Recent progress in the area of ulcer and gastritis is still dominated by findings and reports on Helicobacter pylori and nonsteroidal anti-inflammatory drugs, which in turn are the two major causes of peptic ulcers. Although the prevalence of H. pylori is declining in most developed countries, it is still contributing to a significant proportion of peptic ulcers globally. The interrelationship of H. pylori gastritis in patients with gastroesophageal reflux has become more apparent. H. pylori-induced gastric body gastritis is associated with reduced acid production, and thus with reduced reflux and esophagitis. The controversies regarding the interactions between H. pylori and NSAIDs have still not been settled. With the availability of the new COX-2-specific inhibitors, the current scenario of NSAID-related gastroduodenal complications will certainly change. Short-term usage of these agents has significantly reduced the incidence of endoscopic ulcers, but the benefits in terms of clinical outcomes, such as bleeding or perforation, remain to be determined. This review summarizes the recent literature on peptic ulcer and gastritis.
References
1
Vaira D, Malfertheiner P, Megraud F, et al.
Diagnosis of Helicobacter pylori infection with a new non-invasive antigen-based assay. HpSA European Study Group.
Lancet.
1999;
354
30-33
4
Rinaldi V, Zullo A, de Francesco V, et al.
Helicobacter pylori eradication with proton pump inhibitor-based triple therapies and re-treatment with ranitidine bismuth citrate-based triple therapy.
Aliment Pharmacol Ther.
1999;
13
163-168
5
Lee J M, Breslin N P, Hyde D K, et al.
Treatment options for Helicobacter pylori infection when proton pump inhibitor-based triple therapy fails in clinical practice.
Aliment Pharmacol Ther.
1999;
13
489-496
6
Perri F, Festa V, Clemente R, et al.
Rifabutin-based “rescue therapy” for Helicobacter pylori infected patients after failure of standard regimens.
Aliment Pharmacol Ther.
2000;
14
311-316
8
Yamaoka Y, Kodama T, Gutierrez O, et al.
Relationship between Helicobacter pylori iceA, cagA, and vacA status and clinical outcome: studies in four different countries.
J Clin Microbiol.
1999;
37
2274-2279
9
Yamaoka Y, Kodama T, Kita M, et al.
Relation between clinical presentation, Helicobacter pylori density, interleukin-1β and 8 production, and cagA status.
Gut.
1999;
45
804-811
10
Graham D Y, Osato M S.
H. pylori in the pathogenesis of duodenal ulcer: interaction between duodenal acid load, bile, and H. pylori.
Am J Gastroenterol.
2000;
95
87-91
11
Bodger K, Eastwood P G, Manning S I, et al.
Dyspepsia workload in urban general practice and implications of the British Society of Gastroenterology Dyspepsia guidelines (1996).
Aliment Pharmacol Ther.
2000;
14
413-420
12
Blum A L, Talley N J, O'Morain C, et al.
Lack of effect of treating Helicobacter pylori infection in patients with nonulcer dyspepsia: omeprazole plus clarithromycin and amoxicillin effect one year after treatment (OCAY) study group.
N Engl J Med.
1998;
339
1875-1881
13
Talley N J, Vakil N, Ballard ED I I, Fennerty M B.
Absence of benefit of eradicating Helicobacter pylori in patients with nonulcer dyspepsia.
N Engl J Med.
1999;
341
1106-1111
14
McColl K, Murray L, el-Omar E, et al.
Symptomatic benefit from eradicating Helicobacter pylori infection in patients with nonulcer dyspepsia.
N Engl J Med.
1998;
339
1869-1874
15
Jaakkimainen R L, Boyle E, Tudiver F.
Is Helicobacter pylori associated with non-ulcer dyspepsia and will eradication improve symptoms? A meta-analysis.
Br Med J.
1999;
319
1040-1044
16
Miwa H, Hirai S, Nagahara A, et al.
Cure of Helicobacter pylori infection does not improve symptoms in non-ulcer dyspepsia patients: a double-blind placebo-controlled study.
Aliment Pharmacol Ther.
2000;
14
317-324
17
Moayyedi P, Feltbower R, Brown J, et al.
Effect of population screening and treatment for Helicobacter pylori on dyspepsia and quality of life in the community: a randomised controlled trial. Leeds HELP Study Group.
Lancet.
2000;
355
1665-1669
18
Moayyedi P, Forman D, Braunholtz D, et al.
The proportion of upper gastrointestinal symptoms in the community associated with Helicobacter pylori, lifestyle factors, and nonsteroidal anti-inflammatory drugs. Leeds HELP Study Group.
Am J Gastroenterol.
2000;
95
1448-1455
20
Heaney A, Collins J S, Watson R G, et al.
A prospective randomised trial of a “test and treat” policy versus endoscopy based management in young Helicobacter pylori positive patients with ulcer-like dyspepsia, referred to a hospital clinic.
Gut.
1999;
45
186-190
21
Lassen A T, Pedersen F M, Bytzer P, et al.
Helicobacter pylori test-and-eradicate versus prompt endoscopy for management of dyspeptic patients: a randomised trial.
Lancet.
2000;
356
455-460
23
Ciociola A A, McSorley D J, Turner K, et al.
Helicobacter pylori infection rates in duodenal ulcer patients in the United States may be lower than previously estimated.
Am J Gastroenterol.
1999;
94
1834-1840
24
Lee J M, Breslin N P, Fallon C, O'Morain C A.
