Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present the results of ultrastructural studies of gastric mucosa obtained through upper digestive endoscopy of eight patients with suspicious symptoms of non ulcer dyspepsia or peptic ulcer. Two were male and six female with a median age of 54 years. The urease test to determine the presence of HP and Hematoxylin-Eosin and Warthin-Starry staining techniques were practiced with the purpose of a better detection of bacteria and gastritis. We did not find any correlation between the endoscopic results and the presence of gastritis or HP. Of the 8 patients only one had negative results for HP and for Electron microscopy studies. Chronic active gastritis was seen with light microscopy in all of the cases. Three in this group presented mild focal dysplasia and one case intestinal metaplasia type IIa. The main ultrastructural findings were: a) diminished or absent microvilli underneath the bacteria; b) HP inside phagolysosomes in the cytoplasm of the epithelial cells; c) in some cases, the bacteria was attached to the cell membrane; d) the cellular wall of HP contains mucopolysaccharides and up to four polar flagella; e) there are polymorphonuclear leucocytes in the epithelium. We conclude that Electron Microscopy is not a routine method for studying HP, but it constitutes a good method to study pathogenicity of the bacteria.
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PMID:[Ultrastructural study of the antral mucosa to determine the presence of Helicobacter pylori and its association with chronic active gastritis]. 172 15

This investigation was aimed at assessing whether the Yemeni habit of chewing Qat on a regular basis had a significant effect on the upper alimentary tract. Seventy patients with dyspepsia attending Al-Thawra Hospital in Taiz, Yemen Republic were examined by endoscopy. Biopsies were taken from the oesophagus, stomach and duodenum. The patients included 28 who gave a history of daily Qat intake, 21 with less frequent intake and 21 who took none. The only statistically significant finding associated with daily Qat intake was a higher prevalence of duodenal ulcer, particularly in females. However, a strong association was also found between heavy smoking and ulcer, with most ulcer patients who chewed Qat daily being heavy smokers. Chewing Qat was not associated with a higher prevalence of oesophageal dysplasia, making it unlikely to be the cause of the perceived high incidence of oesophageal carcinoma in Yemen. There was a high prevalence of gastric H. pylori colonization (93%) and columnar-lined lower end of oesophagus (18%), as well as low prevalence of intestinal metaplasia of stomach (4%); this was not, however, related to chewing Qat. Further epidemiological and histological studies are needed to assess the significance of these findings in relation to the incidence of oesophageal and gastric carcinoma in Yemen.
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PMID:Effect of chewing Qat on mucosal histology and prevalence of Helicobacter pylori in the oesophagus, stomach and duodenum of Yemeni patients. 175 83

After definition in the group of the non ulcer dyspepsia (NUD) can be counted all those patients at whom beside the dyspeptical complaints, the radiological and endoscopical examinations didn't show ulcerative changes. The authors made biopsy 550 times on the occasion of 1390 gastroscopical examination (39.5% of the cases). The histological examination showed chronic gastritis in 372 cases (26.7% of all the examinations, 67.6% of the histological examinations). At this group of patients the dyspeptical complaints gave the principal indication of gastroscopical examination. Also it was examined the presence of dysplasia and intestinal metaplasia beside the different severity grade of chronic gastritis. The presence of Helicobacter pylori (Hp) was examined by histological methods. Hp positivity was noticed in 16.4% in the upper group. The authors made Hydrogen-breath examinations in 34 cases between patients with NUD. The results of Hydrogen-breath examinations also raise the multifactorial nature of the NUD. On the basis of examinations chronic gastritis and CP infection can form subdivisions in the heterogenic group of patients with NUD. For exacter judgement of Hp pathogenicity are needed further and wide-spread examinations. The authors would like to call the attention to the indispensability of the biopsy during the gastroscopical examination.
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PMID:[Chronic gastritis and the presence of Helicobacter pylori in patients with non-ulcerative dyspepsia]. 173 39

Biopsy samples were taken endoscopically from the antral-mucosa of 693 patients with peptic ulcer and chronic gastritis presenting dyspepsia symptoms. Campylobacter pyloridis cultures were positive in 59 of 98 (60.2%) cases and histopathologically the organisms were found in 411 of 693 cases (59.3%). Pathologically, Campylobacter pyloridis was positive in 273 out of 300 patients with chronic superficial gastritis (91.0%), in 102 of 249 patients with chronic atrophic gastritis (40.9%), in 36 out of 144 patients with chronic atrophic gastritis with intestinalization or dysplasia (25.0%). We found that there was a significant association between the presence of Campylobacter pyloridis and chronic superficial gastritis, also the degree of lymphocyte infiltration showed a strong inverse association with the presence of Campylobacter pyloridis, suggesting that a local immune response might exert an important action in the eradication of this organism. These findings support the view that Campylobacter pyloridis, may be etiologically related to chronic gastritis and peptic ulceration, even though its role still remains to be determined.
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PMID:Preliminary study on the microbiology of Campylobacter pyloridis and gastric histopathology. 221

