesis, requiring endothelial cell (EC) proliferation and chemotaxis. This study determined whether extracts of H. pylori affected EC proliferation and/or chemotaxis in vitro. Methods: The effects of water and broth extracts of three genotypically different strains of H. pylori and of single strains of Campylobacter jejuni and Escherichia coli on human dermal microvascular EC (HuDMEC) and human umbilical vein EC (HUVEC) were assessed. Tetrazolium dye (MTT) proliferation, dual staining cell viability, flow cytometry, and microchemotaxis assays were performed. Results:H. pylori (all strains) and C. jejuni inhibited HuDMEC (p < 0.01) and HUVEC (p < 0.01) proliferation and decreased the proportion of HUVECs in the S phase of the cell cycle. E. coli had no effect on EC proliferation. The levels of vascular endothelial growth factor stimulated chemotaxis were significantly greater (p < 0.01) than the levels of basal migration for both control and extract-treated ECs. However, none of the bacterial extracts affected EC basal migration or chemotaxis. Conclusion:H. pylori extracts inhibit HuDMEC and HUVEC proliferation in vitro by a cytostatic, strain-independent mechanism. A similar antiproliferative effect of C. jejuni was observed. Our findings suggest that both H. pylori and C. jejuni have the ability to inhibit one of the key stages of angiogenesis which may have implications in peptic ulcer disease.

Helicobacter pylori: Pathology and Diagnostic Strategies

Helicobacter pylori represents one of the most common and medically prominent infections worldwide. Infection with this microaerobic, gram-negative bacterium has been established as an etiologic factor in the development of peptic ulcer disease. In addition, H pylori infection has been associated firmly with the development of gastric neoplasia, including gastric adenocarcinomas and gastric mucosa-associated lymphoid tissue lymphomas. Effective antimicrobial treatment depends on sensitive and accurate diagnostic approaches. This review article discusses invasive and noninvasive strategies for diagnosis of H pylori infection. Invasive methods requiring endoscopic evaluation include bacteriologic culture and susceptibility testing, histopathologic studies, molecular diagnostics, and rapid urease testing. Noninvasive approaches include fecal antigen detection, serologic testing, and urea breath testing.

Helicobacter pylori

Helicobacter pylori represents one of the most common and medically prominent infections worldwide. Infection with this microaerobic, gram-negative bacterium has been established as an etiologic factor in the development of peptic ulcer disease. In addition, H pylori infection has been associated firmly with the development of gastric neoplasia, including gastric adenocarcinomas and gastric mucosa-associated lymphoid tissue lymphomas. Effective antimicrobial treatment depends on sensitive and accurate diagnostic approaches. This review article discusses invasive and noninvasive strategies for diagnosis of H pylori infection. Invasive methods requiring endoscopic evaluation include bacteriologic culture and susceptibility testing, histopathologic studies, molecular diagnostics, and rapid urease testing. Noninvasive approaches include fecal antigen detection, serologic testing, and urea breath testing.