A positive Helicobacter pylori test is associated with low spondylarthritis incidence in a Danish historical cohort study
Ankylosing spondylitis (AS) and undifferentiated spondylarthritis (uSpA) are related inflammatory diseases affecting the spine and joints with infections among possible etiological factors. Helicobacter pylori ( H. pylori ) may affect the development of inflammatory diseases. Thus, we hypothesized t...
Gespeichert in:
Veröffentlicht in: | Rheumatology international 2020-03, Vol.40 (3), p.359-366 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Ankylosing spondylitis (AS) and undifferentiated spondylarthritis (uSpA) are related inflammatory diseases affecting the spine and joints with infections among possible etiological factors.
Helicobacter pylori
(
H. pylori
) may affect the development of inflammatory diseases. Thus, we hypothesized that
H. pylori
infection affects AS and uSpA development. This cohort study was performed in Denmark with 56,000 patients from primary health care centers who were enrolled when a UBT was performed. They were followed for a median time of 8 years. From nationwide administrative registries, we extracted personal, diagnostic, and treatment information. Prevalence at time of UBT was studied on enrollment using logistic regression and incidence in the follow-up time of 8 years after UBT was studied using Cox regression, comparing
H. pylori
positive and
H. pylori
negative patients and adjusting for confounding variables. The prevalence of AS at the time of the UBT was higher among
H. pylori
positive individuals (OR = 2.00, CI 1.17–3.41), but likely to be linked to confounding as trends disappeared when stratifying for country of birth. The incidence of AS after UBT was lower for individuals who were previously
H. pylori
positive (OR = 0.23, CI 0.06–0.93). A similar phenomenon was observed for uSpA. As a novel finding, after UBT, the previously
H. pylori
infected individuals had lower risk of developing AS and uSpA compared to non-infected. This finding may be caused by etiological effects of previous
H. pylori
infection or unknown confounders. This suggests that
H. pylori
may somehow be positively involved in the pathogenesis of AS and uSpA. |
---|---|
ISSN: | 0172-8172 1437-160X |
DOI: | 10.1007/s00296-019-04487-2 |