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Background: It is 40 years since the discovery of Helicobacter pylori infection. Over that time major changes have occurred in esophagogastroduodenoscopy (EGD) findings. The aim of this review is to describe these changes, and the important role H. pylori infection has played in their evolution., Methods: References were identified through searches of PubMed using the search terms-endoscopy time trends, peptic ulcer disease, gastroesophageal reflux disease, upper gastrointestinal cancer, gastric polyps, H. pylori, eosinophilic gastrointestinal disorders, and celiac disease, from 1970 through December 2021., Results: The prevalence of H. pylori infection has fallen and consequently, H. pylori-positive peptic ulcer disease has become rare. Gastroesophageal reflux disease is now the commonest disorder diagnosed at EGD, and Barrett's esophagus has increased in parallel. Cancer of the distal stomach has fallen while esophageal adenocarcinoma and reflux-related cardia cancer have risen. Gastric polyps have changed from hyperplastic and adenomas to sporadic fundic gland polyps. Antimicrobial resistance has made H. pylori infection more difficult to eradicate. Eosinophilic gastrointestinal disorders, particularly eosinophilic esophagitis, have emerged as important new allergic disorders. Celiac disease has changed and increased., Conclusions: EGD findings appear to have changed from features suggesting a H. pylori-positive "phenotype" 40 years ago to a H. pylori-negative "phenotype" today. These changes have major implications for the management of gastrointestinal disorders., (© 2023 John Wiley & Sons Ltd.)

Background/aims: There have been recent reports of reflux esophagitis apparently occurring de novo after cure of H. pylori in peptic ulcer disease. The possibility that this phenomenon might be explained, at least in part, by unmasking of coexistent disease has not been assessed. The aim of this study was to assess the prevalence of esophagitis in H. pylori-positive peptic ulcer disease and examine the short-term impact of H. pylori therapy on the esophagus., Methodology: Esophagitis was systematically graded and the presence of hiatal hernia was noted in 244 peptic ulcer patients (duodenal 223; gastric 21) before and at least four weeks after triple therapy. H. pylori status was assessed using CLO test and histology, and esophagitis grade was assigned without knowledge of H. pylori status., Results: Of the 244 patients, 49 (20%) had esophagitis which was grade 2 or more in over two-thirds. The prevalence of esophagitis was similar in duodenal and gastric ulcer patients. The presence of hiatal hernia was strongly associated with the finding of esophagitis (P < 0.001). Of 241 patients evaluable after therapy, 215 (89%) were H. pylori-negative and 26 remained H. pylori-positive. Esophagitis tended to improve or remain stable after H. pylori therapy and worsened in only 2 of the 49 patients (4%). Of 192 patients with a normal esophagus at baseline endoscopy, 14 (7%) showed evidence of esophagitis after therapy. The presence of hiatal hernia, but not cure of H. pylori, was significantly associated with the development of esophagitis., Conclusions: Our results indicate that esophagitis can coexist with peptic ulcer disease and persists after cure of H. pylori. Development of de novo esophagitis seems uncommon in the short-term after H. pylori therapy. Esophagitis in peptic ulcer disease is strongly associated with the presence of hiatal hernia.

Background: The longterm outlook after Helicobacter pylori (H. pylori) eradication in peptic ulcer disease is unclear., Aim: This study documents H. pylori recurrence, dyspeptic symptoms and anti-secretory therapy in peptic ulcer patients six years or more after H. pylori eradication., Methods: Peptic ulcer patients with H. pylori eradication between 1990 and 1992 were included. Infection recurrence was diagnosed by 13-carbon urea breath test (UBT). Dyspeptic symptoms and anti-secretory therapy use were assessed by questionnaire., Results: Sixty-one patients completed the study protocol. Mean follow-up after eradication was 6.1 years (range 4.8-8.3). Four patients had a positive UBT. H. pylori recurrence rate was 6.6% or 0.02% per patient per year. Forty-two patients (69%) had dyspeptic symptoms. Heartburn and belching were more common than pain (p<0.001). All four patients with H. pylori recurrence had symptoms compared with 38 of 57 H. pylori-negative patients (p>0.05). Ten of 61 patients (16.4%) were taking anti-secretory therapy and their dyspepsia scores were higher., Conclusions: Despite a low H. pylori recurrence rate, longterm dyspeptic symptoms were common in peptic ulcer patients after H. pylori eradication. The symptoms are mainly reflux in type and require anti-secretory therapy in only a minority of patients.

In a prospective study designed to assess the effect of Helicobacter pylori eradication on peptic ulcer healing, 85 consecutive patients with H. pylori-positive peptic ulcer disease were treated with a triple therapy regimen consisting of colloidal bismuth subcitrate 120 mg four times daily for 28 days, with metronidazole 400 mg three times daily and tetracycline 500 mg three times daily for the first seven days of treatment. H. pylori status was assessed by CLO test and histology at least four weeks after completing therapy. Of 75 patients (88%) H. pylori-negative after therapy, 69 (92%) had healed ulcers compared with only five of 10 patients (50%) who remained H. pylori-positive (p = 0.003). Cigarette smoking had no significant effect on ulcer healing. Our results suggest that H. pylori eradication may accelerate ulcer healing and provide further evidence that an effective helicobactericidal regimen is the treatment of choice in H. pylori-positive peptic ulcer.

There is now a persuasive body of evidence linking Helicobacter pylori infection and peptic ulcer disease. Over 90% of duodenal ulcer and 70% of gastric ulcer patients are infected with H. pylori. Only a minority of infected patients develop ulcers, however, and host cofactors, rather than H. pylori strain, are probably critical to the development of peptic ulcer in infected individuals. Conversely, not all ulcers are associated with H. pylori, and in these cases enterogastric reflux and non-steroidal anti-inflammatory drug ingestion may be important. Eradication of H. pylori dramatically reduces ulcer relapse, effectively curing the disease. Eradication may also accelerate duodenal ulcer healing. Triple therapy with bismuth and antibiotics is effective against H. pylori, but there are problems with side effects, compliance and antibiotic resistance. Encouraging results are emerging on the efficacy and safety of omeprazole/antibiotic combination therapy, and this novel approach to H. pylori eradication is an exciting development. H. pylori has established itself as a pivotal factor in peptic ulcer disease and an effective helicobactericidal regimen is now the most rational and cost-effective treatment.

This review presents a critical evaluation of the role of Helicobacter pylori eradication in the management of peptic ulcer disease and non-ulcer dyspepsia. On current evidence, H. pylori eradication therapy seems likely to emerge as the most rational and cost-effective treatment for duodenal ulcer. The role of H. pylori eradication in the treatment of gastric ulcer and non-ulcer dyspepsia is unclear and requires further study. The emerging problem of antibiotic resistance in H. pylori is of major clinical importance and a prime cause of treatment failure. There is increasing evidence of a link between H. pylori and gastric cancer but it is premature to recommend large-scale eradication of H. pylori as a valid strategy for the primary prevention of gastric cancer. The search continues for the ideal H. pylori eradication regimen.