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)

The relation of atrophic gastritis, other gastric lesions and lifestyle factors to stomach cancer risk was prospectively studied among 3,914 subjects who underwent gastroscopic examination and responded to a questionnaire survey at the Aichi Cancer Center Hospital. During 4.4 years of follow-up on average, 45 incident cases of stomach cancer were identified at least three months after the initial examination. If the baseline endoscopic findings indicated the presence of atrophic gastritis, the risk of developing stomach cancer was increased 5.73-fold, compared with no indication at the baseline. The risk further increased with advancing degree of atrophy and increasing extension of atrophy on the lesser curvature. These trends in the relative risks were statistically significant (P = 0.027 and P = 0.041, respectively). The risk of developing stomach cancer was statistically significantly increased among subjects with gastric polyps, but not among those with gastric ulcer. Stomach cancer cases tended to consume more cigarettes, alcohol, rice, pickles and salted fish gut/cod roe and less fruits and vegetables and to have more family histories of stomach cancer than noncases, although these differences were not statistically significant. The results of the present study provide additional evidence on the relation between atrophic gastritis and stomach cancer and suggest a need for intensive follow-up of patients with atrophic gastritis and gastric polyps.
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PMID:A prospective study of atrophic gastritis and stomach cancer risk. 148 28

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

Helicobacter pylori colonization and the incidence, severity, activity and topography of gastritis were investigated systematically in antrum and corpus mucosal biopsies of 1177 subjects undergoing endoscopy in the absence of gastric complaints (asymptomatic, 49) or for non-ulcer dyspepsia (NUD; 631 patients, 72 of whom had gastric and/or duodenal erosions), active gastric ulcer (GU, 76 patients), active duodenal ulcer (DU, 138 patients), and healed gastric (HGU, 39 cases) or duodenal ulcer (HDU, 230 cases). In the antrum, H. pylori colonization and the incidence, severity and activity of gastritis increased progressively in the sequence asymptomatic, erosion-free NUD, erosive NUD, healed ulcer and active ulcer. The same trend was observed in the corpus as regards H. pylori and gastritis incidence, whereas the severity and activity of gastritis were lower in active DU and erosive NUD and higher in active, proximal GU than in the remaining patients. Active DU and erosive NUD showed the highest incidence of non-atrophic gastritis and lowest type-A or AB atrophic gastritis, while active GU had lowest normal mucosa or type-A gastritis and highest type-B atrophic gastritis. In conclusion, H. pylori colonization and gastritis incidence, severity and, especially, activity of the antrum might all contribute to mucosal erosion and ulceration, whereas the same factors, at least in part and with the exception of proximal GU, seem to have a preventive role when affecting corpus mucosa.
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PMID:Helicobacter colonization and histopathological profile of chronic gastritis in patients with or without dyspepsia, mucosal erosion and peptic ulcer: a morphological approach to the study of ulcerogenesis in man. 160 9

Being pepsinogen A (PGA) levels generally reduced and pepsinogen C (PGC) increased in gastric cancer patients, PGA/PGC ratio has been proposed as a useful marker of the tumour. We tested PGA, PGC and Gastrin (G) levels in patients with gastric cancer (39) and, as a control, in patients with epithelial dysplasia (21), chronic atrophic gastritis (57), gastric ulcer (11) or subjects lacking major or minor endoscopic and microscopic changes at gastroscopy (48). PGA and PGA/PGC levels were significantly reduced in gastric cancer patients (p less than 0.005 and p less than 0.0001 respectively with analysis of variance). Gastrin levels were also reduced in the same patients (p less than 0.005). We therefore adopted an index number (PGA x Gastrin) which was also dramatically reduced in gastric cancer (p less than 0.005); using an arbitrarily chosen cut-off, the "marker" showed very high sensitivity (76%), specificity (96%) and overall accuracy (74%, by Youden J test). We therefore suggest the use of the index number PGA x G in the diagnosis of gastric cancer, as the most useful gastrin presently available, to our knowledge.
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PMID:Pepsinogen A/pepsinogen C or pepsinogen A multiplied by gastrin in the diagnosis of gastric cancer? 175 13

