ArticleClinical epidemiology2018
Does low risk of infections as a marker of effective immunity predict increased risk of subsequent giant cell arteritis or polymyalgia rheumatica? A Danish population-based case-control study.
Article in Clinical epidemiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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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
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Association between infection and the onset of giant cell arteritis and polymyalgia rheumatica: a systematic review and meta-analysis.RMD open · 2023Pooled it
- Severe infections in giant cell arteritis - incidence over time and relation to large vessel involvement and comorbidities, a population-based study.BMC rheumatology · 2026Article
- Association between antibiotic use and the onset of giant cell arteritis and polymyalgia rheumatica: A nested case-control study from E3N-European Prospective Investigation into Cancer and Nutrition.Journal of internal medicine · 2025Article
- Infective agents and polymyalgia rheumatica: key discussion points emerging from a narrative review of published literature.Reumatologia · 2024Review
- Influenza A infection as a potential trigger of giant cell arteritis: A case report.SAGE open medical case reports · 2024Article
- Article
- Immunosuppressive Agents and Infectious Risk in Transplantation: Managing the "Net State of Immunosuppression".Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021Review
- A new era for giant cell arteritis.Eye (London, England) · 2020Review
- Polymyalgia rheumatica following infective triggers or vaccinations: a different subset of disease?Reumatologia · 2020Article
- Pathogenesis, Diagnosis and Management of Polymyalgia Rheumatica.Drugs & aging · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIt has been suggested that a hyper-effective immune system ("hyper-immunity") is central to the pathogenesis of giant cell arteritis and polymyalgia rheumatica (GCA/PMR). We examined if a low risk of infections, as a marker of hyper-immunity, can predict increased subsequent risk of GCA/PMR. PATIENTS AND
methodsWe conducted a population-based case-control study including all patients aged ≥50 years with incident GCA/PMR diagnosed between 1997 and 2012 in Northern Denmark. For each case, we selected 10 population controls matched on gender, age, place of residence, and time spent in the region. Complete history of hospital-treated infections and community-based anti-infective prescriptions was assessed in population-based registries. We used conditional logistic regression to compute OR of GCA/PMR associated with infections while adjusting for comorbidities, immunosuppressive treatment, and other potential confounders.
resultsWe included 7,225 GCA/PMR cases and 72,250 controls. When excluding all infections occurring within the last year before GCA/PMR diagnosis, there was no decreased risk for GCA/PMR in people with a history of hospital-treated infection (adjusted OR=1.04, 95% CI: 0.98-1.10) or community anti-infective treatment (adjusted OR=1.07, 95% CI: 0.99-1.16). Within the last year preceding the GCA/PMR index date, patients with hospital-treated infections (adjusted OR=1.59, 95% CI: 1.44-1.75) or community anti-infective treatment (adjusted OR=1.63, 95% CI: 1.48-1.79) had a greatly increased risk of a GCA/PMR diagnosis.
conclusionThese results do not support the hypothesis of "hyper-immunity" leading to GCA/PMR. Instead, incident GCA/PMR is preceded by a slightly increased risk of infection, which may be related to protopathic bias or support theories that infections may be directly involved in the pathogenesis of GCA/PMR.
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