pylori造句
(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./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.
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