Long-term sequelae of Helicobacter pylori gastritis

Kuipers, Ernst J.; Peña, A. S.; Festen, H. P. M.; Meuwissen, S. G. M.; Uyterlinde, Anne M.; Roosendaal, R.; Pals, Gerard; Nelis, G. F.

doi:10.1016/s0140-6736(95)91084-0

Cited by 694 publications

(468 citation statements)

References 18 publications

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“…This IM incidence is significantly higher than that in German patients, in whom we found only 28% in H. pylori-infected subjects, and only 5% in uninfected subjects (Bayerdorffer et al, 1992). Similar observations have been made by other investigators (Eidt and Stolte, 1994;Kuipers et al, 1995). However, as IM was more common in H. pylori-infected carcinoma patients than in infected non-carcinoma patients, and also more common in H. pylori-negative carcinoma patients than in uninfected non-carcinoma patients, it is very possible that IM may be a marker for an increased gastric carcinoma risk in H. pyloriinfected as well as uninfected subjects.…”

Section: Discussionsupporting

confidence: 90%

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori

Miehlke

Hackelsberger²,

Meining³

et al. 1998

Br J Cancer

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Summary In 50 Helicobacterpylori-infected gastric carcinoma patients the corpus gastritis was significantly higher than in matched H. pyloripositive control subjects (P < 0.01). Atrophy and intestinal metaplasia (IM) occurred significantly more often in the antrum of carcinoma patients (P < 0.01). The odds ratio for gastric carcinoma was 8.85 for high-grade corpus gastritis and 8.04 when atrophy in the antrum was present.

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Section: Discussionsupporting

confidence: 90%

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori

Miehlke

Hackelsberger²,

Meining³

et al. 1998

Br J Cancer

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“…Another 4 articles were excluded for the following reasons: all patients had either chronic gastritis or CAG at baseline, incidence of CAG was based on biopsies and not on study participants, incidence of CAG and metaplasia or either of them were grouped together and in one study, no mean follow-up time could be estimated. Due to these exclusions, only 14 studies (from 15 articles) with information on the incidence of CAG could be included in this review [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24]. According to the above described criteria, all of these studies included more than 15 study participants who were diagnosed to be free of CAG at baseline, either by histology ('normal' or 'superficial gastritis') or by serum pepsinogen (PG) levels.…”

Section: Resultsmentioning

confidence: 99%

“…2 of the studies were conducted in multiple centres in different countries [20,22]. Studies were carried out in Sweden, [10] Columbia, [11] the Netherlands, [12,13] the Netherlands and Sweden, [14] Finland, [15] Estonia, [16,24] Japan, [17,23] USA, [18] Slovenia, [19] Australia, Canada, Germany, and the Netherlands, [20] Germany [21] and Denmark, Finland, Norway and Sweden [22]. Most of the studies were not population-based and consisted of symptomatic patients.…”

Section: Resultsmentioning

confidence: 99%

Incidence of chronic atrophic gastritis: systematic review and meta-analysis of follow-up studies

et al. 2010

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Chronic atrophic gastritis (CAG) is an important precursor lesion of intestinal gastric cancer. As it is typically asymptomatic, epidemiological data on the incidence of CAG are sparse. We aimed to provide an overview of published data on CAG incidence (overall and according to risk factors) from follow-up studies. Articles with information on incidence of CAG published in English until 26th of July 2009 were identified through a systematic MEDLINE and EMBASE search. Data extracted include study characteristics and key findings regarding the incidence of CAG. A meta-analysis was performed on the association between Helicobacter pylori infection and CAG incidence. Overall, data on CAG incidence were available from 14 studies, in 7 studies incidence could be estimated according to H. pylori infection. Most studies were conducted in symptomatic or high risk populations and the maximum number of incident cases was 284. Incidence estimates ranged from 0 to 11% per year and were consistently below 1% in patients not infected with H. pylori. The highest incidence was observed in a special study conducted on ulcer patients treated by proximal gastric vagotomy. Rate ratios for the association between H. pylori infection and CAG incidence ranged from 2.4 to 7.6 with a summary estimate of 5.0 (95% confidence interval: 3.1-8.3). Incidence of CAG is very low in the absence of H. pylori infection. There is a need for more population-based studies to provide comparable estimates of incidence and the impact of risk factors in the development of CAG.

