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OP0129 Drug survival on anti-tnf-alpha in psoriatic arthritis patients with axial involvement and analysis of predictors
  1. S. Lopriore,
  2. F. Cacciapaglia,
  3. S. Perniola,
  4. M.G. Anelli,
  5. G. Lopalco,
  6. C. Scioscia,
  7. L. Coladonato,
  8. G. Laselva,
  9. G. Lapadula,
  10. F. Iannone
  1. Department of Emergency and Organ Transplantation (DETO), University of Bari, Rheumatology Unit, Bari, Italy


Background A few studies have focused on the clinical outcomes in predominant axial Psoriatic Arthritis (PsA) patients treated with anti-TNF-α agents1–3 in real-life settings.

Objectives Primary endpoint: to evaluate drug survival on anti-TNF-α agents in PsA patients with axial involvement or axial and either polyarticular or oligoarticular peripheral arthritis. Secondary endpoints: to evaluate the presence of any predictor of discontinuation of anti-TNF in PsA patients with axial involvement and to investigate whether peripheral arthritis may impact the discontinuation for ineffectiveness in patients with axial disease.

Methods 415 biologic therapy-naive PsA patients (CASPAR criteria) starting a first TNF-inhibitor from January 2010 to December 2016 were screened. Among these, 87 had axial involvement (ASAS criteria) with imaging arm (X-ray or MRI) and were enrolled: 40 with axial and polyarticular peripheral PsA (Axe +Poly PsA), 38 with axial and oligoarticular peripheral PsA (Axe +Oligo PsA) and 9 with only axial disease (Ax-PsA). At baseline and at last available visit or drug discontinuation, we collected age, gender, disease duration, BMI, HLA-B27, nail psoriasis and/or dactylitis, TJC, SJC, ESR, CRP, enthesitis, LEI, DAPSA, BASDAI, ASDAS-CRP, PASI, HAQ, intake of glucocorticoids and DMARDs, anti-TNF therapy discontinuation and reasons of discontinuation. Drug survival was evaluated by Kaplan-Meier life table method, comparison of survival curves with Log-rank test and baseline predictors of drug discontinuation with Cox regression analysis.

Results At baseline, Axe +Poly PsA patients had significantly higher peripheral (DAPSA) and axial disease activity (BASDAI, ASDAS-CRP). Stratifying patients by subset of disease, the median of treatment was 51 months (95% IQR 24.87–77.13) for Ax-PsA group, 50 months (95% IQR 28.39–71.61) for Axe +Oligo PsA group, 30 months (95% IQR 11.84–48.15) for Axe +Poly PsA group (figure 1). Axe +Oligo PsA patients had significantly higher persistence on TNFi rather than Axe +Poly PsA patients (log rank test, p=0.03). Axe +Poly PsA patients had higher risk of stopping TNFi (Cox regression, HR 3.75) and significantly higher percentage of discontinuation for ineffectiveness rather than for an adverse event (χ2 test, p=0.0009). At last observation, Axe +Poly PsA patients had higher DAPSA but no difference in axial disease activity (t-STUDENT test, Mann-Whitney test).

Abstract OP0129 – Figure 1

Drug survival on TNF-inhibitor in Ax-PsA, Axe+Oligo-PsA and Axe+Poly-PsA patients (Kaplan-Meier life table method, log rank test)

Conclusions PsA subsets seems to have different features, behaviour, clinical response and drug survival on TNF-inhibitors. Axe +Poly PsA subset seems to be more aggressive and difficult to treat. Anti-TNF-α blockers may perform differently in PsA: a more accurate analysis of the clinical disease subsets may improve our knowledge and better management of PsA in daily practice.

References [1] Lubrano E, et al. Clin Exp Rheumatol2011Jan-Feb;29(1):80–4.

[2] Lubrano E, et al. J Rheumatol2016May;43(5):918–23.

[3] Perrotta FM, et al. J Rheumatol2016Feb;43(2):350–5.

Disclosure of Interest None declared

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