Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred and sixty two patients with upper and intermediate gastrointestinal hemorrhage studied under a prospective protocol are reported. Upper endoscopy revealed lesions of the upper gastrointestinal tract in 137 patients (89%); a barium swallow performed to 92 of them failed to confirm the endoscopic diagnosis in 66 (71.7%). In 99m Tc scan suggested ectopic gastric mucosa in 9 cases; Meckel's diverticulum was confirmed by laparotomy in 7 and gastrointestinal duplication in two of them. Selective mesenteric arteriography demonstrated bleeding ileo-cecal varices in one patient. The main causes of gastrointestinal hemorrhage in the current series were duodenal ulcer (22.8%), esophageal varices (14.8%), stress ulcers (14.2%), reflux esophagitis (7.4%), aspirin-induced gastritis (6.8%), gastric ulcer (5.6%) and ectopic gastric mucosa (5.6%). These diagnosis were characteristically distributed according to pediatric age-groups. The source of bleeding could be detected in 90% of the patients studied. A clinical approach to differential diagnosis of patients with gastrointestinal bleeding is presented.
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PMID:[Usefulness of endoscopy in the differential diagnosis of hemorrhage of the upper digestive tract in children]. 146 73

The aim of this study was to evaluate the prevalence of Helicobacter pylori in 400 patients referred for upper digestive tract endoscopy. In our area it hasn't developed yet any epidemiologic study about this disease. Helicobacter pylori was observed in 281 of the 400 patients studied (70%). No significant differences by sex were found in the subjects analyzed. There was a rise in the percentage of positivities as age increased. Helicobacter pylori were positive in 74 of the 88 patients with chronic superficial gastritis (84.1%), in 53 of the 65 with chronic atrophic gastritis (81.5%), in 16 of the 25 with chronic atrophic gastritis and intestinal metaplasia (64%), in 49 of the 63 with gastric ulcer (77.8%), in 73 of the 85 with duodenal ulcer (85.9%), in 9 of the 24 patients with gastric carcinoma (37.5%), in 5 of the 19 with stump gastritis (26.3%), where as only a few Helicobacter pylori were found in 2 of the 31 histologically normal subjects (6.5%). These findings support the wiew that Helicobacter pylori may be etiologically related to chronic gastritis and peptic ulceration, even though their precise role still remains to be determined.
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PMID:[Prevalence of Helicobacter pylori in gastric pathology in Aragon]. 148 82

Over a period of 3 months, 85 patients who underwent gastroscopy had antral biopsy taken for Clotest, histology and/or culture for Helicobacter pylori (HP). The sensitivity and specificity of Clotest were found to be 77% and 96% respectively with negative predictive value of 63% and positive predictive value of 98%. Ninety-two percent of the positive Clotests were positive within 20 minutes, thus giving rapid result. Therefore, Clotest is a rapid, sensitive and highly specific test for HP infection. A high correlation between HP infection and chronic gastritis was noted and the prevalence of HP infection in patients with duodenal ulcer (90%) was higher than that of gastric ulcer (64%) or non-ulcer group (65%).
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PMID:Clotest (rapid urease test) in the diagnosis of Helicobacter pylori infection. 148 62

Due to increasing number of the elderly, cases of hematemesis and melena in the aged have been increasing. The authors evaluated 69 such cases over 60 years old in whom emergency endoscopy of the upper digestive tract was carried out because of hematemesis and melena. Twenty cases are diagnosed as gastric ulcer (29%), 12 cases as esophageal ulcer and esophageal erosion (17.4%), 9 as duodenal ulcer (13.0%), 7 as gastric cancer (10.1%), 6 as Mallory-Weiss syndrome (8.7%), 6 as esophageal and gastric varices (8.7%), 4 as acute hemorrhagic gastritis (5.8%), 3 as Dieulafoy's ulcer (4.3%), and one case each of chronic pancreatitis (hemosuccus pancreaticus) and hemorrhage due to gastric angiodysplasia (1.4%). Of these cases, blood transfusion was performed in 46 cases (66.7%), and shock occurred in 27 cases (39.1%). The endoscopical hemostatic procedure was effective for detection of underlying diseases in the aged. Surgery was often impossible because of the rapid deterioration of the systemic condition due to the hemorrhage of the digestive tract.
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PMID:[Upper gastrointestinal bleeding in the elderly]. 149 78

