Abstract
BackgroundSeveral studies have demonstrated an association between rheumatoid arthritis (RA) and lymphoproliferative malignancies, but pathogenic mechanisms remain unclear. We investigated 1) the risk of lymphoproliferative malignancies and solid tumors in adults with RA identified in primary care and 2) the possible mediating role of blood eosinophilia in the clonal evolution of cancer in these patients.MethodsFrom the Copenhagen Primary Care Differential Count (CopDiff) Database, we identified 356,196 individuals with at least one differential cell count (DIFF) encompassing the eosinophil count between 2000–2007. From these, one DIFF was randomly chosen (the index DIFF). By linking to the Danish National Patient Register, we categorized the selected individuals according to known longstanding (≥3 years) or recent onset (<3 years) RA prior to the index DIFF. In addition, the cohort was stratified according to management in primary or secondary care. From the Danish Cancer Registry we ascertained malignancies within four years following the index DIFF. Using multivariable logistic regression, odds ratios (OR) were calculated and adjusted for sex, age, year, month, eosinophilia, comorbid conditions and C-reactive protein (CRP).Results921 patients had recent onset RA and 2,578 had longer disease duration. Seventy three percent of RA patients were managed in primary care. After adjustment for sex, age, year, and month, neither recent onset nor long-standing RA was associated with incident lymphoproliferative malignancies or solid cancers. These risk estimates did not change when eosinophilia, CRP, and comorbidities were included in the models.ConclusionsIn this large cohort of patients with RA of short or long duration recruited from a primary care resource, RA was not associated with an increased risk of lymphoproliferative or solid cancers during 4 years of follow-up, when the models were adjusted for confounders. Blood eosinophilia could not be identified as a mediator of cancer development in the present setting.
Highlights
The association between rheumatoid arthritis (RA) and cancer has been investigated in several mainly hospital-based studies
Two major pathways have been suggested to account for the association between RA and malignancy: extrinsic pro-oncogenic effects of disease-modifying antirheumatic drugs (DMARDs) [10,11]; and intrinsic pro-oncogenic effects related to disease activity [6,7,8,12,13,14]
We found that our strategy of randomly choosing one differential cell count (DIFF) per individual to assess incidences of the specified outcomes was feasible for two reasons
Summary
The association between rheumatoid arthritis (RA) and cancer has been investigated in several mainly hospital-based studies. These have indicated that the overall cancer occurrence in patients with RA is only marginally higher than in healthy individuals, while elevated risk figures have been reported for several specific cancers including leukemia [1], non-melanoma skin cancers [2], and lung cancer [3,4]. The pathways by which active RA impose an increased risk of lymphoma are poorly understood In this context, the eosinophilic granulocyte is a pertinent candidate. Eosinophilia has been linked to prognosis and severity of extra-articular manifestations in RA [21] Taken together, these observations support the view that eosinophilia may be associated with cancer risk in RA. We investigated 1) the risk of lymphoproliferative malignancies and solid tumors in adults with RA identified in primary care and 2) the possible mediating role of blood eosinophilia in the clonal evolution of cancer in these patients
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