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At least 109 records · Page 6Linked to original sources
PubMed1998

Helicobacter pylori colonization density and gastric acid output in non-ulcer dyspepsia and duodenal ulcer disease.

BACKGROUND: The pattern of intragastric Helicobacter pylori colonization and its density may be determined by parietal cell function. H. pylori bacterial products can inhibit gastric acid secretion from the parietal cell. The aim of this investigation was to study the relationship between acid output and intragastric H. pylori distribution and colonization density in duodenal ulcer (DU) and non-ulcer subjects. The study included 14 patients with active DU, 10 with inactive DU and 10 non-ulcer dyspeptics. METHODS: Acid output studies in response to fasting and maximal pentagastrin stimulation, basal (BAO) and peak (PAO) acid outputs were calculated. A quantitative assessment of H. pylori colonization density in biopsies from five sites of the gastroduodenum in the active ulcer group, and from the antrum in inactive duodenal ulcer and non-ulcer groups. RESULTS: There were negative correlations between total gastroduodenal bacterial colonization density and, PAO (r - 0.87, p = 0.0025) and BAO (r - 0.635, p < 0.02) in the active ulcer group. There were negative correlations between antral H. pylori colonization density and PAO in the active duodenal ulcer (r - 0.7449, p < 0.01) and non-ulcer (r - 0.5837, p < 0.1) groups but not in the inactive duodenal ulcer group (r - 0.1869, p > 0.2). CONCLUSIONS: An equilibrium is reached between gastroduodenal H. pylori colonization density and gastric acid secretory capacity in active duodenal ulcer disease. It is hypothesized that thresholds of bacterial load and acid secretory capacity, in combination, are required for active ulceration in DU disease.

Adult↗
PubMed2002

Esophageal ulceration activates keratinocyte growth factor and its receptor in rats: implications for ulcer healing.

BACKGROUND & AIMS: Cellular and molecular mechanisms of esophageal ulcer healing remain unexplored. We studied the sequential cellular events and the expression of keratinocyte growth factor (KGF) and its receptor (KGF-R) during the healing of experimental esophageal ulcers. METHODS: Esophageal ulcers were produced in rats by local application of acetic acid. Studies included (1) ulcer size, (2) quantitative histology, and (3) KGF and KGF-R messenger RNA and protein expression by reverse-transcription polymerase chain reaction, Western blotting, and immunostaining. In separate groups, ulcer size and esophageal epithelial proliferation were evaluated after a single injection of recombinant human KGF (1 mg/kg) around the ulcer. RESULTS: Ulcers were fully developed 3 days after induction, and 58% of ulcers were re-epithelialized by 9 days. At 3 days, in esophageal tissue bordering the ulcers, KGF messenger RNA and protein were increased by 191% and 151%, respectively, and KGF-R messenger RNA and protein were increased by 357% and 237%, respectively. KGF was expressed in stromal cells, whereas KGF-R was expressed in epithelial cells. At 6 days, epithelial proliferation at the ulcer margin was increased by 216%, and treatment with KGF further enhanced cell proliferation and accelerated ulcer healing. CONCLUSIONS: KGF is a likely mediator of esophageal epithelial proliferation and ulcer healing.

Animals↗
PubMed2006

Granulocyte/macrophage colony-stimulating factor treatment of human chronic ulcers promotes angiogenesis associated with de novo vascular endothelial growth factor transcription in the ulcer bed.

