Effects of Eradication ofHelicobacter pylorion Gastritis in Duodenal Ulcer Patients

Abstract

of eradication of Helicobacter pylori on gastritis in duodenal ulcer patients. Scand J Gastroenterol 1994;29 Suppl 201:28-34. The incidence and mean score of Helicobacter pylori-related, active antroduodenitis, lesions of superficial antral epithelium and duodenal gastric-type metaplasia were higher in endoscopic biopsies from a large series of patients with duodenal ulcer, when compared with asymptomatic patients or patients with nonulcer dyspepsia. In 65 out of 73 patients with duodenal ulcer who could be followed up, H. pylori was eradicated using a combination of amoxycillin, 3 g daily, metronidazole, 1 g daily, and omeprazole, 20 mg daily. Rapid and permanent (6-month follow-up) abolition of both gastroduodenitis activity and lesions of the gastric surface epithelium was observed in these 65 patients. There was also a progressive decrease in total immune-inflammatory cells but without a substantial change in duodenal gastric-type metaplasia. Similar, but transient and quantitatively less prominent, improvements were observed in the antroduodenal mucosa, which had been temporarily cleared of H. pylori by treatment with omeprazole alone. Conversely, increased gastritis activity, epithelial lesions and immune-inflammatory cell scores were found in the short term in the corpus mucosa. which was not cleared of H. pylori after omeprazole treatment. It is concluded that, of the various H. pylori-related mucosal changes, antroduodenitis activity and antral epithelial lesions most closely reflect the severity of mucosal damage and are probably the most important factors in duodenal ulcerogenesis. Their complete and rapid suppression after bacterial eradication may be a key factor in preventing ulcer relapse. Scand J Gastroenterol Downloaded from informahealthcare.com by Indiana University on 12/13/14 For personal use only. Scand J Gastroenterol Downloaded from informahealthcare.com by Indiana University on 12/13/14 For personal use only. 27. R i b V, Sommi P, Fiocca R, et al. Cytotoxicity of Helicobacter pylon on human gastric epithelial cells in vitro: role of cytotoxin(s) and ammonia. Eur J Gastroenterol Hepatol1993;5:687-94. Scand J Gastroenterol Downloaded from informahealthcare.com by Indiana University on 12/13/14 For personal use only.

Prevention of ulcer recurrence after eradication of Helicobacter pylori: A prospective long-term follow-up study

“…Recrudesrelating to the current H. pylori status. 18,22,23 Furthercence of H. pylori infection was likely in 6 of 7 patients more, patients should only be included in ulcer-relapse (identical DNA pattern pre-eradication and posteradicafollow-up studies after endoscopic proof of healing of the tion). Reoccurrence of H. pylori infection in 1 patient initial ulcer.…”

Pathogenesis of duodenal ulcer disease: the rest of the story

“…49 For example, gastric metaplasia in the duodenum can easily be induced in animals by acid produced in response to repeated injections of gastrin 50 , is extensive in patients with Zollinger±Ellison syndrome 51 , and is markedly uncommon in patients with achlorhydria. 52 The prevalence of gastric metaplasia is increased in patients with duodenal ulcer disease 53 and decreases after acid-lowering operations for this condition 54 , suggesting that the process is reversible, albeit slowly. The initial description of the growth of H. pylori described how it was inhibited by bile.…”

Analysis of Gastroduodenitis and Oesophagitis in Relation to Dyspeptic/Reflux Symptoms

“…In gastric biopsies H. pylori colonisation, neutrophilic granulocytes (gastritis activity) or mononuclear cell infiltration and gland atrophy were evaluated on a four-step scale (0-3), in accordance with the Sydney system [27]. A similar procedure was used for the scoring of H. pylori-related cytotoxic/degenerative lesions of gastric surface foveolar epithelium [28], and of H. pylori, granulocytes, mononuclear cells and gastric-type metaplasia in the duodenal mucosa [29,30]. All histologic evaluations were blind with respect to the symptoms recorded and the endoscopic findings.…”