Helicobacter pylori CagA status associated with gastric cancer incidence rate variability in Costa Rican regions View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2006-06

AUTHORS

Sergio A Con, Ana L Valerín, Hiroaki Takeuchi, Reinaldo Con-Wong, Vicky G. Con-Chin, Gil R Con-Chin, Sachiko N Yagi-Chaves, Fernando Mena U., Fernando Brenes Pino, Guillermo Echandi, Michiya Kobayashi, Mario Monge-Izaguirre, Mitsuaki Nishioka, Norihito Morimoto, Tetsuro Sugiura, Keijiro Araki

ABSTRACT

BackgroundWe evaluated several risk factors for gastric cancer in Costa Rican regions having contrasting gastric cancer incidence rates, despite the small dimensions of the country.MethodsA total of 180 dyspeptic patients were classified into two groups according to the gastric cancer incidence (GCI) rate in their Costa Rican region: group A, with a high GCI rate (n = 91) and group B, with a low GCI rate (n = 89). Helicobacter pylori infection was detected by rapid urease test, Gram staining, and histological observation. Antral and corpus specimens were obtained to assess the grade of inflammation, topography of gastritis, gastric atrophy, and intestinal metaplasia by histological examination. Serum CagA antibody was measured by an antigen-specific enzyme-linked immunosorbent assay.ResultsThere was no significant difference in H. pylori prevalence between groups A (73%) and B (63%); however, serum CagA antibody was more frequently detected in group A (79%) than in group B (54%) [P = 0.02; odds ratio (OR), 2.68]. Among patients under 60 years of age, serum CagA antibody was even more frequently detected in group A (81%) than in group B (49%) (P < 0.01; OR, 4.50). The prevalence of corpus-predominant gastritis, atrophic gastritis, and moderate/severe grades of neutrophilic infiltration was higher in serum CagA antibody-positive patients than in CagA antibody-negative patients (P = 0.003, 0.04, and 0.002, respectively).ConclusionsInfection with H. pylori possessing the cagA gene is associated with the development of severe gastric damage such as gastric atrophy, leading to gastric cancer, and probably influences the differences in GCI between Costa Rican regions. More... »

PAGES

632

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00535-006-1812-3

DOI

http://dx.doi.org/10.1007/s00535-006-1812-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1029028744

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16932999


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27 schema:description BackgroundWe evaluated several risk factors for gastric cancer in Costa Rican regions having contrasting gastric cancer incidence rates, despite the small dimensions of the country.MethodsA total of 180 dyspeptic patients were classified into two groups according to the gastric cancer incidence (GCI) rate in their Costa Rican region: group A, with a high GCI rate (n = 91) and group B, with a low GCI rate (n = 89). Helicobacter pylori infection was detected by rapid urease test, Gram staining, and histological observation. Antral and corpus specimens were obtained to assess the grade of inflammation, topography of gastritis, gastric atrophy, and intestinal metaplasia by histological examination. Serum CagA antibody was measured by an antigen-specific enzyme-linked immunosorbent assay.ResultsThere was no significant difference in H. pylori prevalence between groups A (73%) and B (63%); however, serum CagA antibody was more frequently detected in group A (79%) than in group B (54%) [P = 0.02; odds ratio (OR), 2.68]. Among patients under 60 years of age, serum CagA antibody was even more frequently detected in group A (81%) than in group B (49%) (P < 0.01; OR, 4.50). The prevalence of corpus-predominant gastritis, atrophic gastritis, and moderate/severe grades of neutrophilic infiltration was higher in serum CagA antibody-positive patients than in CagA antibody-negative patients (P = 0.003, 0.04, and 0.002, respectively).ConclusionsInfection with H. pylori possessing the cagA gene is associated with the development of severe gastric damage such as gastric atrophy, leading to gastric cancer, and probably influences the differences in GCI between Costa Rican regions.
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35 CagA antibody
36 ConclusionsInfection
37 Costa Rican regions
38 GCI
39 Gram staining
40 Helicobacter pylori CagA status
41 Helicobacter pylori infection
42 ResultsThere
43 age
44 antibodies
45 antibody-negative patients
46 antibody-positive patients
47 antigen-specific enzyme-linked immunosorbent
48 antral
49 atrophic gastritis
50 atrophy
51 cagA gene
52 cagA status
53 cancer
54 cancer incidence rates
55 corpus specimens
56 corpus-predominant gastritis
57 countries
58 damage
59 development
60 differences
61 dimensions
62 dyspeptic patients
63 enzyme-linked immunosorbent
64 examination
65 factors
66 gastric atrophy
67 gastric cancer
68 gastric cancer incidence rates
69 gastric damage
70 gastritis
71 genes
72 grade
73 grade of inflammation
74 group
75 group A
76 group B
77 histological examination
78 histological observations
79 immunosorbent
80 incidence rate
81 infection
82 infiltration
83 inflammation
84 intestinal metaplasia
85 metaplasia
86 neutrophilic infiltration
87 observations
88 patients
89 prevalence
90 pylori
91 pylori CagA status
92 pylori infection
93 pylori prevalence
94 rapid urease test
95 rate
96 rate variability
97 region
98 risk factors
99 serum CagA antibody
100 severe gastric damage
101 severe grades
102 significant differences
103 small dimensions
104 specimens
105 staining
106 status
107 test
108 topography
109 topography of gastritis
110 total
111 urease test
112 variability
113 years
114 years of age
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