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Risk of nonmelanoma skin cancer in patients with psoriatic arthritis and according to bDMARD treatment-a cohort study from the Nordic Arthritis Research Collaboration.
СтатьяНазвание и аннотация: Перевод в очереди
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Westermann Rasmus, Delcoigne Bénédicte, Cordtz René Lindholm, Provan Sella Aarrestad, Sexton Joe, Nordström Dan, Isomäki Pia, Askling Johan, Dreyer Lene Wohlfahrt, Hellgren Karin
Аннотация
OBJECTIVES: To investigate if psoriatic arthritis (PsA) itself and if biological disease-modifying antirheumatic drugs (bDMARDs) used in PsA are associated with increased risks of nonmelanoma skin cancer (NMSC).
METHODS: From nationwide health and clinical rheumatology registers in 4 Nordic countries, we identified patients with PsA who between 2010 and 2021 started a: (i) tumour necrosis factor inhibitor (TNFi), or (ii) non-TNFi bDMARD, or were (iii) b/targeted synthetic (ts)DMARD naïve. For Sweden and Denmark, we identified incident patients with PsA (2010-2021) and corresponding general population (GP) comparator subjects. Using ever-treated follow-up, incidence rates and adjusted hazards ratios (aHRs) with 95% CIs were calculated for NMSC overall, basal cell carcinoma (BCC), and squamous cell carcinoma (SCC), respectively.
RESULTS: We identified 619 NMSCs among incident patients with PsA (n = 23,553). We observed 221 NMSCs in TNFi-treated (n = 9999), 34 NMSCs in non-TNFi bDMARD-treated (n = 2200), and 433 NMSCs in b/tsDMARD-naïve (n = 19,089) PsA. The aHR of NMSC for incident PsA vs GP was 1.20 (1.11-1.31). Pooled aHRs for NMSC overall were 1.24 (1.03-1.50) with TNFi and 1.11 (0.75-1.63) with non-TNFi bDMARDs vs b/tsDMARD-naïve PsA. Corresponding aHRs of BCC were 1.21 (0.93-1.58) for TNFi and 0.85 (0.42-1.69) for non-TNFi bDMARDs, whereas aHRs for SCC were 1.46 (0.84-2.56) and 2.37 (0.95-5.90).
CONCLUSIONS: Increased risks of NMSC (SCC in particular) were found in patients with PsA compared with the GP. Compared with b/tsDMARD-naïve PsA, TNFi was associated with an increased risk of NMSC overall, whereas a nonsignificantly increased risk of SCC was seen for non-TNFi bDMARDs. However, causality between bDMARD use and NMSC in PsA remains uncertain.
METHODS: From nationwide health and clinical rheumatology registers in 4 Nordic countries, we identified patients with PsA who between 2010 and 2021 started a: (i) tumour necrosis factor inhibitor (TNFi), or (ii) non-TNFi bDMARD, or were (iii) b/targeted synthetic (ts)DMARD naïve. For Sweden and Denmark, we identified incident patients with PsA (2010-2021) and corresponding general population (GP) comparator subjects. Using ever-treated follow-up, incidence rates and adjusted hazards ratios (aHRs) with 95% CIs were calculated for NMSC overall, basal cell carcinoma (BCC), and squamous cell carcinoma (SCC), respectively.
RESULTS: We identified 619 NMSCs among incident patients with PsA (n = 23,553). We observed 221 NMSCs in TNFi-treated (n = 9999), 34 NMSCs in non-TNFi bDMARD-treated (n = 2200), and 433 NMSCs in b/tsDMARD-naïve (n = 19,089) PsA. The aHR of NMSC for incident PsA vs GP was 1.20 (1.11-1.31). Pooled aHRs for NMSC overall were 1.24 (1.03-1.50) with TNFi and 1.11 (0.75-1.63) with non-TNFi bDMARDs vs b/tsDMARD-naïve PsA. Corresponding aHRs of BCC were 1.21 (0.93-1.58) for TNFi and 0.85 (0.42-1.69) for non-TNFi bDMARDs, whereas aHRs for SCC were 1.46 (0.84-2.56) and 2.37 (0.95-5.90).
CONCLUSIONS: Increased risks of NMSC (SCC in particular) were found in patients with PsA compared with the GP. Compared with b/tsDMARD-naïve PsA, TNFi was associated with an increased risk of NMSC overall, whereas a nonsignificantly increased risk of SCC was seen for non-TNFi bDMARDs. However, causality between bDMARD use and NMSC in PsA remains uncertain.