Summary Background Granulocyte/macrophage colony-stimulating factor (GM-CSF), a cytokine with pleiotropic functions, has been successfully employed in the treatment of chronic skin ulcers. The biological effects underlying GM-CSF action in impaired wound healing have been only partly clarified. Objectives To investigate the effects of GM-CSF treatment of chronic venous ulcers on lesion vascularization and on the local synthesis of the angiogenic factors vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF). Methods Patients with nonhealing venous leg ulcers were treated with intradermal injection of recombinant human GM-CSF, and biopsies were taken at the ulcer margin before and 5 days after administration. Wound vascularization was analysed by immunohistochemistry using antiplatelet endothelial cell adhesion molecule-1/CD31 and anti-alpha-smooth muscle actin antibodies. VEGF and PlGF transcription was assessed by in situ hybridization. To identify the cell populations transcribing VEGF within the ulcer bed, the VEGF hybridization signal was correlated with the immunostaining for different cell type markers on serial sections. Direct induction of VEGF transcription by GM-CSF was investigated in GM-CSF-treated cultured macrophages and keratinocytes. Results Blood vessel density was significantly increased in the ulcer bed following GM-CSF treatment. VEGF transcripts were localized in keratinocytes at the ulcer margin both before and after GM-CSF treatment, whereas a VEGF hybridization signal was evident within the ulcer bed only following administration. PlGF mRNA was barely detectable in keratinocytes at the ulcer margin and was not visibly increased after treatment. Unlike VEGF, a specific PlGF hybridization signal could not be detected in cells within the ulcer following GM-CSF administration. Monocytes/macrophages were the main cell population transcribing VEGF after GM-CSF treatment. In vitro analysis demonstrated that VEGF transcription can be directly stimulated by GM-CSF in a differentiated monocytic cell line, but not in keratinocytes. Conclusions Our data show that increased vascularization is associated with GM-CSF treatment of chronic venous ulcers and indicate that inflammatory cell-derived VEGF may act as an angiogenic mediator of the healing effect of GM-CSF in chronic ulcers.

Adult↗
PubMed1988

Risk factors for healing of duodenal ulcer under antacid treatment: do ulcer patients need individual treatment?

In order to identify the risk factors affecting the healing of duodenal ulcer, a clinical trial with effective dose of antacid was carried out in 53 patients. Duration of ulcer history, number of relapses, duration of the last and present relapse, number, duration and severity of pain attacks in the present ulcer relapse, pain radiation to back, vomiting, appetite, smoking habit, intake of analgesics and previous haemorrhage were registered. Number of ulcers, ulcer depth, bublar narrowing, erosions, duodenitis at initial endoscopy and healing of ulcer were assessed by one endoscopist. Basic and peak acid output were measured. The extent of duodenitis on the site opposite the ulcer was determined by histological examination. Sixty per cent of the duodenal ulcers were healed after three weeks. By univariate analysis, the following factors affect the healing; pain radiation to back and pain duration during treatment (p less than 0.001), multiple or deep ulcers, narrowing of duodenal bulb (p less than 0.01), number of pain attacks and poor appetite (p less than 0.05). By the stepwise logistic regression model, the following factors were selected as predictors for healing of duodenal ulcer with 76% correct classification: pain radiation to back (p = 0.002), deep ulcer (p = 0.013), multiple ulcers (p = 0.028). Number of cigarettes/day (p less than 0.007) and male sex (p = 0.036). By this model, the prediction of healing could be accurately assessed in 78% in a new sample. Individual treatment should be carried out on the basis of these factors.

Aluminum Hydroxide↗
PubMed1991

Circadian pattern of intragastric acidity in duodenal ulcer patients: a study of variations in relation to ulcer activity.

The relation between intragastric acidity and duodenal ulcer activity was studied prospectively in 21 patients with endoscopically proved duodenal ulcers. The 24 hour intragastric acidity was measured on four separate occasions by continuous recording using combined glass electrodes: (a) in the presence of an ulcer crater without treatment; (b) during active ulceration being treated with ranitidine; (c) during early healing after a six week course of ranitidine; (d) during late healing six months after acute ulceration. Intragastric acidity was also monitored in 20 healthy subjects. At all stages of ulcer activity and during all predefined time periods, duodenal ulcer patients had significantly higher gastric acidity than healthy control subjects. Duodenal ulcer patients showed a similar circadian pattern of intragastric acidity during exacerbation of ulcer disease and in remission during the early and late ulcer healing periods. These results argue against a direct relation between the activity of duodenal ulcer disease and gastric acidity. It is concluded that the chronic recurrent course of duodenal ulcer disease does not result from a fluctuation in intragastric acidity.

Acute Disease↗