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@ARTICLE{Vavallo:307526,
author = {M. Vavallo and J. Butt$^*$ and S. Cingolani and G. Cozza
and F. P. Schiavone and E. Dilaghi and L. Belloni and M.
Franchitto and B. Annibale and T. Waterboer$^*$ and E.
Lahner},
title = {{H}elicobacter pylori multiplex serology in patients with
autoimmune atrophic gastritis negative for {H}elicobacter
pylori at histology: {A} case-control study.},
journal = {Digestive and liver disease},
volume = {58},
number = {2},
issn = {1590-8658},
address = {[Erscheinungsort nicht ermittelbar]},
publisher = {Saunders},
reportid = {DKFZ-2026-00031},
pages = {212-219},
year = {2026},
note = {2026 Feb;58(2):212-219},
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.},
keywords = {Atrophic gastritis (Other) / Autoimmune gastritis (Other) /
Helicobacter pylori (Other) / Multiplex serology (Other)},
cin = {C230},
ddc = {610},
cid = {I:(DE-He78)C230-20160331},
pnm = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
pid = {G:(DE-HGF)POF4-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:41484031},
doi = {10.1016/j.dld.2025.12.002},
url = {https://inrepo02.dkfz.de/record/307526},
}