Value of Serology (ELISA and Immunoblotting) for the Diagnosis of &lt;i&gt;Campylobacter pylori&lt;/i&gt; Infection

Peña, A. S.; Endtz, Hubert P.; Offerhaus, G.J.A.; Hoogenboom-Verdegaal, A. M. M.; Duijn, Wim van; Vargas, Nancy; Hartog, G. den; Kreuning, J; Reyden, J. van der; Mouton, R. P.; Lamers, C. B. H. W.

doi:10.1159/000199902

Cited by 64 publications

(29 citation statements)

References 25 publications

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“…Specific serum IgG antibodies against H. pylori were measured using an in-house ELISA technique, as described [21]. An absorbance index above 0.32 was considered positive.…”

Section: Methodsmentioning

confidence: 99%

Colonization with cagA-Positive Helicobacter pylori Strains Inversely Associated with Reflux Esophagitis and Barrett’s Esophagus

et al. 2000

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Aim: The hypothesis that colonization with cagA⁺ Helicobacter pylori strains protects against the development of gastroesophageal reflux disease (GERD) and its complications is tested. Methods: Patients with reflux esophagitis and Barrett’s esophagus were studied. Antral biopsy specimens were obtained for detection of H. pylori. A serum sample was obtained for determination of IgG antibodies to H. pylori and to the CagA protein. Results: 736 patients were studied. 118 patients had reflux esophagitis, 36 had Barrett’s esophagus, 108 had hiatal hernia without signs of inflammation (the reflux group), and 20 patients had esophageal or stomach cancer. The remaining 454 patients had no signs of GERD. The 262 patients with reflux disease had a significantly lower prevalence of H. pylori (34.9%) than the 454 controls (54.6%; p < 0.001). Among 310 H. pylori-positive patients from whom serum was available, colonization with cagA⁺ strains was detected in 59% in the control group versus 35% in the reflux group (p < 0.001). Conclusion: Patients with reflux esophagitis and Barrett’s esophagus have a significantly lower prevalence of H. pylori colonization than controls, in particular of the cagA⁺ type. These data suggest that colonization with cagA⁺ H. pylori strains may be protective against the development of GERD

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“…Specific serum IgG antibodies against H. pylori were measured using an in-house ELISA technique, as described [21]. An absorbance index above 0.32 was considered positive.…”

Section: Methodsmentioning

confidence: 99%

Colonization with cagA-Positive Helicobacter pylori Strains Inversely Associated with Reflux Esophagitis and Barrett’s Esophagus

et al. 2000

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“…Severe atrophic gastritis or gastric atrophy were defined as a PGI:PGII < 1.6 combined with a PGI concentration < 17 g/L (32). IgG antibodies to H. pylori were measured with a modified enzymelinked immunosorbent assay (33).…”

Section: Laboratory Techniquesmentioning

confidence: 99%

Role of cobalamin intake and atrophic gastritis in mild cobalamin deficiency in older Dutch subjects

Asselt

Groot

Staveren

et al. 1998

The American Journal of Clinical Nutrition

170

108

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Background:The reason for the high prevalence of mild cobalamin (vitamin B-12) deficiency in the elderly is poorly understood. Objective: We aimed to determine the reason for this high prevalence. Design: We examined cobalamin intake, the presence and severity of atrophic gastritis, the presence of Helicobacter pylori infection, and plasma cobalamin and methylmalonic acid (MMA) concentrations in 105 healthy, free-living, older subjects aged 74-80 y. Results: Mild cobalamin deficiency, ie, low to low-normal plasma cobalamin concentrations (< 260 pmol/L) and elevated plasma MMA concentrations (> 0.32 mol/L), were found in 23.8% of subjects; 25.7% of subjects were not cobalamin deficient (plasma cobalamin ≥ 260 pmol/L and plasma MMA ≤ 0.32 mol/L). Six subjects (5.8%), including 1 with mild cobalamin deficiency, had dietary cobalamin intakes below the Dutch recommended dietary intake of 2.5 g/d. Mildly cobalamin-deficient subjects had lower total (diet plus supplements) cobalamin intakes (median: 4.9 g/d; 25th and 75th percentiles: 3.9, 6.4) than did non-cobalamin-deficient subjects (median: 6.3 g/d; 25th and 75th percentiles: 5.4, 7.9) (P = 0.0336), mainly because of less frequent use of cobalamin supplements (8% compared with 29.6%; 2 = 3.9, P = 0.048). Atrophic gastritis was found in 32.4% of the total study group: mild to moderate in 19.6% and severe in 12.7%. The prevalence of severe atrophic gastritis, but not mild-to-moderate atrophic gastritis, was higher in mildly cobalamin-deficient subjects (25%) than in non-cobalamin-deficient subjects (3.7%) ( 2 = 4.6, P = 0.032). The prevalence of immunoglobulin G antibodies to H. pylori was similar in mildly cobalamin-deficient subjects (54.2%) and in non-cobalamin-deficient subjects (44.4%) ( 2 = 0.5, P = 0.5). Conclusions:The high prevalence of mild cobalamin deficiency in healthy, free-living, older Dutch subjects could be explained by inadequate cobalamin intake or severe atrophic gastritis in only 28% of the study population. Other mechanisms explaining mild cobalamin deficiency in older people must be sought.Am J Clin Nutr 1998;68:328-34.

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“…10 An absorbance index above 0.32 was considered positive. Sensitivity and specificity of this ELISA for the detection of H pylori carriage were 98.5% and 91.7%, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…Sensitivity and specificity of this ELISA for the detection of H pylori carriage were 98.5% and 91.7%, respectively. 10 Determination of the H pylori cagA status was based on the presence of serum IgG antibodies to orv220, a 65 kDa recombinant CagA product purified from Escherichia coli. 9 The presence of these antibodies was assessed by means of ELISA according to previously described methods.…”

Section: Methodsmentioning

confidence: 99%

Colonisation density and topographic localisation of Helicobacter pylori do not depend on the cagA status

Twisk

Kusters²,

Balk³

et al. 2001

Journal of Clinical Pathology

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Value of Serology (ELISA and Immunoblotting) for the Diagnosis of <i>Campylobacter pylori</i> Infection

Cited by 64 publications

References 25 publications

Colonization with <i>cag</i>A-Positive <i>Helicobacter pylori</i> Strains Inversely Associated with Reflux Esophagitis and Barrett’s Esophagus

Colonization with <i>cag</i>A-Positive <i>Helicobacter pylori</i> Strains Inversely Associated with Reflux Esophagitis and Barrett’s Esophagus

Role of cobalamin intake and atrophic gastritis in mild cobalamin deficiency in older Dutch subjects

Colonisation density and topographic localisation of Helicobacter pylori do not depend on the cagA status

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