Publication: Nonenfeksiyöz Üveitli Hastalarda Adalimumab Tedavisinin Etkinliğinin ve Anti-Adalimumab Antikor Oluşumunun Değerlendirilmesi
Abstract
Amaç: Nonenfeksiyöz üveitli hastalarda adalimumab (ADA) tedavisinin etkinliğini, anti-adalimumab antikor (AAA) gelişimini ve AAA gelişiminin tedavi başarısı üzerine etkisini değerlendirmek. Gereç ve Yöntem: Ondokuz Mayıs Üniversitesi, Tıp Fakültesi, Göz Hastalıkları Polikliniği'nde non-enfeksiyoz üveit tanısı ile takip edilen ve en az üç aydır haftada bir veya iki haftada bir ADA tedavisi alan 60 hastanın 117 gözü çalışmaya dahil edildi. Hastaların verileri retrospektif olarak tarandı; demografik verileri ve ADA tedavisi öncesi göz bulguları (görme keskinliği (GK), klinik aktivite bulguları, maküla kalınlığı) kaydedildi. Hastalardan son ADA dozu yapılmadan önce periferik kan örneği alındı. Aynı gün hastalara Snellen ondalık eşeli ile görme keskinliği, aplanasyon tonometrisi ile göz içi basınç ölçümü, yarıklı lamba biyomikroskopi ile ön segment muayenesi ve 90 D mercek ile fundus muayenesini içeren rutin göz muayenesi yapıldı. Maküler kalınlık ölçümü için OKT (Heidelberg Engineering Spectralis HRA+OCT 2015) uygulandı. Mikrobiyoloji laboratuvarında, serum AAA seviyesi ELİSA (BioVision, Inc.155 S Milpitas, CA95035 USA) yöntemi ile ölçüldü. Bulgular: Çalışmamıza dahil edilen hastaların 28'i (%46,7) erkek, 32'si (%53,3) kadındı. Hastaların 19'u (%31,7) idiyopatik üveit olarak takip edilirken, 19 (%31,7) hasta Behçet hastalığı, 9 (%15) hasta sarkoidoz, 4 (%6,7) hasta Vogt-Koyanagi Harada (VKH), 7 (%11,7) hasta ankilozan spondilit, 1 (%1,7) hasta juvenil idiopatik artrit, 1 (%1,7) hasta serpijinöz koroidit tanısı ile takip ediliyordu. Anatomik lokalizasyona göre, 16 (%26,7) hastada anterior, 10 (%16,7) hastada intermediyer, 1 (%1,7) hastada posterior, 33 (%55) hastada panüveit mevcuttu. ADA tedavisi sonrası hastaların GK'de artış (p<0,001), SMK'da (p<0,001) ve atak sayısı/yıl oranında (p<0,001) azalma istatistiksel olarak anlamlı idi. Ek immünsüpresif tedavi kullanımında (p=0,120) istatistiksel olarak anlamlı bir azalma görülmezken steroid kullanımında (p<0,001) istatistiksel olarak anlamlı azalma kaydedildi. İki haftada bir ADA kullanan grupta GK'de artış (p <0,001), SMK'de (p<0,001) ve atak sayısı/yıl oranında (p<0,001) azalma istatistiksel olarak anlamlıydı. Haftada bir ADA kullanan grupta GK'de artış (p=0,102) ve SMK'de azalma (p=0,130) anlamlı değilken, atak sayısı/yıl oranında azalma (p<0,001) anlamlıydı. 15 (%25) hastada, serumda AAA tespit edildi. AAA pozitif grupta GK'de artış (p=0,002), SMK'de (p=0,006) ve atak sayısı/yıl oranında azalma (p<0,001) anlamlı düzeydeydi. Benzer şekilde AAA negatif grupta GK'de artış (p<0,001), SMK'de (p<0,001) ve atak sayısı/yıl oranında azalma (p<0,001) anlamlıydı. İki haftada bir ve haftada bir ADA uygulanan gruplar arasında AAA gelişimi açısından anlamlı fark yoktu (p=0,427). Yan etki açısından AAA pozitif ve AAA negatif gruplar arasında (p=0,164) ve de iki haftada ve haftada bir ADA kullanan gruplar arasında (p=0,773) anlamlı fark saptanmadı. Sonuç: ADA non-enfeksiyöz üveitlerin tedavisinde etkili ve güvenilir bir ajandır. Tedaviye yanıtın yetersiz olduğu hastalarda doz aralığının azaltılması etkili bir yöntem olabilir. ADA kullanan hastalarda AAA gelişebilmektedir ancak çalışmamızda AAA gelişiminin tedaviye cevap üzerine etkisi gösterilememiştir. Anahtar kelimeler: Adalimumab, Anti-TNF, non-enfeksiyöz üveit, anti-adalimumab antikor
