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Clinical and Diagnostic Laboratory Immunology, February 2005, p. 304-309, Vol. 12, No. 2
1071-412X/05/$08.00+0 doi:10.1128/CDLI.12.2.304-309.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Evaluation of Western Blot CagA Seropositivity in Helicobacter pylori-Seropositive and -Seronegative Subjects
J. Henrik Simán,1* Lars Engstrand,2 Göran Berglund,1 Claes-Henrik Florén,3 and Arne Forsgren4Department of Medicine,1 Department of Medical Microbiology, Malmö University Hospital, Lund University, Malmö,4 Department of Medical Epidemiology, Karolinska Institutet, Stockholm,2 Department of Medicine, Lund University Hospital, Lund University, Lund, Sweden3
Received 9 July 2004/ Returned for modification 8 September 2004/ Accepted 11 November 2004
CagA seropositivity is an important risk factor for gastric adenocarcinoma and duodenal ulcer. However, CagA seropositivity is also found in Helicobacter pylori-seronegative subjects. Is CagA seropositivity in these subjects a sign of a past H. pylori infection, or does it represent a false-positive reaction? This study investigates the intensity of the CagA immune reaction and the variation in CagA seroprevalence with year of birth for 650 subjects belonging to the Malmö Preventive Medicine cohort. CagA and H. pylori seroprevalences were determined by Western blot analysis (Helicoblot 2.1) and enzyme-linked immunosorbent assay. The peak intensity of the CagA band was significantly lower in H. pylori-seronegative subjects than in those with concomitant H. pylori seropositivity. In H. pylori-seropositive subjects, peak CagA intensity had a bimodal distribution. The prevalence of CagA-seropositive but H. pylori-seronegative subjects increased successively and significantly with year of birth, in contrast to the prevalence of CagA-seropositive and H. pylori-seropositive subjects, which decreased significantly. However, within H. pylori-seropositive and -seronegative subgroups, CagA seroprevalences were constant for different birth cohorts. If CagA seropositivity in H. pylori-seronegative subjects represents a past H. pylori infection, there must have been some mechanisms of eradication that were more common in younger subjects and that were of more importance than the presence of gastric atrophy and the longer duration and higher prevalence of H. pylori infection found in older subjects. Antibiotic treatment of H. pylori was not common practice at the time of enrollment. On the other hand, a false-positive reaction would be constant and independent of birth cohorts, as with the H. pylori-seronegative subgroup of our study. Peak CagA intensity in H. pylori-seronegative subjects corresponded to the lower part of the bimodal distribution of peak CagA intensity in H. pylori-seropositive subjects. We conclude that a major proportion of CagA seropositivity in H. pylori-seronegative subjects represents a false-positive reaction. Peak CagA intensity has a bimodal distribution in H. pylori-seropositive subjects. Low-intensity CagA seropositivity in H. pylori-seropositive subjects is indeterminate, representing both false-positive and true-positive reactions.
* Corresponding author. Mailing address: Department of Medicine, Malmö University Hospital, S-205 02 Malmö, Sweden. Phone: 46 40 33 10 00. Fax: 46 40 33 62 08. E-mail: henrik.siman{at}skane.se.
Clinical and Diagnostic Laboratory Immunology, February 2005, p. 304-309, Vol. 12, No. 2
1071-412X/05/$08.00+0 doi:10.1128/CDLI.12.2.304-309.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
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