Peptic ulcer disease: current notions
Natalia Castaño-Rodríguez and Hazel M MitchellSchool of Biotechnology and Biomolecular Sciences
The University of New South Wales
Sydney, NSW 2052, Australia
Tel: +61 2 9385 2040
Fax: +61 2 9385 1483
Email: h.mitchell@unsw.edu.au
Microbiology Australia 34(3) 147-150 https://doi.org/10.1071/MA13049
Published: 4 September 2013
Abstract
Helicobacter pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs) are the major aetiological factors in peptic ulcer disease (PUD). A range of H. pylori virulence factors have been linked with both increased levels of inflammation and PUD. Recently, increasing reports of H. pylori-negative PUD has led some to question the role of H. pylori in PUD; however, research would suggest that H. pylori-negative PUDs are mainly due to NSAIDs usage and false negative results in diagnostic methods.
References
[1] Marshall, B.J. et al. (1985) Attempt to fulfil Koch’s postulates for pyloric Campylobacter. Med. J. Aust. 142, 436–439.| 1:STN:280:DyaL2M7mtlWntQ%3D%3D&md5=4ec0452114ba7b08910f8cab8cc6c3d4CAS | 3982345PubMed |
[2] Huang, J.Q. et al. (2002) Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease: a meta-analysis. Lancet 359, 14–22.
| Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease: a meta-analysis.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD38XmsV2msQ%3D%3D&md5=040d7e6a426364b7477dea1b122ee481CAS | 11809181PubMed |
[3] Papatheodoridis, G.V. et al. (2006) Effects of Helicobacter pylori and nonsteroidal anti-inflammatory drugs on peptic ulcer disease: a systematic review. Clin. Gastroenterol. Hepatol. 4, 130–142.
| Effects of Helicobacter pylori and nonsteroidal anti-inflammatory drugs on peptic ulcer disease: a systematic review.Crossref | GoogleScholarGoogle Scholar | 16469671PubMed |
[4] Lau, J.Y. et al. (2011) Systematic review of the epidemiology of complicated peptic ulcer disease: incidence, recurrence, risk factors and mortality. Digestion 84, 102–113.
| Systematic review of the epidemiology of complicated peptic ulcer disease: incidence, recurrence, risk factors and mortality.Crossref | GoogleScholarGoogle Scholar | 21494041PubMed |
[5] Sung, J.J. et al. (2009) Systematic review: the global incidence and prevalence of peptic ulcer disease. Aliment. Pharmacol. Ther. 29, 938–946.
| Systematic review: the global incidence and prevalence of peptic ulcer disease.Crossref | GoogleScholarGoogle Scholar | 1:STN:280:DC%2BD1M3ptlKrtQ%3D%3D&md5=b7179657fd8e8165642c38ad948d1478CAS | 19220208PubMed |
[6] Abraham, N.S. et al. (2005) National adherence to evidence-based guidelines for the prescription of nonsteroidal anti-inflammatory drugs. Gastroenterology 129, 1171–1178.
| National adherence to evidence-based guidelines for the prescription of nonsteroidal anti-inflammatory drugs.Crossref | GoogleScholarGoogle Scholar | 16230071PubMed |
[7] Kusters, J.G. et al. (2006) Pathogenesis of Helicobacter pylori infection. Clin. Microbiol. Rev. 19, 449–490.
| Pathogenesis of Helicobacter pylori infection.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD28XosVaqsrg%3D&md5=40897e42fcfee802406a8dd831547437CAS | 16847081PubMed |
[8] Moss, S.F. et al. (1992) Effect of Helicobacter pylori on gastric somatostatin in duodenal ulcer disease. Lancet 340, 930–932.
| Effect of Helicobacter pylori on gastric somatostatin in duodenal ulcer disease.Crossref | GoogleScholarGoogle Scholar | 1:STN:280:DyaK3s%2FitlaltQ%3D%3D&md5=d9335636502bddd417a9b44333ebbb97CAS | 1357347PubMed |
[9] Craig, P.M. et al. (1992) Helicobacter pylori secretes a chemotactic factor for monocytes and neutrophils. Gut 33, 1020–1023.
| Helicobacter pylori secretes a chemotactic factor for monocytes and neutrophils.Crossref | GoogleScholarGoogle Scholar | 1:STN:280:DyaK3s%2FhtlWguw%3D%3D&md5=aecfc8fa34a1375743f33d69cd783ac6CAS | 1398224PubMed |
[10] Malfertheiner, P. et al. (2009) Peptic ulcer disease. Lancet 374, 1449–1461.
| Peptic ulcer disease.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD1MXhtlSru7jE&md5=b85dd26eaa1dbdbe6cff838d5ee901edCAS | 19683340PubMed |
[11] Backert, S. et al. (2010) Virulence factors of Helicobacter pylori. In Helicobacter pylori in the 21st Century. (First edn) (Sutton, P. and Mitchell, H., eds), pp. 212–247, CAB International.
