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TNF inhibitors, DMARDs yield similar malignancy risk in patients with RA

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MADRID — No significant differences were reported in malignancy incidence among patients with rheumatoid arthritis treated with a cross section of tumor necrosis factor inhibitors and corticosteroid disease-modifying antirheumatic drugs therapies, according to findings presented at the Annual European Congress of Rheumatology 2017.

Associations between malignancy and biological DMARDs are lacking, Johan Askling, MD, PhD, of the department of medicine at Karolinska Institute in Stockholm, said during a press conference. His group investigated cohorts of patients in Sweden from 2006 to 2014.

Eligible participants included patients initiating first-line therapy with tocilizumab (Actemra, Genentech), abatacept (Orencia, Bristol-Myers Squibb), rituximab (Rituxan, Genentech), or a tumor necrosis factor (TNF) inhibitor. Other cohorts included patients beginning a second TNF inhibitor and a group of biologic-naive patients who initiated conventional synthetic DMARD (csDMARD) therapy. A first ever solid tumor served as the primary outcome measure.

Results indicated no statistically significant differences in risk for the primary outcome measure in any of the treatment groups. With the use of csDMARD in patients with rheumatoid arthritis (RA) as the reference (HR = 1), the risk was not increased for tocilizumab (HR = 0.78; 95% CI, 0.54-1.12), abatacept (HR = 0.95; 95% CI, 0.7-1.28), rituximab (HR = 0.86; 95% CI, 0.7-1.04), a first-line TNF inhibitor (HR = 0.91; 95% CI, 0.82-1.01) or a second-line TNF inhibitor (HR = 0.88; 95% CI, 0.73-1.05).

“We didn’t find any relative risk for any of these groups or treatments,” Askling said. “Treatment of RA with available biological drugs was not linked to increased risk of cancer development.”

Askling said there should be caution in interpreting the findings.

“These results apply to most common types of cancer but not all,” he said. “Also, they apply to medium-term treatment, not necessarily to longer treatment.”

He also noted that the results apply to the average patient with RA in routine clinical practice, not necessarily to patients at a particular risk for cancer. “It is difficult to evaluate one signal identified,” he said. “It may be chance, bias or causality.” – by Rob Volansky

Reference:

Wadstrom H, et al. Abstract #OP0100. Presented at: EULAR Annual Congress; June 14-17, 2017; Madrid.

Disclosures: The researchers report no relevant financial disclosures.