Rapid urease tests lack sensitivity in Helicobacter pylori diagnosis when peptic ulcer disease presents with bleeding.
Am J Gastroenterol.
2000;
95
1166-1170
25
Tu T C, Lee C L, Wu C H, et al.
Comparison of invasive and noninvasive tests for detecting Helicobacter pylori infection in bleeding peptic ulcers.
Gastrointest Endosc.
1999;
49
302-306
26
Graham D Y, Genta R, Evans D G, et al.
Helicobacter pylori does not migrate from the antrum to the corpus in response to omeprazole.
Am J Gastroenterol.
1996;
91
2120-2124
27
Sung J J, Lin S R, Ching J Y, et al.
Atrophy and intestinal metaplasia one year after cure of H. pylori infection: a prospective, randomized study.
Gastroenterology.
2000;
119
7-14
28
Nardone G, Staibano S, Rocco A, et al.
Effect of Helicobacter pylori infection and its eradication on cell proliferation, DNA status, and oncogene expression in patients with chronic gastritis.
Gut.
1999;
44
789-799
29
El-Zimaity H M, Graham D Y.
Evaluation of gastric mucosal biopsy site and number for identification of Helicobacter pylori or intestinal metaplasia: role of the Sydney System.
Hum Pathol.
1999;
3
72-77
30
Kuipers E J, Lundell L, Klinkenberg-Knol E C, et al.
Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication.
N Engl J Med.
1996;
334
1018-1022
32
Schenk B E, Kuipers E J, Nelis G F, et al.
Effect of Helicobacter pylori eradication on chronic gastritis during omeprazole therapy.
Gut.
2000;
46
615-621
34
Meining A, Kiel G, Stolte M.
Changes in Helicobacter pylori-induced gastritis in the antrum and corpus during and after 12 months of treatment with ranitidine and lansoprazole in patients with duodenal ulcer disease.
Aliment Pharmacol Ther.
1998;
12
735-740
36
Klinkenberg-Knol E C, Festen H P, Jansen J B, et al.
Long-term treatment with omeprazole for refractory reflux esophagitis: efficacy and safety.
Ann Intern Med.
1994;
121
161-167
37
Meining A, Bosseckert H, Caspary W F, et al.
H2-receptor antagonists and antacids have an aggravating effect on Helicobacter pylori gastritis in duodenal ulcer patients.
Aliment Pharmacol Ther.
1997;
11
729-734
41
Aalykke C, Lauritsen J M, Hallas J, et al.
Helicobacter pylori and risk of ulcer bleeding among users of nonsteroidal anti-inflammatory drugs: a case-control study.
Gastroenterology.
1999;
116
1305-1309
42
Santolaria S, Lanas A, Benito R, et al.
Helicobacter pylori infection is a protective factor for bleeding gastric ulcers but not for bleeding duodenal ulcers in NSAID users.
Aliment Pharmacol Ther.
1999;
13
1511-1518
43
Ng T M, Fock K M, Khor J L, et al.
Non-steroidal anti-inflammatory drugs, Helicobacter pylori and bleeding gastric ulcer.
Aliment Pharmacol Ther.
2000;
14
203-209
45
Cryer B, Feldman M.
Effects of very low dose daily, long-term aspirin therapy on gastric, duodenal, and rectal prostaglandin levels and on mucosal injury in healthy humans.
Gastroenterology.
1999;
117
17-25
47
Dutch TIA Trial Study G roup.
A comparison of two doses of aspirin (30 mg vs. 283 mg a day) in patients after a transient ischemic attack or minor ischemic stroke.
N Engl J Med.
1991;
325
1261-1266
48
Kallmann R, Nieuwenhuis H K, de Groot P G, et al.
Effects of low doses of aspirin, 10 mg and 30 mg daily, on bleeding time, thromboxane production and 6-keto-PGF1 alpha excretion in healthy subjects.
Thromb Res.
1987;
45
355-361
49
Hoffmann W, Nitschke M, Muche J, et al.
Reevaluation of the Cottbus Reinfarction Study with 30 mg aspirin per day 4 years after the end of the study.
Prostaglandins Leukot Essent Fatty Acids.
1991;
42
137-139
51
Muller P, Dammann H G, Marinis E, Simon B.
Gastrointestinal tolerance of 30 mg versus 300 mg acetylsalicylic acid daily: an endoscopically controlled double-blind study of healthy subjects.
Med Klin.
1990;
85
429-431
53
Simon L S, Weaver A L, Graham D Y, et al.
Anti-inflammatory and upper gastrointestinal effects of celecoxib in rheumatoid arthritis: a randomized controlled trial.
JAMA.
1999;
282
1921-1928
54
Laine L, Harper S, Simon T, et al.
A randomized trial comparing the effect of rofecoxib, a cyclooxygenase 2-specific inhibitor, with that of ibuprofen on the gastroduodenal mucosa of patients with osteoarthritis. Rofecoxib Osteoarthritis Endoscopy Study Group.
Gastroenterology.
1999;
117
776-783
55
Hawkey C, Laine L, Simon T, et al.
Comparison of the effect of rofecoxib (a cyclooxygenase-2 inhibitor), ibuprofen, and placebo on the gastroduodenal mucosa of patients with osteoarthritis: a randomized, double-blind, placebo-controlled trial. The Rofecoxib Osteoarthritis Endoscopy Multinational Study Group.
Arthritis Rheum.
2000;
43
370-377