[12] Sahara, S. et al. (2012) Role of Helicobacter pylori cagA EPIYA motif and vacA genotypes for the development of gastrointestinal diseases in Southeast Asian countries: a meta-analysis. BMC Infect. Dis. 12, 223.
| Role of Helicobacter pylori cagA EPIYA motif and vacA genotypes for the development of gastrointestinal diseases in Southeast Asian countries: a meta-analysis.Crossref | GoogleScholarGoogle Scholar | 22994150PubMed |
[13] Hussein, N.R. (2010) The association of dupA and Helicobacter pylori-related gastroduodenal diseases. Eur. J. Clin. Microbiol. Infect. Dis. 29, 817–821.
| The association of dupA and Helicobacter pylori-related gastroduodenal diseases.Crossref | GoogleScholarGoogle Scholar | 1:STN:280:DC%2BC3crivFKqug%3D%3D&md5=49425313762342fabe7d26f0f90e0347CAS | 20419465PubMed |
[14] Shiota, S. et al. (2010) Systematic review and meta-analysis: the relationship between the Helicobacter pyloridupA gene and clinical outcomes. Gut Pathog 2, 13.
| Systematic review and meta-analysis: the relationship between the Helicobacter pyloridupA gene and clinical outcomes.Crossref | GoogleScholarGoogle Scholar | 21040520PubMed |
[15] Basso, D. et al. (2008) Clinical relevance of Helicobacter pylori cagA and vacA gene polymorphisms. Gastroenterology 135, 91–99.
| Clinical relevance of Helicobacter pylori cagA and vacA gene polymorphisms.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD1cXps1Wltrg%3D&md5=73cc04ed79b524b24c2c5ddefb4a422cCAS | 18474244PubMed |
[16] Rhead, J.L. et al. (2007) A new Helicobacter pylori vacuolating cytotoxin determinant, the intermediate region, is associated with gastric cancer. Gastroenterology 133, 926–936.
| A new Helicobacter pylori vacuolating cytotoxin determinant, the intermediate region, is associated with gastric cancer.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD2sXhtFars77M&md5=a830d632e7bc6df20b41e45cf9499af9CAS | 17854597PubMed |
[17] Selbach, M. et al. (2002) Src is the kinase of the Helicobacter pylori CagA protein in vitro and in vivo. J. Biol. Chem. 277, 6775–6778.
| Src is the kinase of the Helicobacter pylori CagA protein in vitro and in vivo.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD38XitV2mtrg%3D&md5=c21bb56bc0c38d2b7789dec13bfd8d38CAS | 11788577PubMed |
[18] Tammer, I. et al. (2007) Activation of Abl by Helicobacter pylori: a novel kinase for CagA and crucial mediator of host cell scattering. Gastroenterology 132, 1309–1319.
| Activation of Abl by Helicobacter pylori: a novel kinase for CagA and crucial mediator of host cell scattering.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD2sXlslKrur0%3D&md5=7b6168457dd44422174777a68165671dCAS | 17408661PubMed |
[19] Argent, R.H. et al. (2005) Simple method for determination of the number of Helicobacter pylori CagA variable-region EPIYA tyrosine phosphorylation motifs by PCR. J. Clin. Microbiol. 43, 791–795.
| Simple method for determination of the number of Helicobacter pylori CagA variable-region EPIYA tyrosine phosphorylation motifs by PCR.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD2MXit1aqsLs%3D&md5=a571247b5d06e69195d873ac334bc35dCAS | 15695681PubMed |
[20] Nomura, A.M. et al. (2002) Relation between Helicobacter pylori cagA status and risk of peptic ulcer disease. Am. J. Epidemiol. 155, 1054–1059.
| Relation between Helicobacter pylori cagA status and risk of peptic ulcer disease.Crossref | GoogleScholarGoogle Scholar | 12034584PubMed |
[21] Schöttker, B. et al. (2012) Helicobacter pylori infection is strongly associated with gastric and duodenal ulcers in a large prospective study. Clin Gastroenterol. Hepatol. 10, 487–493.e481.