The risk of developing gastric cancer has been investigated in a case-control study and in a prospective investigation. In the case-control study, 1495 cases of gastric cancer were identified in five city hospitals and matched with autopsy controls from the same hospitals. The frequency of operations for benign ulcer [partial gastrectomy (PG) and gastroenterostomy] was similar in the two groups. Thus, there was no increased risk for late gastric cancer after an ulcer operation. A total of 140 operated ulcer subjects [80 truncal vagotomy and drainage (TVD), 60 PG and 78 nonoperated cases attending with dyspepsia (C)] were examined by endoscopy, multiple gastric biopsy and analysis of gastric juice for nitrite. Biopsies were graded for gastritis and a gastritis index was derived (normal, 1; superficial gastritis, 2; chronic atrophic gastritis: mild, 3; moderate, 4; severe, 5). More atrophic gastritis was found in operated subjects than in controls: TVD, 2.3 +/- 0.08 (mean +/- SE); PG, 2.6 +/- 0.1 versus C, 1.8 +/- 0.08, p less than 0.01. The severity of atrophic gastritis increased after an operation interval of 20 years in PG subjects (p less than 0.05). Intestinal metaplasia was a common change, but unequivocal epithelial dysplasia was not observed. Two cases of operated stomach cancer were found. High levels of nitrite were positively correlated with pH and a high gastritis index. This evidence does not suggest that ulcer surgery leads to either an increased risk of cancer or a precancerous condition.
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PMID:An investigation of possible risk factors associated with gastric cancer after benign ulcer operations. 367 37

Seventy-two patients with endoscopically proven gastric ulcers were entered into a prospective controlled trial to assess the efficacy of ranitidine and cimetidine in ulcer healing. All patients were biopsied on entry and at subsequent endoscopies. After exclusion of 7 patients during the first month of treatment, the remaining 65 patients, 47 males and 18 females, mean age 48.2 +/-1.5 years, at 1 month had a healing rate of 47% and 52% respectively. The non-healers continued their treatment for a further 4 weeks. This increased the healing rate to 77% and 76% respectively. If the defaulters and poor compliers are withdrawn the healing rate rises to 58% and 57% at 4 weeks and to 91% and 79% at 8 weeks respectively. There was no significant difference between the two groups as regarded initial ulcer size and severity of dyspepsia. Antacid tablet consumption during the study was comparable. The initial size of the ulcers which failed to heal after 4 weeks of treatment tended to be larger than those which healed (P less than 0.05), but smoking did not appear to influence ulcer healing. No obvious side-effects or evidence of dysplasia were found. The study shows that ranitidine is at least as effective as cimetidine in gastric ulcer healing.
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PMID:Ranitidine in the treatment of gastric ulceration. 627 19

Progressive anemia, melena, and sudden massive upper gastrointestinal bleeding in a man with cutaneous neurofibromatosis (von Recklinghausen's disease) since childhood prompted endoscopic demonstration of multiple gastric neurofibromas. One source of gastric bleeding removed by endoscopic electrosurgery proved to be a malignant schwannoma (spindle cell sarcoma). A pulmonary schwannoma, multifocal intracerebral spindle cell sarcomas, an extra-adrenal pheochromocytoma, and ocular neurofibromas were other features of this neuroectodermal dysplasia. Neurogenic tumors of the gastrointestinal tract are rare, commonly present with dyspepsia, abdominal pain, anemia, or hemorrhage, and should be suspect in the clinical setting of cutaneous neurofibromatosis. In the patient with systemic neurofibromatosis, endoscopic removal represents a safe method of diagnosis and treatment of bleeding neoplasms in the stomach or duodenum.
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PMID:Gastrointestinal neurofibromatosis. 643 77

In order to ascertain the role of gastric carcinoembryonic antigen (CEA) determination in detecting patients with a risk for gastric cancer, 69 subjects were studied; 23 were referred for endoscopy because of dyspepsia but without obvious macroscopic lesions, 27 with duodenal ulcer, 11 with benign gastric ulcer, 8 with gastric cancer. The following results were obtained by subdividing the material according to the histologic interpretation of the results of gastric mucosal biopsies: (1) in the presence of minor histologic abnormalities of the gastric mucosa, CEA in gastric juice was under 100 ng/ml in all but five cases; and (2) in moderate or severe chronic atrophic gastritis (associated or otherwise with intestinal metaplasia or dysplasia), and in gastric cancer, gastric CEA ranged between 224 and 3120 ng/ml in all but two cases. Although not diagnostic for gastric cancer, gastric CEA is a promising test in detecting patients at risk, including those with dysplasia of the gastric mucosa.
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PMID:Carcinoembryonic antigen in gastric juice collected during endoscopy. Value in detecting high-risk patients and gastric cancer. 664 May 4

