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At least 19 recordsLinked to original sources

A prospective comparative study of clinical and pathological characteristics in Icelandic and Danish patients with gastric ulcer, duodenal ulcer, and X-ray negative dyspepsia. II. Histological results.

The occurrence of gastritis in antral and body mucosa is compared in an Icelandic and a Danish group of patients with gastric ulcer, duodenal ulcer, and X-ray negative dyspepsia. In all 93 Icelandic and 88 Danish patients were examined. All signs of antral gastritis were more frequent in Icelandic than in Danish patients, but only the incidence of superficial inflammation and decreased mucus content in surface and crypt epithelium differed significantly. In body mucosa pseudopyloric metaplasia was more frequent in Iceland and occurred equally freqeuntly in all three diseases. A statistically significant correlation was found between macroscopic gastritis and occurrence of antral superficial inflammation and between smoking and superficial inflammation and decreased mucus content in the pyloric biopsy specimen. The presence of histological gastritis was not correlated to the intake of alcohol and salicylic acid, nor to the presence of pain at the time of investigation.

Adult↗

A prospective comparative study of clinical and histological characteristics in Icelandic and Danish patients with gastric ulcer, duodenal ulcer, and X-ray negative dyspepsia. I. Design and clinical features.

Iceland (IS) and Denmark (DK) are ethnically, culturally, and economically closely related Nordic countries, but gastric cancer is much more frequent in Iceland, and other differences in the occurrence rates of gastric diseases are also suspected. Therefore a cooperative study was initiated comparing Icelandic and Danish patients with gastric ulcer (GU), duodenal ulcer (DU), and X-ray negative dyspepsia (XND) as regards clinical features, external factors of possible importance for gastritis and cancer, gastroscopic appearance, and histological gastric mucosal changes. The project lasted one year and comprised 93 Icelandic and 88 Danish patients. A large number of comparisons showed a high degree of similarity between Icelandic and Danish patients. Significant differences were found in tobacco consumption (DK greater than IS), duration of symptoms in XND (IS greater than DK), whereas the positon ratio of GU (IS less than DK) and acetylsalicylic acid consumption (DK greater than IS) showed non-significant trends. Significant difference was found between the occurrence of diffuse macroscopic changes of the gastric mucosa (IS greater than DK), which corresponds to the histological differences to be described in a subsequent article.

Adolescent↗

Refractory duodenal ulcers (nonhealing duodenal ulcers with standard doses of antisecretory medication).

To evaluate possible differences between patients with refractory duodenal ulcers and those with duodenal ulcers that respond to standard doses of antisecretory medications, we determined basal acid outputs by nasogastric suction and daily smoking histories in 75 patients with endoscopically documented active duodenal ulcers. Patients were treated for at least eight weeks with standard doses of antisecretory medications and endoscopic healing or nonhealing was documented. Fifty-five patients that had complete healing of their duodenal ulcers had a mean basal acid output of 6.6 +/- 5.3 meq/hr, and 18/55 had daily cigarette smoking histories, whereas 20 patients that had nonhealing duodenal ulcers had a mean basal acid output of 20.0 +/- 9.6 meq/hr, and 8/20 had daily cigarette smoking histories. There were no significant differences between the two groups with regard to age, duodenal ulcer size, or cigarette smoking history. However, there were significant differences in male-female ratio (P less than 0.02) and in mean basal acid output (P less than 0.001), and all patients with nonhealing duodenal ulcers had basal acid outputs of greater than 10.0 meq/hr. Patients with nonhealing duodenal ulcers were treated with increased doses of ranitidine, mean 675 mg/day (range 600-1200 mg/day), and all had complete healing endoscopically documented. These results indicate that patients treated with standard doses of antisecretory medications with nonhealing duodenal ulcers have increased basal acid outputs of greater than 10.0 meq/hr, and the duodenal ulcers heal with increased doses of antisecretory medication.

