Helicobacter pylorhassodated antibodies in patients with duodenal ulcer, gastric and oesophageal adenocarcinoma

Ce, Grimley; Rl, Holder; De, Loft; Morris, Arthur J.; Nwokolo, CU

doi:10.1097/00042737-199905000-00007

Cited by 25 publications

(26 citation statements)

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“…The view that these reciprocal trends of OA and H pylori may be associated is supported by several studies showing that virulent strains of H pylori are found less commonly among patients with Barrett's oesophagus and OA when compared with controls. [1][2][3] This has led to the suggestion that H pylori colonisation may protect against gastro-oesophageal reflux (GORD) and OA. Others, arguing that there is no plausible biological mechanism, have suggested that the observed trends are purely coincidental.…”

mentioning

confidence: 99%

Plasma ghrelin following cure of Helicobacter pylori

Nwokolo

2003

Gut

220

159

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mentioning

confidence: 99%

Plasma ghrelin following cure of Helicobacter pylori

Nwokolo

2003

Gut

220

159

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“…The results of serological tests have done much to establish H. pylori as a causative agent of peptic ulcer disease and gastric cancer (13,17). Serological detection of the cytotoxin-associated gene product A (CagA) of H. pylori appears to correlate with further increases in risk for peptic ulcer disease and gastric cancer (3,11,25).…”

mentioning

confidence: 99%

Reliability of Helicobacter pylori and CagA Serological Assays

Everhart

Kruszon-Moran

Pérez-Pérez

2002

Clin Vaccine Immunol

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Background serological assays for Helicobacter pylori are commonly used without knowledge of reliability. This information is needed to define the ability of serological tests to determine either new cases of infection or loss of infection in longitudinal studies. We evaluated the reproducibility and the interrelationships of serological test results for H. pylori and cytotoxin-associated gene product A (CagA) enzyme-linked immunoassays within a subset of participants in a population-based study. Stored samples from 1,229 participants in the third U.S. National Health and Nutrition Examination Survey were replicate serologically tested for H. pylori and CagA. Overall disagreement was 3.4% between duplicate tests for H. pylori (or 2.3% if equivocal results were disregarded). Six percent of samples positive on the first test had an immune serum ratio at least 30% lower on repeat testing. The odds ratio for H. pylori seropositivity on retesting was 2.8 (95% confidence interval [CI] ‫؍‬ 1.8 to 4.5) when CagA serology was positive versus when it was negative. CagA antibody was found among 47.8% of H. pylori-equivocal and 7.0% of H. pylori-negative samples. CagA-positive yet H. pylorinegative samples were more likely to occur among Mexican Americans (odds ratio, 5.2; 95% CI ‫؍‬ 2.4 to 11.4) and non-Hispanic blacks (odds ratio, 5.5; 95% CI ‫؍‬ 2.3 to 13.0) than among non-Hispanic whites. Relying on repeated H. pylori serological tests over time to determine infection rates may result in misinterpretation due to limits in test reproducibility. CagA testing may have a role in verifying infection.

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“…Reports of the prevalence of HP infection in esophageal disease vary from 14% to 40% in GERD/esophagitis and 25% to 62% in CLO [22][23][24][25][26][27], although the prevalence of HP in esophageal adenocarcinoma seems to be much lower and reports have suggested anything from 0% to 20% [23,25,28]. From our study of a cohort of patients with CLO, the prevalence of HP infection in patients that had been tested was fairly high, at 55.7%.…”

Section: Discussionmentioning

confidence: 65%

“…Even if the remaining 571 patients who were not tested for HP were found to be negative, this would give an overall prevalence of HP infection of 24.5%. As we would reasonably predict this to be higher, it may be that the prevalence of HP in the entire cohort would have been greater than the reported prevalence of HP infection in normal/control populations, which ranges from 17% to 36% [24,28]. Whether it would have reached reported prevalence rates seen in patients with PUD, 48-94% [24,28], however, seems unlikely.…”

Section: Discussionmentioning

confidence: 77%

Helicobacter pylori Infection and Severity of Reflux-Induced Esophageal Disease in a Cohort of Patients with Columnar-Lined Esophagus

Ramus¹,

Gatenby²,

Caygill³

et al. 2007

Dig Dis Sci

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The relationship between Helicobacter pylori infection and reflux-induced esophageal diseased is controversial. We examined esophageal disease severity in patients with columnar-lined esophagus and compared results between patients with and without Helicobacter pylori infection. Medical records of 1000 patients diagnosed with columnar-lined esophagus were examined. Endoscopic and histological findings of reflux-induced esophageal disease were compared between H. pylori-positive and H. pylori-negative patients. Four hundred twenty-nine patients (42.9%) showed evidence of H. pylori status, of whom 239 (55.7%) were positive and 190 (44.3%) negative. There were no significant differences in length of columnar-lined segment (P = 0.305), frequency of associated esophagitis (P = 0.583), or presence of gastroduodenal inflammation (P = 0.335, P = 0.131) between the two groups. Histological grade of esophageal disease severity was similar between them, with no statistically significant differences (P = 0.231). We conclude that in patients with established columnar-lined esophagus, there appears to be no difference in severity of reflux-induced esophageal disease between those with and those without H. pylori infection.

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Helicobacter pylorhassodated antibodies in patients with duodenal ulcer, gastric and oesophageal adenocarcinoma

Cited by 25 publications

References 0 publications

Plasma ghrelin following cure of Helicobacter pylori

Plasma ghrelin following cure of Helicobacter pylori

Reliability of Helicobacter pylori and CagA Serological Assays

Helicobacter pylori Infection and Severity of Reflux-Induced Esophageal Disease in a Cohort of Patients with Columnar-Lined Esophagus

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