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Query: UMLS:C0851341 (infestation)
 10,121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the study was to evaluate the long-term effects of vagotomy on the morphological status and Helicobacter pylori infestation of the gastric mucosa. Endoscopy with biopsies (2 from antrum and 2 from corpus) was performed in 317 patients on whom vagotomy had been performed on an average 8 years earlier. The success of the vagotomy was estimated by the endoscopic Congo Red technique in 270 cases. Non-operated 187 duodenal ulcer patients were examined endoscopically and bioptically in a similar way and used as a reference series. Helicobacter pylori (HP) was determined by Giemsa staining of biopsy specimens in both series. In non-operated dudoenal ulcer patients, gastritis and HP behaved as expected from the data in literature: antral gastritis was present in nearly all cases (96%), while the corpus mucosa was normal or the process was retarded at the stage of superficial gastritis (76%) and atrophic changes were virtually lacking (1%). On the basis of the Congo Red test the vagotomized patients were separated into two groups: successfully operated, i.e., complete vagotomy, and incomplete vagotomy groups. The results of the examinations were independent of the kind of vagotomy performed, but related significantly to its completeness. The incomplete and complete groups differed significantly. The prevalence of atrophic changes (29%) in the corpus was significantly higher and that of superficial gastritis (69%) lower in the complete than in the incomplete vagotomy group, in which the prevalences were 12% and 85%, respectively. Likewise the prevalence and density of HP was lower in the complete vagotomy group but the difference was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term effect of vagotomy on gastric mucosa and Helicobacter pylori in duodenal ulcer patients. 175 34

The efficacy of omeprazole in the elimination of Helicobacter pylori was investigated in a prospective randomized-controlled trial. 50 patients with upper gastrointestinal symptoms and chronic active H. pylori-associated gastritis were allocated to one of the following four therapeutic schedules: 1) omeprazole 40 mg/d for 4 weeks (n = 13); 2) bismuth subsalicylate (BSS) 3 x 600 mg for 4 weeks (n = 12); 3) omeprazole plus BSS for 4 weeks (n = 13); 4) triple therapy (BSS for 4 weeks, amoxicillin 3 x 750 mg and metronidazole 3 x 400 mg for 10 days) (n = 12). Clinical symptoms, endoscopic and histologic findings, and H. pylori status were reassessed immediately after therapy, and 1 and 6 months later. After cessation of therapy bacterial clearance rates were: 1) omeprazole 2/13 (15%); 2) BSS 6/12 (50%); 3) omeprazole plus BSS 5/13 (38%); 4) triple therapy 10/12 (83%). The degree of density of gastric mucosal infestation with H. pylori and the degree of activity of gastritis was reduced in all treatment groups but was most prominent after triple therapy. Clinical symptoms improved in all treatment groups. One and six months after completion of therapy H. pylori eradication rates were: 1) omeprazole 0/13 (0%); 2) BSS 1/12 (8%); 3) omeprazole plus BSS 1/13 (8%); 4) triple therapy 10/12 (83%). Our study shows that 40 mg/d omeprazole is ineffective in eradicating H. pylori. Dual therapy with omeprazole and bismuth subsalicylate does not improve bacterial elimination. Only triple therapy effectively eradicates H. pylori.
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PMID:The role of omeprazole (40 mg) in the treatment of gastric Helicobacter pylori infection. 177 34

The authors analyse the results of esophago-gastro-duodenal fibroscopy in 930 symptomatic patients. Ninety one per cent of them had lesions. Inflammatory pathology was predominant: esophagitis, gastritis and duodenitis were seen in 21.5%, 47% and 29.08% respectively of the patients investigated. Gastritis accompanied 75.13% of cases of esophagitis and 76.4% of duodenitis, and was associated with the demonstration of the presence of Helicobater pylori in gastric biopsies in 56.41% of patients with that lesion. The relatively high incidence of carcinoma of the esophagus (2.7%) is a particular feature of this study, while that of carcinoma of the stomach (1%) was in accordance with classical data. Duodenal ulcer was found in 18% of patients as compared with 5.16% for gastric ulcer. From a pathophysiological standpoint, mention is made of traditional diet (hot, highly spiced), self-medication and intestinal parasite infestation in causing inflammatory lesions. Finally, emphasis is placed upon the role of Helicobacter infection in the development of chronic gastritis. The high rate of infection with this organism and its involvement in the mechanisms of duodenal ulcerogenesis could explain the high incidence of duodenal ulcers in our group and in studies emanating from developing countries.
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PMID:[The contribution of endoscopy in the diagnosis of esophago-gastro-duodenal disorders in a tropical milieu. Experience in Benin with 930 examinations]. 177 37

