ArticleRheumatology international2020
A positive Helicobacter pylori test is associated with low spondylarthritis incidence in a Danish historical cohort study.
Article in Rheumatology international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- Association Between Infections and Risk of Ankylosing Spondylitis: A Systematic Review and Meta-Analysis.Frontiers in immunology · 2021Pooled it
- TNF ınhibitor resistance in ankylosing spondylitis: is Helicobacter pylori the overlooked culprit?Clinical rheumatology · 2025Article
- Environmental and Genetic Determinants of Ankylosing Spondylitis.International journal of molecular sciences · 2024Review
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
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