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Treating the skin with biologics in patients with psoriasis decreases the incidence of psoriatic arthritis
  1. Maria Laura Acosta Felquer1,
  2. Luciano LoGiudice1,
  3. Maria Laura Galimberti2,
  4. Javier Rosa1,
  5. Luis Mazzuoccolo2,
  6. Enrique R Soriano1
  1. 1Rheumatology Unit, Internal Medicine Service, Hospital Italiano de Buenos Aires and Instituto Universitario Hospital Italiano de Buenos Aires, Buenos Aires, Argentina
  2. 2Dermatology Service, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina
  1. Correspondence to Dr Enrique R Soriano, Rheumatology Unit, Internal Medicine Service, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina; enrique.soriano{at}hospitalitaliano.org.ar

Abstract

Objectives To compare the incidence of psoriatic arthritis (PsA) in patients with psoriasis (PsO) according to different treatments for their skin: topics/no treatment, conventional disease-modifying antirheumatic drugs (DMARDs) (cDMARDs) or biological DMARDs (bDMARDs).

Methods Patients with PsO without PsA followed at a university hospital were included in this retrospective cohort study. Patients were classified according to their treatment in topics (topics, phototherapy or no treatment), cDMARDs (methotrexate and cyclosporine) and bDMARDs (tumour necrosis factor inhibitors (TNFi), interleukin 17 inhibitors (IL-17i) and IL-12-23i ((interleukin (IL) 12/IL-23 inhibitor))) groups. Incident cases of PsA were attributed to one treatment if developed during the administration of that treatment. A Cox proportional hazards model was used to evaluate the adjusted risk of PsA development by treatment group.

Results 1719 patients with PsO contributed a total of 14 721 patient/years (py). 1387 (81%) patients were in the topics, 229 (13%) in cDMARDs and 103 (6%) in the bDMARDs group. During follow-up, 239 patients (14%) developed PsA (231 under topics, six under cDMARDs and two under bDMARDs). Global incidence was 1.6 per 100 py. The risk of developing PsA in patients with PsO treated with bDMARDs was significantly lower (incidence rate ratio (IRR)=0.26; 95% CI 0.03 to 0.94; p=0.0111), compared with topics, but not compared with cDMARDs (IRR=0.35; 95% CI 0.035 to 1.96; p=0.1007). Adjusted Cox proportional hazards regression analysis showed that male sex, nail involvement and higher body max index were associated with increased risk of developing PsA, while biologics use was protective (HR: 0.19; 95% CI 0.05 to 0.81).

Conclusion Treatment with biologics in patients with PsO reduced the risk of PsA development.

  • psoriatic arthritis
  • biological therapy
  • epidemiology

Data availability statement

Data are available upon reasonable request. Our data are not in a repository; data are available upon request to ERS.

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Data availability statement

Data are available upon reasonable request. Our data are not in a repository; data are available upon request to ERS.

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Footnotes

  • Handling editor Josef S Smolen

  • Presented at Preliminary data from this study were previously presented at 2019 ACR Meeting: Lo Giudice L, Acosta Felquer M, Mazzuoccolo L, Galimberti M, Soriano E. Can Biologics “Prevent” the Development of Psoriatic Arthritis in Psoriasis Patients? Data from a Large University Hospital Cohort in Argentina [abstract]. Arthritis Rheumatol. 2019; 71 (suppl 10). https://acrabstracts.org/abstract/can-biologics-prevent-the-development-of-psoriatic-arthritis-in-psoriasis-patients-data-from-a-large-university-hospital-cohort-in-argentina/. Accessed May 25, 2021. And at the 2020 EULAR Meeting: Lo Giudice L, Acosta Felquer ML, Galimberti ML, et al. Sat0426 can biologics “prevent” the development of psoriatic arthritis in psoriasis patients? Data from a large university hospital cohort in Argentina. Annals of the Rheumatic Diseases 2020;79:1167-8.

  • Contributors MLAF and ERS: designed the study and performed data analysis and interpretation. LLG and MLG: contributed to data collection, data quality control and interpretation of the data. JR and LM: contributed to data quality control and interpretation of the data. All authors contributed intellectual content during the drafting and revision of the work and approved the final version to be published.

  • Funding This study was supported by a grant from PANLAR (Pan-American League of Associations for Rheumatology).

  • Competing interests ERS received grants from AbbVie, Janssen, Novartis, Pfizer and Roche, outside the submitted work, and consulting/speaker’s fee from AbbVie, Amgen, BMS, Janssen, Novartis, Lilly, Pfizer, Roche, Sandoz and UCB outside the submitted work. MLAF received consulting/speaker’s fee from AbbVie, Janssen, Novartis, Lilly and Pfizer outside the submitted work. JR received consulting/speaker’s fee from AbbVie, Amgen, Janssen, Novartis, Lilly and Pfizer outside the submitted work. LM received consulting/speaker’s fee from AbbVie, Janssen, Novartis and Lilly outside the submitted work.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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