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“…In senescence, the current view claims that (1) prolonged infection with H. pylori is the major determinant for development of IM in the stomach; (2) with aging, the inflammation of the antrum burns out (as measured by a decrease of the antrum gastritis sum score); (3) the microbes, the inflammation process and the corpus-antrum border are consecutively shifting (as measured by an increase of the corpus gastritis sum score); and (4) the gastric acid secretion declines. [18][19][20][21][22][23][24][25] The prevalence of H. pylori infection is generally supposed to increase with age. 26 More recently, it was reported in Japan, that the prevalence of positive rate of serum anti-H. pylori-IgG as well as H. pylori infection detected histological and by the 13 C-urea breath test is decreasing in longliving elderly, leading to a concomitant decrease of Helicobacter pylori virulence factors A Soltermann et al the prevalence of gastric cancer in subjects older than 85 years.…”

Section: Discussionmentioning

confidence: 99%

Correlation of Helicobacter pylori virulence genotypes vacA and cagA with histological parameters of gastritis and patient's age

et al. 2007

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The histological parameters of Helicobacter pylori (H. pylori) gastritis are dependent on the virulence factor profile of the microbe, which includes the cytotoxins vacA (vacuolating cytotoxin A) and cagA (cytotoxinassociated gene A) as well as the duration of infection. The virulence factor genotypes vacA and cagA were assessed by the line probe reverse hybridization assay INNO-LiPA and correlated with the histological parameters of H. pylori infection, in particular intestinal metaplasia (IM) as well as with the patient's age. A total of 120 patients were analyzed; 47 patients with IM in the antrum and 73 control patients without this alteration. The vacA s1 cagA þ genotype (high virulence) correlated with the presence of antral IM, a more intense acute inflammation in both antrum and corpus and the formation of ulcer. The vacA m1 genotype (high virulence) correlated with a more intense acute inflammation in only the corpus as well as more prominent Russell bodies in the antrum. H. pylori strains with the vacA s2 m2 cagAÀ genotype (low virulence) were rarely found in these conditions (all P o0.05). No correlation with the virulence status was found for the type and extent of IM, the intensity of chronic inflammation, the formation of lymphoid follicles and the microbial density. Furthermore, patients with IM were 7 years older than their counterparts without (Po0.05). Finally, there was a trend for more virulent vacA s1 m1 cagA þ strains to be found in younger individuals (P40.05). The virulence genotype of the microbe is an important determinant for the severity of the gastritis and the formation of antral IM. Age is an additional factor for the development of IM. Keywords: Helicobacter; virulence; gastritis; histology; resistance The Gram-negative bacteria Helicobacter pylori colonize the human stomach. 1 Prolonged infection is associated with several diseases like chronic gastritis, peptic ulcer disease and stomach carcinoma or lymphoma. This association depends on bacterial, host and environmental factors. Among the bacterial factors, several virulence proteins determine the severity of inflammation and the formation of intestinal metaplasia (IM). [2][3][4][5] The most studied virulence proteins are vacA and cagA, which are injected into the gastric epithelial cell through a multimeric protein complex. 6 This protein complex is elaborated from the PAI (pathogenicity-island), a 40 kb DNA segment. CagA makes part of the PAI and targets particularly the phosphorylation cascade and the tight junctions. 7-9 H. pylori are either cagA-positive or -negative. VacA, present in all H. pylori, is located outside the PAI and forms an oligomeric pore with channel activity. 10,11 VacA has two variable parts: The s (signal peptide) region exists as allele s1 or s2. The m (middle) region occurs as m1 or m2 allelic type. The allele combination s1 m1 confers high, s1 m2 intermediate and s2 m2 low toxin activity. Most vacA s1 strains are cagA-positive, thus the two markers are closely related. 12 H. pylori infection is normal...

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Long-term sequelae of Helicobacter pylori gastritis

Cited by 694 publications

References 18 publications

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori

Incidence of chronic atrophic gastritis: systematic review and meta-analysis of follow-up studies

Correlation of Helicobacter pylori virulence genotypes vacA and cagA with histological parameters of gastritis and patient's age

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