The frequency of Helicobacter pylori (H.p.) infestation in antral mucosa and the presence of gastritis were investigated in different states of gastric acid secretion. Biopsies were stained by the Warthin-Starry technique and hematoxylin-eosin. Antral H.p. was found in similar frequencies in Zollinger-Ellison syndrome (n = 17; profound acid hypersecretion, associated with duodenal ulcer disease in most cases) and the same number of age-matched controls (35% in each group) whereas H.p. could be detected in 31 out of 33 duodenal ulcer patients (94%). The incidence of H.p. infestation in H2-blocker refractory reflux oesophagitis was low (24%). Treatment of peptic lesions with omeprazole (drug-induced hypochlorhydria) led to a reduction or disappearance of H.p. in 7 out of 10 H.p.-positive patients whereas none of 19 primarily H.p.-negative patients became infected with H.p. during prolonged omeprazole therapy. It is concluded that (1) development of duodenal ulcers (as in gastrinomas) does not necessarily require H.p., and (2) at least in some patients H.p. is reduced in antral mucosa by omeprazole.
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PMID:Antral Helicobacter pylori-like organisms in different states of gastric acid secretion. 180 Jan 86

Helicobacter pylori can cause acute gastritis. It is also associated with chronic gastritis and peptic ulcers. The clinical significance of chronic gastritis is not clear, there are apparently no connections between chronic gastritis and dyspeptic complaints. There is hitherto no reason to treat Helicobacter pylori infestation in patients with gastritis or non ulcerating dyspeptic disease. In patients with ulcers several studies have suggested that the rate of recurrence of ulcers is diminished after eradication of Helicobacter. Unfortunately most of these studies have methodologic deficiencies. Treatment with the goal to eradicate helicobacter is tedious, carries a substantial risk of side effects and has a limited chance for success. These treatments are of an experimental nature and should essentially be reserved for controlled studies. These will have to compete with the established and safe treatment by H2-antagonists.
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PMID:[Helicobacter pylori and ulcer disease: significance for diagnosis and therapy]. 194 43

One hundred and thirty-nine subjects representing a randomly selected sample of an Estonian urban population examined endoscopically, bioptically and bacteriologically in 1979 was re-examined in 1985. In the antrum the development of superficial gastritis was clearly associated with the appearance or persistence of Helicobacter pylori (HP) infestation. The further progression of superficial gastritis could less clearly be related to HP infestation, although regression and progression of antral superficial gastritis was significantly associated with the disappearance or presence of the bacteria. The progression of atrophic antral gastritis as well as the development and progression of all body gastritis seemed unrelated to the HP infestation. It is concluded, that HP infestation is in some way involved in the appearance of the first stages of chronic gastritis, but is less related or unrelated to its further progression, which is probably determined mainly by factors other than HP.
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PMID:Helicobacter (Campylobacter) pylori infestation and the development and progression of chronic gastritis: results of long-term follow-up examinations of a random sample. 235 34

