Histology and culture results among subjects with antibodies to CagA but no evidence of Helicobacter pylori infection with IgG ELISA.
OBJECTIVE
Serological evidence of antibodies to cytotoxin-associated gene A (CagA) antigens may exist without concomitant Helicobacter pylori IgG enzyme linked immunosorbent assay (ELISA) seropositivity. In a recent case-control study, this serological pattern was strongly linked to stomach cancer, and it was hypothesized to represent "burned-out" CagA-positive infections. The aim of this analysis was to test this hypothesis.


METHODS
We used data from a Swedish endoscopy clinic-based case-control study with 64 gastric cancer cases and 281 age-matched and gender-matched non-cancer patients who had other gastric diseases or normal endoscopy. HM-CAP ELISA and Helicoblot 2.0 immunoblot results were compared with culture and histology.


RESULTS
Overall, 86 out of 345 (25%) subjects were CagA seropositive but ELISA seronegative. This proportion was similar among cancer and non-cancer patients. Current H. pylori infection could be verified by culture or histology in only 15% of these patients. Forty-three percent of subjects with this isolated CagA seropositivity had histological evidence of corpus and/or antral atrophy. This was higher than in those who were negative in both tests (15%), but lower than among those seropositive for both tests (53%). The percentage of isolated CagA-seropositive patients who had atrophy was similar among those with or without evidence of current infection.


CONCLUSIONS
Although false-positive tests for CagA, or false-negative ELISA tests, may explain the serologic pattern in some of the subjects with isolated CagA seropositivity, healed infections are estimated to account for the majority. Unless the histology is often restituted after spontaneous disappearance of the infection, atrophy does not appear to be a mandatory intermediate step leading to this serology.
Ye
Weimin
W
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. weimin.ye@meb.ki.se
Held
Maria
M
Enroth
Helena
H
Kraaz
Wolfgang
W
Engstrand
Lars
L
Nyrén
Olof
O
D000230:Adenocarcinoma / Q000097:blood / Q000473:pathology; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood* / Q000276:immunology; D000942:Antigens, Bacterial / Q000235:genetics / Q000276:immunology*; D001426:Bacterial Proteins / Q000235:genetics / Q000276:immunology*; D001706:Biopsy; D004269:DNA, Bacterial / Q000032:analysis; D003937:Diagnosis, Differential; D016145:Endoscopy, Digestive System; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005748:Gastric Fundus / Q000473:pathology; D005753:Gastric Mucosa / Q000473:pathology*; D005756:Gastritis / Q000097:blood / Q000473:pathology; D016481:Helicobacter Infections / Q000097:blood / Q000382:microbiology / Q000473:pathology*; D016480:Helicobacter pylori / Q000276:immunology / Q000302:isolation & purification*; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology*; D008297:Male; D016133:Polymerase Chain Reaction; D011706:Pyloric Antrum / Q000473:pathology; D015203:Reproducibility of Results; D012189:Retrospective Studies; D013274:Stomach Neoplasms / Q000097:blood / Q000473:pathology
D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D004269:DNA, Bacterial; D007074:Immunoglobulin G; C080866:cagA protein, Helicobacter pylori