Abstract
To investigate the efficacy of adalimumab in the cases with refractory non-infectious uveitis and evaluate retinal vascular leakage changes on ultra-widefield fundus fluorescein angiography. Twenty-three patients with refractory uveitis were included in study. Forty-four eyes of 23 patients with non-infectious uveitiswere evaluated. Clinically active inflammation was present in 19 eyes (43.18%), while 25 (56.8%) were inactive. The mean drug burden was a 9.91 ± 3.78 (5-21) in baseline, 7.3 ± 4.25 at third and 8.0 ± 4.71 at sixth month (p = 0.022). The mean choroidal thickness was 256.65 ± 43.63μm in baseline, 240.49 ± 36.73μm at third and 224.81 ± 34.91μm at sixth month (p ≤ 0.05). In terms of leakage extend, leakage was initially present in a mean of 2.95 ± 4.55 clock hours, 2.41 ± 3.91 at third and 1.76 ± 3.44 at sixth month (p < 0.001). Adalimumab was found to be effective in establishing inflammation control by reducing drug burden, controlling retinal vascular leakage and choroidal inflammation in refractory uveitis.
Highlights
Uveitis is a sight-threatening intraocular inflammation andour understanding of the pathogenesis of the disease, other than infectious causes, is still limited
Adalimumab was found to be effective in establishing inflammation control by reducing drug burden, controlling retinal vascular leakage and choroidal inflammation in refractory uveitis
The efficacy of adalimumab in uveitis and inflammation control has been proved in several studies, especially evaluating retinal vascular and optic discleakages in posterior segment have been investigated in a few studies.The purpose of the present study was to investigate retrospectively the efficacy of adalimumab in retinal vascular leakage, and controlling vascular and choroidal inflammation in patients with non-infectious uveitis, which is refractory to conventional immune suppressive therapy, by evaluating the posterior segment and peripheral retina with ultra-widefield fundus fluorescein angiography
Summary
Uveitis is a sight-threatening intraocular inflammation andour understanding of the pathogenesis of the disease, other than infectious causes, is still limited It is responsible 5–20% of legal blindness in developed countries.[1, 2] Systemic autoimmune diseases such as Behçet disease, sarcoidosis, spondyloarthropathies, and Vogt-Koyanagi-Harada syndrome or unclassifiable idiopathic uveitis constitute non-infectious uveitis.[3, 4] The main objective in the treatment of uveitis is to keep the intraocular inflammation under control, to prevent recurrences, to establish full remission, and to protect the vision.[5] Steroids are used as the first therapeutic choice in active inflammations.,severe ocular and systemic side-effects may develop with long-term steroid use. Since recurrences are common under steroid monotherapy, conventional immunosuppressive agents are employed in long-term treatment. Some patients are resistant to treatment, and the disease cannot be brought under control, despite the use of combination therapies
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