| Helicobacter pylori infection is strongly associated with gastric and duodenal ulcers in a large prospective study.Crossref | GoogleScholarGoogle Scholar | 22230167PubMed |
[22] Batista, S.A. et al. (2011) Higher number of Helicobacter pylori CagA EPIYA C phosphorylation sites increases the risk of gastric cancer, but not duodenal ulcer. BMC Microbiol. 11, 61.
| Higher number of Helicobacter pylori CagA EPIYA C phosphorylation sites increases the risk of gastric cancer, but not duodenal ulcer.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC3MXks1Kks70%3D&md5=aaaad74381f5e6ddff177f9563120defCAS | 21435255PubMed |
[23] Atherton, J.C. and Blaser, M.J. (2009) Coadaptation of Helicobacter pylori and humans: ancient history, modern implications. J. Clin. Invest. 119, 2475–2487.
| Coadaptation of Helicobacter pylori and humans: ancient history, modern implications.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD1MXhtFWgsrbI&md5=45f2b312983594efcb3f1f6fb84562b8CAS | 19729845PubMed |
[24] Atherton, J.C. et al. (1995) Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori. Association of specific vacA types with cytotoxin production and peptic ulceration. J. Biol. Chem. 270, 17771–17777.
| Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori. Association of specific vacA types with cytotoxin production and peptic ulceration.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DyaK2MXnt1Crt7Y%3D&md5=04005d2c14d6beedd190b9440f8dff2eCAS | 7629077PubMed |
[25] Lu, H. et al. (2005) Duodenal ulcer promoting gene of Helicobacter pylori. Gastroenterology 128, 833–848.
| Duodenal ulcer promoting gene of Helicobacter pylori.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD2MXjvV2qtrg%3D&md5=8fd37361cdc75e9050eb086d57ed9cc9CAS | 15825067PubMed |
[26] Arachchi, H.S. et al. (2007) Prevalence of duodenal ulcer-promoting gene (dupA) of Helicobacter pylori in patients with duodenal ulcer in North Indian population. Helicobacter 12, 591–597.
| Prevalence of duodenal ulcer-promoting gene (dupA) of Helicobacter pylori in patients with duodenal ulcer in North Indian population.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD1cXjs1SisA%3D%3D&md5=816927e83ca7acb90292e044693a586bCAS | 18001398PubMed |
[27] Hussein, N.R. et al. (2008) Differences in virulence markers between Helicobacter pylori strains from Iraq and those from Iran: potential importance of regional differences in H. pylori-associated disease. J. Clin. Microbiol. 46, 1774–1779.
| Differences in virulence markers between Helicobacter pylori strains from Iraq and those from Iran: potential importance of regional differences in H. pylori-associated disease.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD1cXmvV2mt7g%3D&md5=afc7e885bd2114845802cca008c46eafCAS | 18353934PubMed |
[28] Zhang, Z. et al. (2008) The Helicobacter pylori duodenal ulcer promoting gene, dupA in China. BMC Gastroenterol. 8, 49.
| The Helicobacter pylori duodenal ulcer promoting gene, dupA in China.Crossref | GoogleScholarGoogle Scholar | 18950522PubMed |
[29] Argent, R.H. et al. (2007) The presence of dupA in Helicobacter pylori is not significantly associated with duodenal ulceration in Belgium, South Africa, China, or North America. Clin. Infect. Dis. 45, 1204–1206.
| The presence of dupA in Helicobacter pylori is not significantly associated with duodenal ulceration in Belgium, South Africa, China, or North America.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD2sXht1ykt7jI&md5=2d5fadaceb61e8533fce36ea144e180cCAS | 17918084PubMed |
[30] Schmidt, H.M.A. et al. (2009) The prevalence of the duodenal ulcer promoting gene (dupA) in Helicobacter pylori isolates varies by ethnic group and is not universally associated with disease development: a case-control study. Gut Pathog 1, 5.
| The prevalence of the duodenal ulcer promoting gene (dupA) in Helicobacter pylori isolates varies by ethnic group and is not universally associated with disease development: a case-control study.Crossref | GoogleScholarGoogle Scholar |
[31] Jung, S.W. et al. (2012) The intact dupA cluster is a more reliable Helicobacter pylori virulence marker than dupA alone. Infect. Immun. 80, 381–387.
| The intact dupA cluster is a more reliable Helicobacter pylori virulence marker than dupA alone.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC38XktlGntQ%3D%3D&md5=87699ffdafe41a4c24f6f729e3135298CAS | 22038914PubMed |
[32] Wallace, J.L. (2008) Prostaglandins, NSAIDs, and gastric mucosal protection: why doesn’t the stomach digest itself? Physiol. Rev. 88, 1547–1565.