Objective: To evaluate the efficacy of adalimumab (ADA) treatment, anti-adalimumab antibody (AAA) development, and the effect of AAA development on treatment success in patients with non-infectious uveitis. Materials and Methods: 117 eyes of 60 patients who were followed up with the diagnosis of non-infectious uveitis in Ondokuz Mayıs University, Faculty of Medicine, Ophthalmology Outpatient Clinic and who received ADA treatment once a week or every two weeks for at least 3 months were included in the study. The data of the patients were evaluated retrospectively, and demographic data and eye findings (visual acuity (VA), clinical activity findings, macular thickness) before ADA treatment were recorded. Peripheral blood samples were obtained from the patients included in the study before the last dose of ADA was administered. Routine eye examination including visual acuity (VA) with Snellen decimal chart, intraocular pressure measurement with applanation tonometry, anterior segment examination with slit lamp biomicroscopy and fundus examination with 90 D lens were underwent to patients on the same day. Macular thickness was performed with optical coherence tomography [OCT (Heidelberg Engineering Spectralis HRA+OCT 2015)]. The serum AAA level was determined by ELISA (BioVision, Inc.155 S Milpitas, CA95035 USA) method in the blood sample taken in the microbiology laboratory. Results: Of the patients included in this study, 28 (46.7%) were male and 32 (53.3%) were female. While 19 (31.7%) of the patients were followed with idiopathic uveitis, 19 (31.7%) patients had Behçet's disease, 9 (15%) patients had sarcoidosis, 4 (6.7%) patients had Vogt-Koyanagi Harada (VKH), 7 (11%) patients had ankylosing spondylitis, 1 (1.7%) patient had juvenil idiopathic arthritis, and 1 (1.7%) patient had serpiginous choroiditis. According to anatomical localization, 16 (26.7%) patients had anterior, 10 (16.7%) patients had intermediate, 1 (1.7%) had posterior, and 33 (55%) patients had panuveitis. The increase in VA (p<0.001), decrease in central macular thickness CMT (p<0.001) and the number of attacks per year (p<0.001) in patients after ADA treatment were statistically significant. While no statistically significant decrease was observed in the use of additional immunosuppressive therapy (p=0.120), a statistically significant decrease was observed in the use of steroids (p<0.001). The increase in VA (p <0.001), decrease in CMT (p<0.001) and the number of attacks per year (p<0.001) were statistically significant in the group using ADA every other week. While the increase in VA (p=0.102) and decrease in CMT (p=0.130) before and after the treatment in the group using ADA once a week were not significant, the decrease in the number of attacks per year (p<0.001) was significant. AAA was detected in the serum 15 (25%) of the patients. In the AAA positive group, an increase in VA (p=0.002), a decrease in CMT (p=0.006) and in the number of attacks per year (p<0.001) were significant. Similarly, an increase in VA (p<0.001), a decrease in CMT (p<0.001) and the number of attacks per year (p<0.001) were significant in the AAA negative group. There was no significant difference in the development of AAA between the groups in which ADA was applied every other week and ADA applied once a week (p=0.427). In terms of side effects, there was no significant difference between the AAA positive and AAA negative groups (p=0.164), and between the groups using ADA every other week and those using ADA once a week (p=0.773). Conclusion: ADA is an effective and safe agent in the treatment of non-infectious uveitis. Reducing the dose interval may be an effective method in patients with inadequate response to treatment. AAA may develop in patients using ADA, but the effect of AAA on response to treatment was not demonstrated in this study. Key words: Adalimumab, Anti-TNF, non-infectious uveitis, anti-adalimumab antibody
