1567: Refractory Macular Edema Due to Behçet's Disease. Multicenter Comparative Study of Adalimumab and Certolizumab Pegol

José Luis Martín-Varillas¹, Lara Sánchez-Bilbao², Vanesa Calvo Río³, Alf Adán⁴, Inés Hernanz Rodríguez⁴, Miguel Cordero Coma⁵, David Díaz Valle⁶, Patricia Fanlo⁷, Juan Ramón de Dios⁸, A. Garcia-Aparicio⁹, Sergio Rodriguez Montero¹⁰, Vega Jovani Casano¹¹, Patricia Moya Alvarado¹², eva Peña Sainz-Pardo¹³, José Luis Hernández² and Ricardo Blanco¹⁴, ¹Hospital de Laredo, Laredo, Cantabria, Spain, ²Hospital Universitario Marqués de Valdecilla, Santander, Spain, ³Valdecilla Hospital, Santander, Spain, ⁴H. Clinic, Barcelona, Spain, ⁵Hospital de León, León, Spain, ⁶Hospital Clínico San Carlos, Madrid, Spain, ⁷Complejo Hospitalario de Navarra, Navarra, Spain, ⁸Hospital de Araba, Araba, Spain, ⁹Hospital Universitario de Toledo, Toledo, Spain, ¹⁰Virgen de Valme University Hospital, Sevilla, Spain, ¹¹National Health system, Alicante, Spain, ¹²Hospital Parc Tauli, Barcelona, Spain, ¹³Hospital Universitario 12 de Octubre, Madrid, Spain, ¹⁴Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Spain

Background/Purpose: Cystoid 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. Our aims wereto compare the efficacy and safety of Certolizumab Pegol (CZP) and Adalimumab (ADA) in CME due to BD refractory to conventional therapy.

Methods: multicenter 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.

Results: We 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). Improvement in visual acuity and a GC-sparing effect was also observed (TABLE). No serious adverse events were observed in either group.

Conclusion: Our 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.
TABLE. main ocular parameters compared in the CZP-treated group vs. ADA-treated group.
Disclosures: J. Martín-Varillas, AbbVie/Abbott, Pfizer, Janssen, UCB, Celgene; L. Sánchez-Bilbao, Eli Lilly; V. Calvo Río, AbbVie/Abbott, Eli Lilly, Merck/MSD, UCB; A. Adán, None; I. Hernanz Rodríguez, None; M. Cordero Coma, None; D. Díaz Valle, None; P. Fanlo, None; J. de Dios, None; A. Garcia-Aparicio, None; S. Rodriguez Montero, None; V. Jovani Casano, None; P. Moya Alvarado, None; e. Peña Sainz-Pardo, None; J. Hernández, None; R. Blanco, Eli Lilly, Pfizer, Roche, Janssen, MSD, AbbVie, Amgen, AstraZeneca, Bristol Myers Squibb, Galapagos, Novartis, Sanofi.