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(31) Twelve of these children received previous antibiotic therapy for various reasons, with possible inadvertent effects on the diagnosis of H pylori.

(32) However, acid secretion in old subjects without atrophy was not different to that in young subjects, irrespective of H pylori status.

(33) These differences persisted when subgroups of patients were analysed according to Helicobacter pylori colonisation or degree of mucosal injury.

(34) Endoscopy in the nine H pylori positive non-uraemic patients showed oesophagitis in one patient and active duodenal ulcer in another.

(35) In healthy men without atrophy, gastric acid secretion is preserved with ageing and is independent of H pylori status.

(36) Further studies are needed to clarify the presence of H pylori in saliva or plaque, and also in faeces.

(37) It has previously been reported that H pylori infection raises serum pepsinogen I in non-uraemic patients but only by about 25%.

(38) Similarly our study found a strong association between dyspepsia and colonisation by Helicobacter pylori in patients taking NSAIDs.

(39) In the present study we also analysed the relation between active H pylori infection and serum pepsinogen-I and pepsinogen-II concentrations.

(40) We conclude from this study that H pylori eradication enhances gastric juice ascorbate secretion, and thus increases intragastric anti-oxidant protection.

(41) Activated pepsinogen was significantly reduced in the stomach of H pylori positive patients only.

(42) Decreased concentrations of activated pepsinogen were found in H pylori positive patients only. Duodenal biopsies were tested in 76 patients.

(43) H pylori has variable effects on serum gastrin concentrations and gastric acid secretion.

(44) Patients classified as having H pylori infection received an eradication regimen; 107 were reassessed 4 weeks after therapy.

(45) Helicobacter pylori increases plasma gastrin concentrations by 50% to 100% and values fall to normal after the organism has been eradicated.

(46) The mechanism by which H pylori infection stimulates the release of G17 is not known.

(47) The strong association between antral tumours and chronic active gastritis suggests the possibility that H pylori infection may have a pathogenic role.

(48) Demanding oral triple therapy eradicates H pylori in up to 96% of patients treated but does have considerable side effects.

(49) This led us to ask if there was intrafamilial spread of H pylori.

(50) Can gastric juice ascorbic acid secretion be restored by eradication of H pylori?

(51) H pylori positive gastritis, and the combination of active duodenitis and gastric metaplasia were independent predictors of duodenal ulceration.

(52) The finding of enhanced fasting gastrin concentrations in H pylori positive subjects and in duodenal ulcer disease can not easily be explained.

(53) These tests have been shown to be reliable in detecting H pylori infection in patients with and without renal failure.

(54) Decreased concentrations of activated pepsinogen were found in H pylori positive patients only.sentencedict.com/pylori.html

(55) Helicobacter pylori also tended to increase thromboxane B 2 synthesis although this was not statistically significant.

(56) In the nine H pylori negative non-uraemic patients, one had erosive duodenitis and another a deformed duodenum.

(57) Although H pylori does not invade the mucosa, bacterial proteins may activate monocytes with a local T-cell mediated immune response.

(58) In healthy volunteers, H pylori state was determined by the C urea breath test.

(59) In addition, H pylori eradication speeds up ulcer healing and is associated with healing of previously refractory ulcers.

(60) Thus, in addition to duodenal ulcer disease, H pylori eradication may also cure gastric ulcer disease.