Objective: To evaluate the efficacy of adalimumab (ADA) treatment, anti-adalimumab antibody (AAA) development, and the effect of AAA development on treatment success in patients with non-infectious uveitis. Materials and Methods: 117 eyes of 60 patients who were followed up with the diagnosis of non-infectious uveitis in Ondokuz Mayıs University, Faculty of Medicine, Ophthalmology Outpatient Clinic and who received ADA treatment once a week or every two weeks for at least 3 months were included in the study. The data of the patients were evaluated retrospectively, and demographic data and eye findings (visual acuity (VA), clinical activity findings, macular thickness) before ADA treatment were recorded. Peripheral blood samples were obtained from the patients included in the study before the last dose of ADA was administered. Routine eye examination including visual acuity (VA) with Snellen decimal chart, intraocular pressure measurement with applanation tonometry, anterior segment examination with slit lamp biomicroscopy and fundus examination with 90 D lens were underwent to patients on the same day. Macular thickness was performed with optical coherence tomography [OCT (Heidelberg Engineering Spectralis HRA+OCT 2015)]. The serum AAA level was determined by ELISA (BioVision, Inc.155 S Milpitas, CA95035 USA) method in the blood sample taken in the microbiology laboratory. Results: Of the patients included in this study, 28 (46.7%) were male and 32 (53.3%) were female. While 19 (31.7%) of the patients were followed with idiopathic uveitis, 19 (31.7%) patients had Behçet's disease, 9 (15%) patients had sarcoidosis, 4 (6.7%) patients had Vogt-Koyanagi Harada (VKH), 7 (11%) patients had ankylosing spondylitis, 1 (1.7%) patient had juvenil idiopathic arthritis, and 1 (1.7%) patient had serpiginous choroiditis. According to anatomical localization, 16 (26.7%) patients had anterior, 10 (16.7%) patients had intermediate, 1 (1.7%) had posterior, and 33 (55%) patients had panuveitis. The increase in VA (p<0.001), decrease in central macular thickness CMT (p<0.001) and the number of attacks per year (p<0.001) in patients after ADA treatment were statistically significant. While no statistically significant decrease was observed in the use of additional immunosuppressive therapy (p=0.120), a statistically significant decrease was observed in the use of steroids (p<0.001). The increase in VA (p <0.001), decrease in CMT (p<0.001) and the number of attacks per year (p<0.001) were statistically significant in the group using ADA every other week. While the increase in VA (p=0.102) and decrease in CMT (p=0.130) before and after the treatment in the group using ADA once a week were not significant, the decrease in the number of attacks per year (p<0.001) was significant. AAA was detected in the serum 15 (25%) of the patients. In the AAA positive group, an increase in VA (p=0.002), a decrease in CMT (p=0.006) and in the number of attacks per year (p<0.001) were significant. Similarly, an increase in VA (p<0.001), a decrease in CMT (p<0.001) and the number of attacks per year (p<0.001) were significant in the AAA negative group. There was no significant difference in the development of AAA between the groups in which ADA was applied every other week and ADA applied once a week (p=0.427). In terms of side effects, there was no significant difference between the AAA positive and AAA negative groups (p=0.164), and between the groups using ADA every other week and those using ADA once a week (p=0.773). Conclusion: ADA is an effective and safe agent in the treatment of non-infectious uveitis. Reducing the dose interval may be an effective method in patients with inadequate response to treatment. AAA may develop in patients using ADA, but the effect of AAA on response to treatment was not demonstrated in this study. Key words: Adalimumab, Anti-TNF, non-infectious uveitis, anti-adalimumab antibody
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