The following is a summary of “Impact of high rheumatoid factor levels on treatment outcomes with certolizumab pegol and adalimumab in patients with rheumatoid arthritis,” published in the September 2024 issue of Rheumatology by Smolen et al.

Researchers conducted a retrospective study to investigate the relationship between baseline rheumatoid factor (RF) levels and the drug concentrations and efficacy of certolizumab pegol (CZP) with (TNF inhibitor (TNFi) without a crystallizable fragment (Fc)] and adalimumab (ADA); in patients with rheumatoid arthritis (RA).

They conducted the phase 4 EXXELERATE study (NCT01500278), a 104-week, randomized, single-masked (double-masked until week 12; investigator-blind after that) comparing CZP and ADA in patients with RA. In this post hoc analysis, they reported drug concentration and efficacy outcomes stratified by baseline RF quartile (≤Q3 or >Q3).

The results showed the baseline data by RF quartiles were available for 453 and 454 CZP and patients who are ADA-randomized (≤Q3: ≤204 IU/ml; >Q3: >204 IU/ml), respectively. From week 12 onward, the area under the curve (AUC) for ADA concentration was lower in patients with RF >204 IU/ml compared to those with RF ≤204 IU/ml. The AUC for CZP concentration was similar in patients with RF ≤204 IU/ml and >204 IU/ml. In patients with RF ≤204 IU/ml, the disease activity score (DAS28)-C-reactive protein (CRP) was similar between CZP- and ADA-treated patients through week 104. For patients with RF >204 IU/ml, the mean DAS28-CRP was lower in those treated with CZP than those treated with ADA at week 104. Additionally, the proportion of patients with RF >204 IU/ml achieving DAS28-CRP low disease activity at week 104 was greater among those treated with CZP than those treated with ADA.

They concluded that CZP was associated with drug concentration and efficacy in patients with RA and high RF, making it a more suitable therapeutic option than TNF with an Fc fragment for these patients.

Source: academic.oup.com/rheumatology/advance-article/doi/10.1093/rheumatology/keae435/7747837