A series of 38 patients with high gastric ulcer (GU) was examined twice a seven-year interval. One-third of the patients had an active ulcer at the second examination. Chronic gastritis was evaluated, and the level of Helicobacter pylori (HP) colonisation assessed semiquantitatively. The results were compared with age and sex matched non-ulcer controls. The GU series differed from the controls in having a higher degree of HP colonisation in gastric mucosa. The relative risks (RR) in predicting high GU connected with high HP colonisation were significantly elevated, both in the antrum (RR = 6.0-4.8) and in the corpus (RR 5.0-4.4), and still higher when combined HP colonisation values were used (RR 9.5-7.1). The persistence of active ulcer (GU+) was associated with a very high level of HP colonisation, with absence of corpus atrophic gastritis at the first examination and with young patients. Half of the GU+ patients had the maximum grade of combined HP colonisation in both examinations. The study indicates that the presence of HP infection as well as the level of HP colonisation are of importance in both the development and chronicity of peptic GU disease.
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PMID:Grade of Helicobacter pylori colonisation, chronic gastritis and relative risks of contracting high gastric ulcers: a seven-year follow-up. 175 32

Argyrophil cell (AC) hyperplasia in corpus mucosa was investigated in 53 patients with chronic gastric ulcer disease not previously treated with antisecretory drugs. Mucosal biopsies were taken stepwise from the posterior wall in the corpus area of the stomach. Of 117 biopsy sites, 28 showed gastritis without atrophy, 85 showed chronic atrophic gastritis of varying degrees while 4 biopsies showed a normal mucosa. About one third (38%) showed a normal AC pattern. Of the remaining two thirds (62%), 45% had simple AC hyperplasia, 18% had linear and 37% had micronodular AC hyperplasia. A strong association was found between focal (linear/micronodular) AC hyperplasia and chronic atrophic gastritis. It is concluded that focal AC hyperplasia is a common phenomenon in gastric ulcer patients and is inherently related to the spontaneous development of atrophy in the corpus mucosa of these patients.
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PMID:Argyrophil cell hyperplasia associated with chronic corpus gastritis in gastric ulcer disease. 175 36

A new monoclonal antibody has been developed which is capable of detecting structures in gastric mucus glycoproteins expressed in the fetus and in adult gastric mucosa in conditions such as gastric carcinoma. Cancer associated monoclonal antibodies were selected by testing them against various mucous glycoprotein samples from the alimentary tract, including salivary glycoproteins from both secretory and non-secretory subjects, and cancerous and normal gastric juice glycoproteins. They were tested against 1000 samples of gastric juice from an unselected population. Immunochemical characterisation suggested that the glycoproteins picked up by P4 and i11 include one of the compounds reacting with rabbit anti-fetal sulphoglycoprotein antigen serum. On the basis of a clinical trial and immunohistological evaluation further evidence was obtained of P4 as the most promising antibody for further experimentation. A total of 302 gastric juice specimens from patients with various gastric symptoms were analysed using the enzyme linked immunosorbent assay technique and P4 antibody. Of 10 gastric cancers, nine had P4 in the gastric juice. A positive correlation was found between gastric ulcer and the appearance of P4. Duodenal ulcers were not correlated to P4. Atrophic gastritis and P4 coincided less frequently. Raised P4 values were found in between 3% and 9% of subjects, depending on the population. Cancer cases showed high P4 values, which allows adjustment of the lower limit of a positive result to high level whereby a considerable number of non-cancerous P4 positives are omitted.
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PMID:Gastric cancer associated structure in mucus glycoproteins shown as a clinically useful marker. 148 73

