Gastric Cancer Risk in Achlorhydric Patients: A Long-Term Follow-up Study

Svendsen, J H; Dahl, Claus; Svendsen, Lars Bo; Christiansen, Peer

doi:10.3109/00365528609034615

Cited by 70 publications

(41 citation statements)

References 12 publications

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“…Hypochrolhydria, which is a well known high-risk factor for gastric cancer (Siurala et al 1966;Svendsen et al 1986;Correa et al1990), accompanied by corpus atrophy, should be at similar levels in CPG and MAG (Derakhshan et al 2006). Simply, the larger area undergoing atrophic changes including intestinal metaplasia in MAG may result in a higher risk of developing cancer (Cassaro et al 2000;Faraji and Frank 2002).…”

Section: Discussionmentioning

confidence: 98%

“…Atrophic gastritis is a well-recognized high-risk condition for developing gastric cancer, especially for intestinaltype cancer (Siurala et al 1966;Svendsen et al 1986;Correa et al 1990), and the risk varies depending on the severity or topography of the atrophic change (Cassaro et al 2000;Uemura et al 2001). Although corpus atrophy and its accompanying hypochlorhydria is known to be a primarily important risk factor for gastric cancer, histological analyses suggest that co-existing antral atrophy could represent additional substantial risk for gastric cancer in individuals with corpus atrophy (Sipponen and Stolte 1997;Rugge et al 2007).…”

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confidence: 99%

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Low Serum Levels of Pepsinogen and Gastrin 17 Are Predictive of Extensive Gastric Atrophy with High-Risk of Early Gastric Cancer

Kikuchi

Abe

Iijima

et al. 2011

Tohoku J. Exp. Med.

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Atrophic gastritis (AG) is a well-recognized high-risk condition for developing gastric cancer (GC). Gastrin 17 (G17), a hormone secreted from antral G cells, regulates gastric acid secretion, and its serum level is a possible indicator of antral atrophy. Serum pepsinogen is well established as the indicator of AG involving the corpus. Here we investigated whether serum PG and G17 levels would be useful for determining the topographic pattern of AG and estimating the risk of GC. Enrolled were 122 Japanese patients with early GC (114 well-to moderate-differentiated cancers and 8 poorly-differentiated cancers). In addition, 178 subjects without GC were recruited as control from those undergoing endoscopic examination (non-GC group). All subjects were histologically assigned to the following four groups: non-AG, antrum-predominant AG, corpus-predominant AG, and multifocal AG, affecting the antrum and corpus. Serum concentrations of pepsinogen and G17 were determined using ELISA. Multifocal AG was more frequent in the GC group than in the adjusted non-GC group, and had the highest risk of GC (OR 25.1). Serum G17 was significantly decreased with the exacerbation of antral atrophy in the coexistence of corpus atrophy. Serum biomarker profiles showed that the low levels of pepsinogen and G17 could discriminate between multifocal AG and other types of AG, but not with pepsinogen level alone. Serologically defined multifocal AG had the highest cancer risk among other serologically defined AG groups (OR 26.9). In conclusion, the low serum levels of pepsinogen and G17 are predictive of extensive gastric atrophy with high-risk of early GC.

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Section: Discussionmentioning

confidence: 98%

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confidence: 99%

Low Serum Levels of Pepsinogen and Gastrin 17 Are Predictive of Extensive Gastric Atrophy with High-Risk of Early Gastric Cancer

Kikuchi

Abe

Iijima

et al. 2011

Tohoku J. Exp. Med.

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“…The possibility was considered that excluding men with a history of gastric surgery may have introduced some bias into the area comparisons, more having been omitted in Caerphilly than in Bath. If it is assumed that none of these men had severe atrophic gastritis, the prevalence of this condition falls to 7.5%, 13.6%, and 11 .8% respectively in Bath, Caerphilly and Caerphilly adjusted for social class, the two Caerphilly rates (Correa et al, 1975 (Siurala et al, 1968), and that severe atrophic gastritis is associated prospectively with a four to six fold increase in the risk of stomach cancer (Svendsen et al, 1986). If (Varis et al, 1979).…”

Section: Resultsmentioning

confidence: 99%

Atrophic gastritis and vitamin C status in two towns with different stomach cancer death-rates

