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| Home > Publications database > Helicobacter pylori multiplex serology in patients with autoimmune atrophic gastritis negative for Helicobacter pylori at histology: A case-control study. |
| Journal Article | DKFZ-2026-00031 |
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2026
Saunders
[Erscheinungsort nicht ermittelbar]
Abstract: Autoimmune atrophic gastritis (AAG) is an immune-mediated disorder affecting the gastric oxyntic mucosa. Two pathogenetic models are proposed: a pure autoimmune disorder or gastric autoimmunity triggered by Helicobacter pylori (Hp)-infection. In AAG, histological diagnosis of Hp may be challenging and serology can help assess exposure to Hp-infection. This study aimed to determine seroreactivity to Hp-antigens in AAG patients by using Hp-multiplex serology assay.A single-centre case-control study on 178 adults: 75 patients with serological and histological AAG diagnosis, 25 controls with histologically Hp-positive-non-atrophic gastritis (Ctr-NAG-Hp+) and 78 subjects with a healthy stomach (Ctr-HS). Sera were analysed using Hp-multiplex serology assay allowing simultaneous detection of antibodies to 13 Hp-proteins. Overall positivity cutoff: seroreactivity to more than 3 Hp-antigens.The number of seroreactive Hp-antigens was higher in AAG than in Ctr-HS(mean±SEM 2.2±0.3 vs 1.4±0.22,p=0.02) and lower than in Ctr-NAG-Hp+ patients (mean±SEM 5.4±0.5,p<0.001).Overall Hp-seropositivity in AAG was two-fold higher than in Ctr-HS but not statistically significant (21.1% vs 10.3%,p=0.06) and lower than in Ctr-NAG-Hp+(80%,p<0.0001). Complete absence of seroreactivity was similar in AAG and Ctr-HS (29.3% vs 38.5%, p=0.23) and significantly higher than in Ctr-NAG-Hp+ (4%, p=0.009). Main immunogenic Hp-proteins were HP0010(GroEL),HP1098(HcpC),HP0695(HyuA),HP0875(Catalase),HP1564,HP0547(CagA) and HP0243(NapA) with seroreactivity in >50% of AAG patients.By Hp-multiplex serology, 30% of histologically Hp-negative AAG pts had no seroreactivity, likely belonging to the pure AAG type. Conversely, 20% of AAG pts showed Hp exposure, indicating that infection might have triggered gastric autoimmunity. The remaining AAG patients showed seroreactivity below cut-off for seropositivity and thus not definitively categorisable by this approach.
Keyword(s): Atrophic gastritis ; Autoimmune gastritis ; Helicobacter pylori ; Multiplex serology
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