To assess the evolution of gastric epithelial dysplasia (GED), a prospective multicenter study was based on a protocol of repeated endoscopies and biopsies. To date, 134 cases (0.4% of all patients endoscopically examined in the same period) have been diagnosed as having GED and 80 of those have had an "adequate" follow-up (at least three endoscopies). Mean follow-up time was 18 months. Gastric epithelial dysplasia was mild in 59% of cases, moderate in 25%, and severe in 10%. Six percent of the patients had lesions that were "indefinite for dysplasia." Chronic atrophic gastritis (40%), gastric ulcer (32%), gastrectomy (10%), and polyps (9%) were the most frequently associated lesions. The term "regression" was adopted for GED no longer detectable during follow-up and the term "progression" was used when more severe changes or cancer was detected. Mild GED regressed in 66% of cases, persisted in 15%, and progressed in 19% (three cases to moderate, one to severe, and five to cancer). Moderate GED regressed in 30% of patients, persisted in 30%, and progressed in 40% (one to severe GED and seven to cancer). Severe GED regressed in 12.5% of patients, persisted in 12.5%, and progressed to cancer in 75%. Of the five patients with lesions indefinite for dysplasia, two had no dysplastic changes at follow-up and three had cancer diagnosed. Ten of 21 cases of cancer (48%) were at the early stage. The diagnosis was reached within the first year of follow-up in 14 cases and after 1 year in seven (13 to 39 months). Fifteen of 21 cases of cancer were diagnosed in gastric ulcer patients. In conclusion, GED is an infrequent finding and its biologically neoplastic significance is confirmed by the results of the follow-up study: (1) in its mild form, it tends to regress but adequate subsequent check-ups are mandatory as it may associate with or evolve as cancer; (2) patients with moderate GED require strict follow-up since the lesion shows a higher cancer risk; (3) surgery is indicated for severe GED because gastric cancer develops in 75% of cases; and (4) patients with lesions indefinite for dysplasia should immediately undergo repeat endoscopy and biopsy. Such an approach allows gastric cancer to be detected at an early stage in a much higher percentage of cases than may be expected.
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PMID:Gastric epithelial dysplasia: a prospective multicenter follow-up study from the Interdisciplinary Group on Gastric Epithelial Dysplasia. 184 72

Peripheral blood monocytes from healthy subjects, patients with gastric precancer disease (chronic gastric ulcer, stomach polyps and chronic atrophic gastritis) and different stages of gastric cancer were used. Spontaneous and lipopolysaccharide (LPS)-stimulated TNF-like factors production by monocytes was significantly higher in the precancer gastric disease patients than in the healthy subjects. At the same time the spontaneous capacity of monocytes to produce NTF-like factors was 2.5 lower in the gastric cancer patients compared to the healthy subjects. Moreover, in 5/13 of the gastric cancer patients in TNF-like factors production by the LPS-stimulated and non-stimulated monocytes was 1 unit/ml less. Spontaneous and reactive CL indexes were higher in the cancer patients monocytes than in the healthy subjects. The obtained results suggest that reactive oxygen species production can be an alternative mechanism by which a cytotoxic action of monocytes is regulated.
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PMID:[Changes in the profile of cytotoxic mediator monocytes in patients with cancer and precancerous conditions of the stomach]. 185 63

A total of 129 consecutive gastrectomy specimens from Japanese (99), Philippinos (11), Hawaiians (8), Koreans (5), Chinese (4) and Caucasians born in Hawaii (2) were examined under high-power light microscopy (1000 x) for the presence of ciliated gastric cells. Fifty-two of the 129 gastrectomy specimens (40.3%) contained ciliated cells. Ciliated cells were found in the basal segments of antral glands (usually cystically dilated) whose superficial segments had undergone intestinal metaplasia. The presence of ciliated cells in the gastric mucosa was influenced by the age of the patient and by the degree of intestinal metaplasia: the older the patient, the greater the degree of intestinal metaplasia and the greater the frequency of specimens with ciliated cells. The presence of ciliated cells was also influenced by the type of lesion in the specimen. Although the highest frequency (47.2%) was found in stomachs removed for adenocarcinoma, a substantial number of stomachs removed for gastric ulcer also showed that change (36%). The data suggest that increasing age and advanced atrophic gastritis, especially of the antrum, provide the necessary conditions that lead to the development of cilia, not only in Japanese subjects, but in other Hawaiian ethnic groups as well.
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PMID:Ciliated gastric cells among Japanese living in Hawaii. 190 Feb 73


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