Burr

Samloff²,

Bates³

et al. 1987

Br J Cancer

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Summary A survey was conducted of 513 men aged 65-74 years living in two British towns with high and low stomach cancer death-rates. The prevalence of severe atrophic gastritis (defined as a serum pepsinogen I <20pg I) was significantly higher in the high-risk than in the low-risk town (14.5% and 7.7% respectively); it also tended to be higher in the manual workers, who are known to have a greater risk of stomach cancer than non-manual workers. The manual workers in the high-risk town were particularly likely to have had a partial gastrectomy. Plasma ascorbate concentration and fruit intake were lower in the high-risk area and lower social classes, suggesting a poorer vitamin C status. There was, however, no direct relationship between ascorbate concentration and the presence of severe atrophic gastritis. These findings are consistent with the hypothesis that risk of stomach cancer is determined in two stages -a long-term effect, producing atrophic gastritis; and a short-term effect in which vitamin C is protective.It has been suggested that the pathogenesis of stomach cancer involves two stages (Correa et al., 1975). Firstly, there seems to be a long-term effect, possibly initiated in childhood, and leading to severe atrophic gastritis and intestinal metaplasia in the gastric mucosa. Secondly, carcinogenesis occurs in some stomachs which have undergone these mucosal changes. Fresh fruit and vegetables seem to protect against this effect, possibly because of their vitamin C content. If this sequence is correct, populations with a high risk of stomach cancer should have a higher prevalence of severe atrophic gastritis and a lower vitamin C status than others.Stomach cancer death rates show wide geographical variations. Even within the United Kingdom there are substantial local differences, death rates being substantially higher in Wales than in much of Southern England. There is also a marked social class gradient in the disease; for men aged 15-64 years the standardized mortality ratio (SMR) rises steadily from 50 in social class I (professional people) to 147 in social class V (unskilled manual workers) (Office of Population Censuses and Surveys, 1978).A survey was therefore designed to discover whether the geographical and social-class differences in stomach cancer mortality are reflected by similar differences in vitamin C status (as represented by plasma ascorbate concentration) and the prevalence of severe atrophic gastritis. Diagnosis of severe atrophic gastritis was based on serum pepsinogen (PG), which exists in two forms, PG I and PG II (Samloff et al., 1982). Chronic atrophic gastritis and intestinal metaplasia are characterised by a low serum PG I (below 20 pg 1-) due to a preferential loss of the fundal chief cells which produce this enzyme. A low PG I correlates very well with the degree of severity of gastritis, pernicious anaemia (Samloff et at., 1982), achlorhydria (Levine & Beer, 1984), and the risk of subsequent stomach cancer (Nomura et at., 1980). Subjects and methodsIn view of the steep rise...

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“…[10][11][12][13]43 We found no obvious difference in dietary factors, such as the total energy intake or total fat, salt, vitamin, and dietary fiber intakes between the sexes. Although smoking habits and alco- hol consumption are more common in men than in women, our stratified analysis did not demonstrate an interaction between these factors and H pylori infection (data not shown).…”

Section: Commentmentioning

confidence: 99%

Impact of Helicobacter pylori Infection on Gastric Cancer Incidence in a General Japanese Population

Yamagata¹,

Kiyohara²,

Aoyagi³

et al. 2000

Arch Intern Med

107

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Background: Several nested case-control studies have reported the potentially causal relationship between Helicobacter pylori infection and the development of gastric cancer. However, there has been no prospective study evaluating this issue. The purpose of this study is to examine the impact of H pylori infection on gastric cancer occurrence in a general Japanese population (Hisayama, Japan) stratified according to sex, using a prospective study design.Methods: A total of 2602 subjects aged 40 years or older (1070 men; mean age, 57 years; 1532 women; mean age, 59 years) without a history of gastrectomy or gastric cancer were classified according to the status of the serum IgG antibodies to H pylori and observed prospectively for 9 years from 1988. Results:Infection of H pylori was more common in men (71.5%) than in women (62.5%; PϽ.001). The ageadjusted incidence of gastric cancer for men (5.3 per 1000 person-years) was 4-fold higher than that for women (1.3; PϽ.001). In men, the age-adjusted incidence of gastric cancer was significantly higher in the subjects with H pylori infection than in those without it (6.2 vs 2.5; relative risk, 2.59 [95% confidence interval, 1.03-6.50]), whereas no significant difference was observed in women (1.2 vs 1.1; relative risk, 0.99 [95% confidence interval, 0.36-2.68]). These results were similar even after controlling for other risk factors in multivariate analysis. It was estimated that 40.1% of gastric cancers for men in this cohort were attributable to H pylori infection.Conclusion: A significant relationship exists between infection with H pylori and subsequent occurrence of gastric cancer for men but not for women in this Japanese population. Med. 2000;160:1962-1968 S INCE THE discovery of Helicobacter pylori in 1983, much research has focused on the relationship of this bacterium to gastric cancer. A number of clinical case-control studies have found positive associations between H pylori infection and gastric cancer. Arch Intern1 In addition, 8 prospective, nested case-control studies on this issue have since been reported. [2][3][4][5][6][7][8][9] Of these nested casecontrol studies, five [2][3][4]8,9 have shown a significant association between IgG seropositivity for H pylori and gastric cancer, and one 7 has shown that the risk of gastric cancer was significantly increased among subjects showing positive IgA antibodies against H pylori, but not among those showing positive IgG antibodies. Another 2 studies from Asian countries 5,6 have failed to reveal a significant relationship between IgG seropositivity and gastric cancer. Since all previous studies were of crosssectional or nested case-control design, the possibility of selection bias could not be ruled out, and the impact of H pylori infection on the development of gastric cancer in a general population could not be fully evaluated. Further, a number of additional factors that might influence gastric cancer, such as smoking habits, alcohol intake, history of peptic ulcer disease, and dietary factors, 10-14 shoul...

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Gastric Cancer Risk in Achlorhydric Patients: A Long-Term Follow-up Study

Cited by 70 publications

References 12 publications

Low Serum Levels of Pepsinogen and Gastrin 17 Are Predictive of Extensive Gastric Atrophy with High-Risk of Early Gastric Cancer

Low Serum Levels of Pepsinogen and Gastrin 17 Are Predictive of Extensive Gastric Atrophy with High-Risk of Early Gastric Cancer

Atrophic gastritis and vitamin C status in two towns with different stomach cancer death-rates

Impact of Helicobacter pylori Infection on Gastric Cancer Incidence in a General Japanese Population

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