| Home > Publications database > Helicobacter pylori multiplex serology in patients with autoimmune atrophic gastritis negative for Helicobacter pylori at histology: A case-control study. > print |
| 001 | 307526 | ||
| 005 | 20260126103124.0 | ||
| 024 | 7 | _ | |a 10.1016/j.dld.2025.12.002 |2 doi |
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| 024 | 7 | _ | |a 1590-8658 |2 ISSN |
| 024 | 7 | _ | |a 1878-3562 |2 ISSN |
| 037 | _ | _ | |a DKFZ-2026-00031 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Vavallo, Marica |b 0 |
| 245 | _ | _ | |a Helicobacter pylori multiplex serology in patients with autoimmune atrophic gastritis negative for Helicobacter pylori at histology: A case-control study. |
| 260 | _ | _ | |a [Erscheinungsort nicht ermittelbar] |c 2026 |b Saunders |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1769419844_3933356 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 500 | _ | _ | |a 2026 Feb;58(2):212-219 |
| 520 | _ | _ | |a 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. |
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| 650 | _ | 7 | |a Atrophic gastritis |2 Other |
| 650 | _ | 7 | |a Autoimmune gastritis |2 Other |
| 650 | _ | 7 | |a Helicobacter pylori |2 Other |
| 650 | _ | 7 | |a Multiplex serology |2 Other |
| 700 | 1 | _ | |a Butt, Julia |0 P:(DE-He78)31d7c3e829be03400641f80b821ef728 |b 1 |u dkfz |
| 700 | 1 | _ | |a Cingolani, Sophia |b 2 |
| 700 | 1 | _ | |a Cozza, Giulio |b 3 |
| 700 | 1 | _ | |a Schiavone, Francesco Paolo |b 4 |
| 700 | 1 | _ | |a Dilaghi, Emanuele |b 5 |
| 700 | 1 | _ | |a Belloni, Laura |b 6 |
| 700 | 1 | _ | |a Franchitto, Matteo |b 7 |
| 700 | 1 | _ | |a Annibale, Bruno |b 8 |
| 700 | 1 | _ | |a Waterboer, Tim |0 P:(DE-He78)6b4ebb9791b983b5620c0caaf3468e30 |b 9 |u dkfz |
| 700 | 1 | _ | |a Lahner, Edith |b 10 |
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