Adult↗

[Role of duodenogastric reflus in pathogenesis of duodenal ulcer].

Duodenal ulcer is characterized by certain recurrence and occurs more often in men than in women. One can assume that functional changes, which are characterized by the seasonal nature and sex differences, play some role in its pathogenesis. There was a study of the duodenogastric reflux role in the pathogenesis of duodenal ulcer. It was revealed that duodenal reflux is provoked in about one half of patients sent for an endoscopic examination, less frequently--in spring and autumn, and least of all--in male patients with duodenal ulcer during seasons of the maximum frequency of duodenal ulcer exacerbations. The frequency of duodenogastric reflux provocation went down on days of geomagnetic storms. One could observe certain dependence between the extent and duration of reflux, on the one hand, and clinical registration of the disease, on the other hand.

Duodenal Ulcer↗

Effects of smoking and Helicobacter pylori on prostaglandin concentrations in gastric and duodenal mucosa of patients with duodenal ulcer and duodenitis.

The aim of this study was to determine the level of endogenous prostaglandin E2 (PGE2), prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) in the gastric and duodenal mucosa of patients with duodenal ulcer and duodenitis. Besides, the investigation aimed at determining the effect of smoking and infection by Helicobater pylori on prostaglandin synthesis. The investigation comprised 62 patients with duodenal ulcer, 46 patients with duodenitis and 44 controls. The results of our investigation indicate that the decreased prostaglandin synthesis in gastric and duodenal mucosa determined in patients with duodenal ulcer may have a considerable role in development of duodenal ulcer. Furthermore, the harmful effects of smoking on the gastric and duodenal mucosa may be mediated by the decreased prostaglandin synthesis in the gastric and duodenal mucosa. However, Helicobacter pylori seems to affect the development of duodenal ulcer through other mechanisms.

Analysis of Variance↗

[Piracetam in combined pathogenetic therapy of recurrent duodenal ulcer].

Duodenal ulcer cure, as a systemic gastroenterologic disease, can be achieved in some patients by the addition of the nootropic drug piracetam to current antisecretory and antihelicobacter therapy. Piracetam corrects vegetative and psychoemotional disorders in duodenal ulcer, normalizes gastric motility, has an antioxidant effect and improves cerebral circulation. An optimal effect on clinico-endoscopic manifestations of recurrent duodenal ulcer was achieved in combination of piracetam with current antisecretory (omeprazole) and antihelicobacter (de-nol, amoxicillin, metronidazole) medicines. Such combination improves both short- and long-term outcomes of duodenal ulcer treatment.

Adolescent↗

Age at establishment of Helicobacter pylori infection and gastric carcinoma, gastric ulcer, and duodenal ulcer risk.

Helicobacter pylori is an important risk factor for gastric cancer, gastric ulcer, and duodenal ulcer, yet most infected persons do not develop disease. We examined two correlates of acquisition age, sibship size and birth order, to evaluate the hypothesis that early life acquisition of H. pylori is a risk factor for the development of these illnesses. In earlier nested case-control studies of a cohort of Japanese American men in Hawaii, evidence of H. pylori infection was associated with the development of gastric cancer or gastric or duodenal ulceration during the subsequent period, 1968-1989. The present analysis included 102, 147, and 64 men who developed adenocarcinoma of the distal stomach, gastric ulcer, and duodenal ulcer, respectively, and a matched control for each. Sibship size and birth order data were analyzed as risk factors for development of these diseases. H. pylori-infected but not H. pylori-uninfected men from larger sibships (odds ratio, 2.06) and of higher birth order (odds ratio, 1.67) were at increased risk for developing gastric cancer. H. pylori- infected men but not uninfected men at higher birth order had increased risk of gastric (odds ratio, 1.64) but not duodenal ulcers. These data are consistent with the hypothesis that early life acquisition of H. pylori increases the risk of developing both gastric cancer and gastric ulcer but not duodenal ulcer.

Adenocarcinoma↗