Adalimumab (humira™) in ophthalmology: a review of the literature.

Tumor Necrosis Factor alpha (TNF-α) is a pleiotropic cytokine which plays a primary role in the induction of inflammation in autoimmune diseases. The newest anti-TNF-α agent is adalimumab (Humira, Abbott Pharmaceutical Inc.), a human-derived antibody. This review summarizes the characteristics of adalimumab, highlighting its clinical use in systemic and ocular inflammatory disorders, and the possible therapeutic strategies. Adalimumab has been successfully used for the treatment of rheumatoid arthritis, ankylosing spondylitis, and psoriasis arthritis. More recently, adalimumab has shown promising qualities in controlling intraocular inflammations, even though this has been used prevalently as a rescue therapy for unresponsive cases. This biologic agent was also used in pediatric cases, showing a good safety and efficacy profile. Albeit no direct comparison with other biologics has been done, and adalimumab seems to be equivalent to the other anti-TNF-α, the switching to adalimumab can offer a better uveitic control. Adalimumab is a promising drug for the treatment of uveitis, even though further studies are needed on its application as a primary therapy in uveitis.

Association of systemic steroids and mycophenolate mofetil as rescue therapy for uveitic choroidal neovascularization unresponsive to the traditional immunosuppressants: interventional case series.

To study the efficacy of systemic steroids (SS) associated with mycophenolate mofetil (MMF) for the control of juxta/sub-foveal uveitic choroidal neovascularization (CNV) unresponsive to the traditional immunosuppressive agents. Patients with juxta/sub-foveal uveitic CNV unresponsive to the traditional immunosuppressive drugs were treated with SS and MMF. The study was designed as a prospective, consecutive, open-label, interventional case series. Visual gain and loss were defined as improving or worsening of two or more lines of best-corrected visual acuity (BCVA), respectively. CNV size outcome was dichotomized as "increased" or "stable/reduced", if increased >200 µm(2), or reduced ≥ 200 µm(2) or not modified by 200 µm(2), respectively. Nine cases (12 eyes) have been considered; ages ranged from 27 to 56 years. The mean follow-up time was 18.2 ± 2.9 months (min: 14 months, max: 23 months). At base-line, the mean BCVA was 0.3 ± 0.17, improving up to 0.57 ± 0.25 and to 0.63 ± 0.22 (P < 0.001, paired t-test) at the 6 and 12-month follow-ups, respectively. At the last follow-up, all the patients had stable/improved BCVA (P < 0.0001, Fisher's exact test) and stable/reduced lesion size (P < 0.0001, Fisher's exact test). None of the patients complained of any severe adverse event during the treatment. The combination of SS and MMF seems to be a promising strategy in order to control uveitic CNVs unresponsive to the traditional immunosuppressive agents. Further studies are needed to validate the data of this case series.

Inflammatory choroidal neovascularization.

PURPOSE AND METHODS: Choroidal neovascularization (CNV) can be a severe sight-threatening sequela, which can be secondary to both infectious and noninfectious uveitis. This review summarizes the different diseases associated with CNV, highlighting new treatment modalities and the possible strategies, which could be applied for the therapy of this occurrence. RESULTS: Since CNV can often originate from posterior pole lesions and can be hard to identify, an accurate examination is mandatory in order to identify the correct diagnosis. In the majority of cases, fluorescein angiography (FA), indocyanine green angiography (ICGA) and optical coherence tomography (OCT) enable the determination of the clinical characteristics of the CNV. An infectious disease should be looked for to include a suitable therapy when available. The treatment strategy for CNV secondary to noninfectious uveal inflammations should be directed at controlling the inflammatory process. Systemic corticosteroids with or without immunosuppressive agents are indicated even when the CNV occurs with apparently inactive uveitis: Chronic subclinical inflammation can be the basis for the pathogenesis of CNV. Additional therapies aimed directly at the neovascular process, such as the intravitreal anti-Vascular Endothelial Growth Factor (VEGF) agents, are recommended particularly when the therapy shows an insufficient response. CONCLUSION: CNV secondary to uveitis is a severe sequela leading to significant visual impairment. ICGA is mandatory in order to obtain relevant information about the choroidal status. Several therapeutic options have been considered, but no guidelines are provided at the moment. Moreover, the current data are still only based on case reports or small series. For such reasons, further trials are mandatory to validate the preliminary available results.