A consecutive series of 71 children (mean age 8.6 years) with recurrent abdominal pain underwent endoscopic oesophageal, gastric and duodenal biopsy in order to determine whether the pain was of gastro-intestinal origin. Of these 71 children, 27 (38%) showed oesophagitis, 14 (20%) cardiac gastritis, 29 (41%) body gastritis, 38 (54%) antral gastritis, and 29 (41%) duodenitis. Thus, 66 of the 71 children studied had an inflammatory lesion explaining their complaints. One of the patients had a gastric ulcer. Helicobacter pylori colonisation was found in 5 of the children: One had H. pylori associated antral and body gastritis and 4 H. pylori associated antral gastritis only. Body gastritis without H. pylori was present in three of these four children. Our data do not support the widespread assumption that recurrent abdominal pain for which no medical cause can be found, is psychogenic; neither do they establish an association between H. pylori antral gastritis and recurrent abdominal pain. However, our data provide strong evidence that there is a gastro-intestinal origin of these patients' complaints.
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PMID:Recurrent abdominal pain of gastro-intestinal origin. 150 71

We have assessed 270 consecutive patients (age range 0.8-20 years) referred for endoscopic study because of abdominal pain during 32 months. Helicobacter pylori (HP) was detected by culture in 91 cases (33.7%). HP colonization increased significantly with age (p less than 0.01). Nine patients less than 5 years of age were colonized by HP. A previous history of peptic ulcer disease in first-degree relatives was significantly more frequent in the HP-positive group (p less than 0.001). The frequency of HP positiveness as related to diagnosis was: normal, 3.3%; nonactive chronic gastritis, 100%; active chronic gastritis, 97.2%; gastric ulcer, 75%; and duodenal ulcer, 90.9% (p less than 0.001). Endoscopic nodular antritis was a frequent (67%) and specific finding; this presence was associated with that of lymphoid follicles in the histopathological study. Signs of histological activity were observed in 55.9% of the HP-positive patients. The histological colonization by HP was assessed semiquantitatively, and a significantly greater HP colonization score was observed in patients with signs of histological activity (p less than 0.001). A significant correlation was found between HP colonization score and histological score (rs = 0.574), with a significant association between the degree of HP colonization and the histologic categories (p less than 0.001). The present study suggests a pathogenic role of HP in the development of gastroduodenal disease in children.
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PMID:Helicobacter pylori infection in children: clinical, endoscopic, and histologic correlations. 835 Feb 6

The association and causative role of Helicobacter pylori infection of the stomach with gastric ulcer, duodenal ulcer, non-ulcer dyspepsia, and gastritis has remained controversial. The authors studied the effects of daily intragastric administration of H. pylori suspension in saline (10(8) CFU/ml) and bacteria-free filtrates of saline H. pylori suspensions in 85 Sprague-Dawley rats (weight, 150 to 200 g) with normal mucosa and with surgically produced experimental gastric ulcers. Group I rats (n = 30) with pre-existent experimental gastric ulcers received H. pylori suspension (ATCC 43504, 10(8) CFU/ml); Group II rats (n = 20) with experimental gastric ulcers received bacteria-free H. pylori filtrates; Group III rats with ulcers (n = 20) received saline alone; and Group IV control rats (n = 15) without ulcers received intact H. pylori organisms in suspension (ATCC 43504, 10(8) CFU/ml). At death, ulcer surface areas were measured with a dissecting microscope. Full-thickness sections were obtained for quantitative and qualitative histologic parameters, including the area of remaining mucosal necrosis; characteristics and cellular composition of restored mucosal architectures; and presence or absence of inflammation including counts of neutrophils and lymphocytes. H. pylori organisms were identified within the surface mucus and crypts using routine, special, and immunohistochemical stains. Our results indicate that the continued presence of either intact H. pylori organisms or bacteria-free H. pylori filtrates in the stomachs of rats with pre-existent gastric ulcers resulted in delayed healing of the ulcers and persistence of chronic active inflammation. Daily administration of suspensions of H. pylori organisms to sham-operated rats with intact gastric mucosa, however, resulted in no ulceration or inflammation despite identification of surface H. pylori organisms at death. The authors conclude that H. pylori alone causes little or no effect on an intact gastric mucosa in the rat, that either intact organisms or bacteria-free filtrates cause similar prolongation and delayed healing of pre-existing ulcers with active chronic inflammation, and that the presence of predisposing factors leading to disruption of gastric mucosal integrity may be required for the H. pylori enhancement of inflammation and tissue damage in the stomach.
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PMID:Helicobacter pylori. Its role in the pathogenesis of peptic ulcer disease in a new animal model. 151 73

