Clinical Significance of IgG Antibody Titer against Helicobacter pylori

Tatemichi, Masayuki; Sasazuki, Shizuka; Inoue, Manami; Tsugane, Shoichiro

doi:10.1111/j.1523-5378.2009.00681.x

Cited by 35 publications

(49 citation statements)

References 28 publications

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“…As shown in Table 2, a ''low risk'' stomach reflects less mucosal inflammation and atrophy with preserved acid secretion, which is in line with previous results, indicating that ''low risk'' stomachs according to our criteria have a low likelihood of future cancer development [13,14,16,17,25]. The low incidence of gastric cancer in persons with ''low risk'' stomachs has also been widely reported from Japan as well as other Asian countries, including Korea and China [13,14,16,17,[24][25][26]. Conversely, in terms of the incidence of ''low risk'' stomach among gastric cancer subjects, only 1% to 2% of gastric cancer patients (including cases of noncardia and cardia gastric cancer) showed lack of infection with H. pylori and normal pepsinogen-I levels [27].…”

Section: Discussionsupporting

confidence: 88%

“…Ohata [17] reported that no cancer developed in subjects with negative H. pylori infection and normal pepsinogen status during a follow-up of 4655 patients for a period of 7.7 years, and several other investigators [13,14,16] also reported an extremely low incidence of gastric cancer in subjects without gastric mucosal atrophy and inflammation. However, it is important to evaluate atrophy using only objective endoscopic findings during routine endoscopy.…”

Section: Introductionmentioning

confidence: 93%

“…of Pages 8 FGPs predict low gastric carcinogenesis 3 infection-positive. Stomachs were defined as ''atrophic'' when the criteria of both pepsinogen-I ≤ 70 ng/mL and pepsinogen-I/II ratio ≤ 3 were satisfied, and the rest were defined as ''normal'' [11][12][13][14][15].…”

Section: Assays For Antibodies Against H Pylori and For Serum Pepsinmentioning

confidence: 99%

“…Reduced levels of serum pepsinogen-I and the ratio of serum pepsinogen-I/II are reliable markers for atrophic gastritis, a high risk precursor of gastric cancer [11][12][13][14][15]. The recent combined analysis of H. pylori seropositivity and mucosal atrophy determined by the serum pepsinogen method allows better stratification of the risk for development of gastric cancer than pepsinogen measurement alone [13][14][15][16][17]. This screening method is also effective for detecting the population exhibiting a low risk of stomach carcinogenesis, i.e., without gastric mucosal atrophy and inflammation [13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

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Fundic gland polyps accurately predict a low risk of future gastric carcinogenesis

Kishikawa

Kaida

Takarabe

et al. 2014

Clinics and Research in Hepatology and Gastroenterology

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 93%

Section: Assays For Antibodies Against H Pylori and For Serum Pepsinmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Fundic gland polyps accurately predict a low risk of future gastric carcinogenesis

Kishikawa

Kaida

Takarabe

et al. 2014

Clinics and Research in Hepatology and Gastroenterology

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“…Subjects with an antibody concentration <10 U/mL were classified into the infection-negative group according to the manufacturer's recommended cutoff value; this cutoff value has been widely used in previous studies [6,7,8,11,23,24]. Using these criteria, subjects with a normal PG test and negative status for H. pylori antibody titer were classified into Group A [6,7,8,11].…”

Section: Methodsmentioning

confidence: 99%

Cutoff Pepsinogen Level for Predicting Unintendedly Eradicated Cases of Helicobacter pylori Infection in Subjects with Seemingly Normal Pepsinogen Levels

Kishikawa¹,

Kimura²,

Ito³

et al. 2017

Digestion

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Backgrounds/Aims: In the ABC method, which is a method for risk stratification of gastric cancer using serum anti-Helicobacter pylori antibody and pepsinogen (PG) test, subjects with normal PG and seronegative for H. pylori are named as “Group A” and are regarded as having a low risk of gastric cancer. These “Group A” subjects include unintentionally eradicated cases at relatively high risk, and this study aimed to identify these subjects. Methods: Of the 109 subjects, 76 were classified as uninfected Group A subjects with negative histologic H. pylori infection and no histologic and endoscopic atrophy, and 33 subjects were classified serologically as Group A after successful eradication, which are serologically equal to the unintendedly eradicated cases in Group A. The usefulness of measuring PG levels to detect post-eradication cases was validated by using a receiver operating characteristic (ROC) curve analysis. Results: The area under the ROC curve for PGI level was 0.736 ± 0.06 (p < 0.01; cutoff value, 37.0 ng/mL; sensitivity, 77.6%; specificity, 72.7%), and that for the PGI/II ratio was 0.660 ± 0.06 (p < 0.01; cutoff value, 5.1; sensitivity, 84.2%; specificity, 43.4%). Conclusion: PGI levels of ≤37 ng/mL and PGI/II ratios of ≤5.1 effectively identified unintendedly eradicated cases in Group A.

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Additive interactions between PRKAA1 polymorphisms and Helicobacter pylori CagA infection associated with gastric cancer risk in Koreans

et al. 2016

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Although several studies reported genetic polymorphisms in protein kinase AMP‐activated alpha 1 catalytic subunit (PRKAA1) and their associations with gastric cancer risk, few have evaluated associations between Helicobacter pylori infection and PRKAA1 gene‐environment interactions. Here, we evaluated the effects of interactions between H. pylori infection and PRKAA1 polymorphisms on gastric cancer risk in Koreans. In this hospital‐based case–control study, PRKAA1 genotypes were analyzed and H. pylori infection and CagA status were examined using a serologic method in 846 pairs of gastric cancer patients and controls matched for age and sex. H. pylori seropositivity was associated with a 1.43‐fold [95% confidence interval: 1.12–1.81] increase in the risk of gastric cancer, and CagA low‐positive titers during H. pylori infection increased the risk by 1.85‐fold (95% confidence interval, 1.38–2.48). Significant positive interaction between the PRKAA1 rs13361707 genotype and H. pylori infection was verified on an additive scale [relative excess risk due to interaction, 0.55; 95% confidence interval, 0.05–1.04; P = 0.030], and the gene‐environment interaction between PRKAA1 rs13361707 and CagA status was also statistically significant (relative excess risk due to interaction, 0.50; 95% confidence interval, 0.30–0.70; P < 0.001). Our results indicated that H. pylori infection, CagA status, and PRKAA1 polymorphisms were risk factors for gastric cancer in Koreans, and that the combination of two of these factors rather than their independent effects synergistically increased the risk.

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Clinical Significance of IgG Antibody Titer against Helicobacter pylori

Cited by 35 publications

References 28 publications

Fundic gland polyps accurately predict a low risk of future gastric carcinogenesis

Fundic gland polyps accurately predict a low risk of future gastric carcinogenesis

Cutoff Pepsinogen Level for Predicting Unintendedly Eradicated Cases of <b><i>Helicobacter pylori</i></b> Infection in Subjects with Seemingly Normal Pepsinogen Levels

Additive interactions between PRKAA1 polymorphisms and Helicobacter pylori CagA infection associated with gastric cancer risk in Koreans

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