| Prostaglandins, NSAIDs, and gastric mucosal protection: why doesn’t the stomach digest itself?Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD1cXhtlGgtbbM&md5=5e53e9a68afb8face1d77317efeae79aCAS | 18923189PubMed |
[33] Wallace, J.L. et al. (1990) Gastric ulceration induced by nonsteroidal anti-inflammatory drugs is a neutrophil-dependent process. Am. J. Physiol. 259, G462–G467.
| 1:CAS:528:DyaK3cXlvVCns7c%3D&md5=b7d3bf6b3f2eeba43be4f34d5752c26aCAS | 2169206PubMed |
[34] Kelly, J.P. et al. (1996) Risk of aspirin-associated major upper-gastrointestinal bleeding with enteric-coated or buffered product. Lancet 348, 1413–1416.
| Risk of aspirin-associated major upper-gastrointestinal bleeding with enteric-coated or buffered product.Crossref | GoogleScholarGoogle Scholar | 1:STN:280:DyaK2s%2FptFKitg%3D%3D&md5=1b3f18fc585ec495a4a169d5f6353e93CAS | 8937281PubMed |
[35] Chan, F.K. et al. (2013) Effects of Helicobacter pylori infection on long-term risk of peptic ulcer bleeding in low-dose aspirin users. Gastroenterology 144, 528–535.
| Effects of Helicobacter pylori infection on long-term risk of peptic ulcer bleeding in low-dose aspirin users.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC3sXislyrsb4%3D&md5=6d356c0bb7937b96cb05df0181fab959CAS | 23333655PubMed |
[36] Tovey, F.I. et al. (2012) Dietary phosphilipids and sterols protective against peptic ulceration. Phytother Res: PTR.
[37] Eastwood, G.L. (1997) Is smoking still important in the pathogenesis of peptic ulcer disease? J. Clin. Gastroenterol. 25, S1–S7.
| Is smoking still important in the pathogenesis of peptic ulcer disease?Crossref | GoogleScholarGoogle Scholar | 9479620PubMed |
[38] Hofner, P. et al. (2007) Genetic polymorphisms of NOD1 and IL-8, but not polymorphisms of TLR4 genes, are associated with Helicobacter pylori-induced duodenal ulcer and gastritis. Helicobacter 12, 124–131.
| Genetic polymorphisms of NOD1 and IL-8, but not polymorphisms of TLR4 genes, are associated with Helicobacter pylori-induced duodenal ulcer and gastritis.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BD2sXjvFKqtL0%3D&md5=99acd21b00e22dca854a823e7d2c5800CAS | 17309748PubMed |
[39] Musumba, C.O. et al. (2013) CYP2C19*17 gain-of-function polymorphism is associated with peptic ulcer disease. Clin. Pharmacol. Ther. 93, 195–203.
| CYP2C19*17 gain-of-function polymorphism is associated with peptic ulcer disease.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC3sXhsVars70%3D&md5=af29633dd1b05ea16292da0fc25f4fa2CAS | 23267857PubMed |
[40] Yin, Y.W. et al. (2013) Association between interleukin-8 gene-251 T/A polymorphism and the risk of peptic ulcer disease: a meta-analysis. Hum. Immunol. 74, 125–130.
| Association between interleukin-8 gene-251 T/A polymorphism and the risk of peptic ulcer disease: a meta-analysis.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC38XhsFGjtrjN&md5=9bc9807af34f39dc3dfdd6df7e87869bCAS | 23000201PubMed |
[41] Yang, C.A. et al. (2013) A frequent Toll-like receptor 1 gene polymorphism affects NK- and T-cell IFN-γ production and is associated with Helicobacter pylori-induced gastric disease. Helicobacter 18, 13–21.
| A frequent Toll-like receptor 1 gene polymorphism affects NK- and T-cell IFN-γ production and is associated with Helicobacter pylori-induced gastric disease.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC3sXotl2kug%3D%3D&md5=a8dde51c9bd4b977b8d90eb21f2dc2edCAS | 23067142PubMed |
[42] Zhang, B.B. et al. (2012) No association between IL-1beta -511 C/T polymorphism and the risk of duodenal ulcer: a meta-analysis of 4667 subjects. Gene 506, 188–194.
| No association between IL-1beta -511 C/T polymorphism and the risk of duodenal ulcer: a meta-analysis of 4667 subjects.Crossref | GoogleScholarGoogle Scholar | 1:CAS:528:DC%2BC38XhtVKnt7jO&md5=e29416827b1096ee50d78ac527f3af58CAS | 22759516PubMed |