Endocrine cells of the gastric oxyntic mucosa, and especially the enterochromaffin-like (ECL) cells, are the progenitors of gastrin-promoted proliferative lesions whose tumorigenic potential largely depends on the background condition in which they arise. Hypertrophic gastropathy due to the familial multiple endocrine neoplasia (MEN-1)-associated or sporadic Zollinger-Ellison syndrome (ZES), diffuse chronic atrophic gastritis restricted to the corpus-fundus (type A CAG), with or without associated pernicious anemia, and Helicobacter pylori-related multifocal chronic atrophic gastritis are the usual background for such growths. The endocrine cell lesions have been classified as pseudohyperplasia (cell clustering unassociated with cell proliferation), hyperplasia (diffuse, linear, micronodular, adenomatoid), dysplasia (enlarged, adenomatous or fused micronodules, microinfiltration, nodular growth), and neoplasia (intramucosal or invasive carcinoids). The entire spectrum of endocrine cell proliferation, from hyperplasia to dysplasia and neoplasia, has been observed in MEN-ZES and diffuse type A CAG. Both hyperplastic and pseudohyperplastic changes occur with some frequency in the H. pylori-related chronic gastritis associated with ulcer disease or dyspepsia. However, because no progression to dysplastic or neoplastic lesions has thus far been documented in these latter conditions, their role in gastric endocrine cell tumorigenesis appears negligible.
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PMID:Hyperplastic, dysplastic, and neoplastic enterochromaffin-like-cell proliferations of the gastric mucosa. Classification and histogenesis. 776 35

Recently many reports have shown a strong association between Helicobacter pylori infection in the stomach and recurrent peptic ulcer. Moreover, prospective cohort serological studies showed that H. pylori infected individuals have significantly increased rate of gastric cancer in the USA. H. pylori is a gram-negative spiral organism which has urease activity and produces ammonia and CO2 from urea, and nestles in the gastric pits and overlaying mucus gel layer. Many diagnostic methods of H. pylori infection are available; ie bacterial culture, 13C-urea breath test, histology, serum IgG antibody against H. pylori. We developed a new method, ie tissue IgA antibody against H. pylori and detection of H. pylori DNA in the gastric juice by PCR method. Triple therapies with metronidazole, bismuth compounds, and amoxicillin or tetracyclin are difficult to use in Japan because of their sever side effects. Thus, new methods with proton pump inhibitor (PPI) and amoxicillin have been introduced. We treated 14 patients of whom were H. pylori positive-active peptic ulcer with 30 mg/day of lansoprazole, a new PPI, plus 1,500 mg/day of amoxicillin for 2 weeks and 8 (57%) patients were eradicated. Gastric carcinogenesis are multi-steps and multifactorials process. Hypothetical sequence of intestinal type of gastric cancer is that superficial gastritis-->atrophic gastritis-->intestinal metaplasia-->dysplasia-->gastric cancer and H. pylori infection may play a role in the early stage of the sequence. We examined mucosal IgA antibody against H. pylori in chronic gastritis and intestinal metaplasia detected by the Tes-Tape method in 25 resected specimens after gastrectomy for gastric cancer. Positivity rates of tissue H. pylori IgA antibody were lower in the mucosa of intestinal metaplasia than in non-metaplastic gastric mucosa and were negative in carcinoma. Causal relationship between H. pylori infection and gastric cancer is not proven and factors other than H. pylori infection are also important in the gastric carcinogenesis. Finally we introduce 2 reports: (1) NIH Consensus Conference: Helicobacter pylori in peptic ulcer disease (JAMA. 1994; 272: 65-69). The consensus panel concluded that 1. ulcer patients with H. pylori infection require treatment with antimicrobial agents in addition to antisecretory drugs whether on first presentation with the illness or on recurrence; 2. the value of treating nonulcerative dyspepsia patients with H. pylori infection remains to be determined; and 3. the interesting relationship between H. pylori infection and gastric cancer requires further exploration. (2) World Health Organization: Working Group Meeting (Reported in World Congress of Gastroenterology, Los Angeles, 1994). H. pylori plays a causal role in the chain of events leading to cancer of the stomach. Group I: definite carcinogen.
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PMID:[Helicobacter pylori in peptic ulcer and gastric cancer]. 785 88


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