The occurrence of Campylobacter pylori (CP) was examined in 179 subjects representing a sample collected from the population of South Finland. In a normal antral and body mucosa CP was present in 5% and 11% and in superficial gastritis (SG) in 71% and 91% of subjects, respectively. In atrophic gastritis (AG) of antrum and body the prevalence of CP decreased significantly with an increasing degree of atrophy, so that CP was not found in severe body AG. Different combinations of antral and body gastritis revealed a characteristic pattern. Campylobacter pylori was lacking when antral and body mucosa were normal, but was present in 41% when normal mucosa was associated with gastritis in the opposite area. In SG affecting diffusely antrum and body, the bacterium was present in every case, but when SG was associated with AG in the opposite area it was lacking in 29% of the subjects. When SG affecting both areas was compared with SG accompanied by different degrees of AG in the body, there was a highly significant decrease of the prevalence of CP in antrum and body along with an increasing degree of AG in the body. This decrease showed a highly significant positive correlation with the acid output. On the whole, acid output correlated well with the occurrence of CP in both antrum and body. Thus the prevalence of CP was 10% in achlorhydria and rose up to 100% in cases with acid output above 30 mmol/h. The presence of CP did not correlate with signs of acute inflammation, but correlated significantly with those of chronic inflammation. No correlation was found in the antrum and a significant negative one in the body, between CP infestation and the extension of intestinal metaplasia. It is concluded that increased pH of gastric contents and mucus secreted by intestinalised glands may create unfavourable conditions for survival of the bacteria and might explain the decrease in the prevalence of CP in the more severe degrees of AG. The present results, however, give no definite answer to the question of the pathogenic significance of CP in the development of chronic gastritis.
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PMID:Campylobacter pylori in a sample of Finnish population: relations to morphology and functions of the gastric mucosa. 339 64

After oral infection of domesticated rabbits with 1,500 Graphidium strigosum-larvae III third-stage larvae were discovered in the stomach during the next 6 d, fourth-stage larvae from the 8th d and mature nematodes from the 34th d onwards. In 26 rabbits infected with 75...2,000 larvae III the prepatent period of Graphidium strigosum-infestation varied from 40 to 60, in most cases from 40 to 50 d. After one oral infection with 500...1,000 Graphidium strigosum-larvae III 3-month old domesticated rabbits showed no clinical symptoms, their performance was impaired but only insignificant and a population of 154 to 765 mature nematodes parasitizing in the stomach caused a gastritis catarrhalis chronica, partly a fibrosing gastritis.
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PMID:[Experimental studies on the course and consequences of infection with Graphidium strigosum (Nematoda, Trichostrongylidae) in Oryctolagus cuniculus (domestic rabbit)]. 380 49

A chronic gastritis caused by an infestation with O. tricuspis is described. The differential-diagnostic importance of this parasitosis in chronic maldigestive diseases is emphasized. Conventional coproscopic diagnostic procedures fail as the life cycle of the parasite is confined to the gastrum of the host.
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PMID:[Chronic gastritis caused by Ollulanus tricuspis (Leuckart, 1865) in a tiger]. 845 85

The aim was to determine the prevalence of Helicobacter heilmannii-like organisms in human gastric biopsies and the associated histology compared with that of Helicobacter pylori-bearing gastric biopsies. Furthermore, the feasibility of culturing H. heilmannii was examined. A consecutive series of 727 gastric biopsies from 650 patients were prospectively scrutinized for H. heilmannii. Their distribution pattern was recorded as well as the affiliated morphology of the gastric mucosa. Additional biopsies from some of the patients were examined microbiologically. Four cases (0.6%)(95% confidence intervals: 0.01-1.2%) of the examined material harboured H. heilmannii. The bacterial burden was graded as sparse in three cases, moderate in one case. The distribution pattern was patchy; thus, in no case did all biopsies from one endoscopy comprise H. heilmannii. Adhesion to epithelial cells was infrequent. A mild gastritis, active in three cases, characterized all biopsies. Lymphoid aggregates occurred in biopsies from three patients. Micropapillary tufting of the epithelial layer and intestinal metaplasia were not apparent. Culture studies proved successful in the one of the four cases assayed. In conclusion the morphology of H. heilmannii-bearing mucosa deviates from that of H. pylori-associated mucosa by the absence of epithelial damage in the former. This observation can in part be explained by the predominant location of H. heilmannii at a distance from the epithelium in contrast to the conspicuous H. pylori adhesion to epithelial cells, coupled with a usually low bacterial burden and patchy occurrence of H. heilmannii as opposed to the generally more heavy infestation with H. pylori.
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PMID:The histopathology of human gastric mucosa inhabited by Helicobacter heilmannii-like (Gastrospirillum hominis) organisms, including the first culturable case. 936 89


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