POS1351 CERTOLIZUMAB PEGOL VS ADALIMUMAB IN THE TREATMENT OF REFRACTORY CYSTOID MACULAR EDEMA DUE TO BEHÇET’S DISEASE. MULTICENTER STUDY.

Abstract

BackgroundCystoid Macular Edema (CME) is the leading cause of blindness in non-infectious uveitis. Behçet’s disease (BD) is one of the diseases most frequently associated with CME [1-4].Objectivesto compare the efficacy and safety of Certolizumab (CZP) and Adalimumab (ADA) in CME due to BD refractory to conventional therapy.Methodsmulticenter study of patients with CME secondary to BD refractory to glucocorticoids (GC) and at least 1 conventional immunosuppressant. All patients had CME (OCT>300µ) at baseline. Efficacy was assessed with the following ocular parameters: macular thickness (µm), visual acuity (BCVA) and GC-sparing effect. The efficacy of CZP vs. ADA was compared between the baseline visit, 1st and 6th month, and 1st and 2nd year. Statistical analysis was performed with IBM SPSS Statistics v.23.ResultsWe studied 21 patients/38 affected eyes were studied. 10 patients were treated with CZP (200 mg c/2 weeks) and 11 with ADA (loading dose of 80 mg and subsequently 40 mg c/2 weeks).No statistically significant baseline differences were observed in both groups (CZP vs. ADA) in sex (♂/♀; 3/7 vs 5/6; p=0.65) and mean age (36.1±8.0 vs 42.2±8.6; p=0.10). However, CZP group was more severe with a longer time between EB diagnosis and biologic initiation (91.6±71.4 vs 34.4±21.3 months, p=0.02), and a greater median [IQR] number of previous biologic drugs (2 [0.75-3] vs 0 [0-0]). In CZP group, 8 patients were previously treated with ADA.Combined therapy with conventional DMARDs was used with ADA in 81.8% vs. 18.2% of CZP patients.Regarding the efficacy outcomes analyzed, a rapid and maintained improvement in macular thickness, measured by OCT, was observed after 2 years of follow-up in both groups with no statistically significant differences between them (Table 1). Improvement in visual acuity and a GC-sparing effect was also observed (Table 1).Table 1.main ocular parameters compared in the CZP-treated group and in the ADA-treated group.CZP(n=10)ADA(n=11)PBaseline  OCT (µm, mean±SD)380.7±96.4416.9±171.10.56 BCVA (mean±SD)0.72±0.300.57±0.200.21 Prednisone (mg/dl, mean±SD)13.1±11.434.1±18.90.071st month  OCT (µm, mean±SD)333.7±60.4302±44.20.19 BCVA (mean±SD)0.80±0.270.72±0.180.45 Prednisone (mg/dl, mean±SD)8.1±5.5112.1±6.40.316th month  OCT (µm, mean±SD)284.4±45.5272.8±38.90.53 BCVA (mean±SD)0.82±0.230.86±0.160.65 Prednisone (mg/dl, mean±SD)6.8±6.66.1±2.80.921st year  OCT (µm, mean±SD)269.0±46.8260.9±39.50.67 BCVA (mean±SD)0.82±0.230.89±0.170.48 Prednisone (mg/dl, mean±SD)6.2±3.05.8±2.10.872nd year  OCT (µm, mean±SD)289.4±49.3248.0±42.00.16 BCVA (mean±SD)0.87±0.200.87±0.171.0 Prednisone (mg/dl, mean±SD)3.7±1.23.1±2.30.90No serious adverse events were observed in either group.ConclusionOur study suggests that both CZP and ADA are effective in the treatment of CME due to BD refractory to conventional treatment. CZP was equally effective despite most patients were refractory to ADA.References[1]Schaap-Fogler M, et al. Graefes Arch Clin Exp Ophthalmol. 2014 Apr;252(4):633-40. doi: 10.1007/s00417-013-2552-8.[2]Martín-Varillas JL, et al. Ophthalmology 2018; 125:1444-1451 doi: 10.1016/j.ophtha.2018.02.020[3]Martín-Varillas JL, et al. J Rheumatol. 2021;48:741-750. doi: 10.3899/jrheum.200300[4]Vegas-Revenga N et al Am J Ophthalmol. 2019;200:85-94. doi: 10.1016/j.ajo.2018.12.019Disclosure of InterestsNone declared