Role of intravitreal steroids

There is no standard treatment for a choroidal osteoma. Various treatments for CNV have been tried, but they do not usually halt visual loss. The results of one study showed that photocoagulation of an extrafoveal classic CNV was successful in closing CNV in 25% of treated eyes [ 2 ]. However, photocoagulation can stimulate rapid vascular remodeling and anastomoses in choroidal osteoma [ 3 ]. Another study reported that the CNV can be surgically removed, but the postoperative visual acuity was poor at 6/95 (20/320) [ 4 ]. PDT has been partially successful in treating CNV in eyes with choroidal osteoma. Earlier studies showed that, 6 months after a single PDT, the metamorphopsia can resolve completely; in one study, the visual acuity was not changed [ 5 ] and in another study it improved from 6/60 (20/200) to 6/6 (20/20) [ 6 ]. Another study reported that four PDT applications led to closure of the CNV, but the final vision was 6/35 (20/120) [ 7 ]. PDT has successfully caused closure of extrafoveal CNV in choroidal osteoma [ 6 ]. Laser photocoagulation or PDT in choroidal osteomas with or without CNV may carry the risk of decalcification of choroidal osteoma [ 10 ]. Shields et al. [ 10 ] proposed that photodynamic therapy could be a therapeutic modality for choroidal neovascularization and induction of decalcification of extrafoveal osteoma to prevent tumor growth into the foveola. However, these results should not be extrapolated to subfoveal choroidal osteoma because decalcification of subfoveal choroidal osteoma could result in worse visual acuity because of loss of retinal pigment epithelium and choroidal perfusion [ 1 , 3 , 6 , 10 ].

In addition to data from the 2 phase III clinical trials, data from phase I/II studies were also included in the FDA review.  In an open-label, 2-center, uncontrolled, randomized, phase I clinical trial, Rosenfeld and colleagues (2006) examined if multiple intravitreal doses of up to 2 mg of ranibizumab can be tolerated and are biologically active when injected using a dose-escalating strategy in eyes of patients with neovascular AMD.  A total of 32 patients with primary or recurrent sub-foveal choroidal neovascularization secondary to AMD were enrolled.  Baseline best-corrected VA in the study eye was from 20/40 to 20/640 (Snellen equivalent).  Treatment regimens consisted of 5, 7, or 9 intravitreal injections of ranibizumab at 2- or 4-week intervals for 16 weeks, with escalating doses ranging from to mg.  Patients were evaluated through day 140, 4 weeks after their last injection.  Safety was assessed based on ocular and non-ocular adverse events, changes in VA, changes in intraocular pressure (IOP), slit-lamp ocular examination, changes in lesion characteristics based on fluorescein angiography and color fundus photography, and the presence of anti-ranibizumab antibodies.  A total of 29 patients received an injection at baseline, and 27 patients completed the study through day 140.  Results were similar across the 3 treatment groups.  All patients experienced ocular adverse events, most of which were mild.  The most common ocular adverse events were iridocyclitis (83 %), and injection-site reactions (72 %).  Inflammation did not increase with repeated injections, despite the increasing ranibizumab doses.  Transient mild IOP elevations were common after ranibizumab injection.  No serum anti-ranibizumab antibodies were detected.  In general, median and mean VAs in the study eyes improved by day 140 in all 3 groups.  Only 3 of the 27 patients lost significant vision.  There was no significant lesion growth, and a decrease in area of leakage from choroidal neovascularization was detected through day 140.  The authors concluded that multiple intravitreal injections of ranibizumab at escalating doses ranging from to mg were well-tolerated and biologically active in eyes with neovascular AMD through 20 weeks.  Mild transient ocular inflammation was the most common post-injection adverse event.

AB - Purpose: To evaluate the safety and efficacy of intravitreal methotrexate in the management of primary central nervous system lymphoma (PCNSL) involving the eye. Design: Retrospective noncomparative interventional case series. Participants: Sixteen human immunodeficiency virus-negative white patients (5 males and 11 females, aged 30-76 years) with intraocular B cell lymphoma treated with intravitreal methotrexate at Oregon Health & Science University or Hadassah University Hospital between August 1995 and September 2000. Intervention: Patients were treated with intravitreal methotrexate (400 μg/ ml) according to a standard induction-consolidation-maintenance regimen and monitored by serial examinations, including measurement of visual acuity, slit-lamp biomicroscopy, and dilated funduscopy. Main Outcome Measures: Clinical response to intravitreal chemotherapy, number of injections for clinical remission, visual acuity, complications during study period, length of survival from diagnosis, and cause of death. Results: Time of follow-up from commencement of the methotrexate injections was 6 to 35 months (median, months). Twenty-six of 26 eyes (100%) were cleared clinically of malignant cells after a maximum of 12 methotrexate injections. A second remission was induced in three patients, who were treated with a further course of intravitreal chemotherapy after their tumor recurred within the eye. Complications that occurred during the period of treatment and follow-up included cataract (73% of 26 eyes), corneal epitheliopathy (58% of 26 eyes), maculopathy (42% of 26 eyes), vitreous hemorrhage (8% of 26 eyes), optic atrophy (4% of 26 eyes), and sterile endophthalmitis (4% of 26 eyes). No patient had irreversible loss of vision that could be definitely attributed to the intravitreal injection of methotrexate. Conclusions: Intravitreal chemotherapy with methotrexate is effective in inducing clinical remission of intraocular tumor in PCNSL with acceptable morbidity. Further study is indicated to determine whether this approach extends life expectancy.

Role of intravitreal steroids

role of intravitreal steroids

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