ArticleThe Journal of rheumatology2026
Association of Early-Life Exposures With Later Diagnosis of Spondyloarthritis: A Population-Based Case-Control Study.
Article in The Journal of rheumatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
objectiveTo assess whether early-life antibiotics are associated with spondyloarthritis (SpA) diagnosed by age 21.
methodsIn this population-based, matched case-control study, we used Danish live births (1997-2023) restricted to those reaching the following minimum relevant ages by December 31, 2024: 1-21 years for psoriatic arthritis (PsA), and 6-21 years for peripheral/axial SpA and inflammatory bowel disease (IBD)-associated arthritis. Cases (n = 560) had physician-recorded SpA (peripheral/axial SpA, PsA, or IBD-associated arthritis). Controls were matched 1:50 by birth year, sex, and calendar year of diagnosis. Primary exposure was systemic antibiotic use the first year of life; secondary exposures included antibiotic class, number of courses, delivery mode, early upper respiratory tract infection (URTI), and systemic nonbacterial antimicrobials. Conditional logistic regression estimated adjusted odds ratios (aORs); dose response was tested with the Wald test.
resultsAmong cases (median age 16.8 years; 59% peripheral/axial SpA, 28% PsA, 13% IBD-associated arthritis), 50% received antibiotics, vs 42% of controls. First-year antibiotic exposure was associated with higher odds of SpA (aOR 1.35, 95% CI 1.14-1.59). Broad-spectrum penicillins had the strongest class-specific association (aOR 1.42, 95% CI 1.19-1.70). Early URTI was independently associated with SpA (aOR 1.88, 95% CI 1.32-2.67); delivery mode and systemic nonbacterial antimicrobials were not. In SpA subgroup analysis, the association with first-year antibiotics was significant only for PsA (aOR 1.75, 95% CI 1.27-2.41).
conclusionAntibiotic exposure in the first year of life, particularly broad-spectrum penicillins, was associated with increased odds of SpA by age 21, supporting the hypothesis that early-life microbiome disruption may increase later SpA risk.
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