One hundred eighty-nine consecutive gastric biopsies showing colonization by Helicobacter pylori (HP) were studied. Epigastric pain and bleeding were the clinical presentations in 167 cases (88.4%). Major endoscopic findings were gastritis (n = 72, 38.1%) and ulceration (n = 101, 53.4%). Duodenal ulcer was associated with 32 (44.4%) and 29 (28.7%) cases of gastritis and gastric ulcer, respectively. Histologically, the HP-colonized gastric epithelium showed characteristic degenerative changes that were topographically related to the bacteria but unrelated to the inflammatory infiltrate. Disintegration and loss of apical mucus with formation of epithelial pits was seen in nearly all cases. Other changes included microerosion, conventional erosion, and frank ulceration. Only the disintegration of apical mucus, epithelial pit, and microerosion were specific for HP colonization. These conditions were absent in areas not colonized by HP and in 79 consecutive HP-negative gastric biopsies seen during the same study period. The epithelial degenerative changes in HP-colonized gastric mucosa are easy to recognize in routine hematoxylin-eosin-stained sections and they could serve as histologic guides to the localization of the bacteria. It is proposed that HP-colonized gastric mucosa is a distinct pathologic entity with a pathologic spectrum ranging from active chronic gastritis to erosion and frank ulcer. Damage to the mucin-containing portion of the gastric epithelial cells appears to be the basic cytopathologic effect of HP on the gastric mucosa. As effective specific treatment for HP infection is available, identification of HP colonization in gastric biopsies should be attempted in all cases of gastritis and gastric ulcer.
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PMID:Pathologic changes of gastric mucosa colonized by Helicobacter pylori. 142 63

Helicobacter pylori (Hp) is considered to be one of the causes of gastric mucosal injury. Using biopsy specimens from the gastric mucosa of patients with gastritis or gastric ulcer, the intramucosal mucus was quantified by computer image analysis to evaluate its relationship with Hp. In gastric mucosa positive for Hp, the mucus content within the gastric mucosa was significantly decreased. Ammonia was administered based on its assumed role in decreasing the mucus content of the gastric mucosa, and resulted in a decrease in rats to whom it was administered. Based on these results, cases of intractable gastric ulcer were studied. In these intractable cases, Hp was present significantly more often than in other cases and the intramucosal mucus content was significantly lower. These findings suggest that Hp may be a factor in the resistance of gastric ulcer to treatment.
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PMID:[Relation between Helicobacter pylori and intractable gastric ulcer--PAS positive intramucosal mucus as an index]. 157 1

The variation in the healing and the relapse rates of peptic ulcer disease has led to the search for other factors in the pathogensis of peptic ulcer disease. Helicobacter pylori is believed to be responsible for these different patterns of healing. The results of a study to detect Helicobacter pylori in Sri Lankan patients having duodenal ulcer, gastric ulcer, gastritis and non-ulcer dyspepsia are presented in this paper. The method employed was the urease test which detects the urease enzyme of H. pylori in gastric mucosal biopsies taken during upper gastrointestinal endoscopy. There is a high incidence in those with gastritis and duodenitis.
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PMID:Helicobacter pylori and peptic ulcer disease in Sri Lanka. 158 90


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