New data continues to be released on the role that inflammation plays in the disease process of DME. Effective treatment addresses the underlying inflammation to prevent the recurrence and slows the progression of vascular changes to preserve a patient’s vision.
Diabetes causes hyperglycemia resulting in chronic low-grade, systemic inflammation. This inflammation is a major contributor to the progression and complications of DME.1
DME has historically been considered an ocular microvascular complication of diabetes. Recent scientific evidence indicates an earlier role of chronic, low-grade neuroinflammation in DME. In the eye, chronic low-grade inflammation causes damage to neuronal cells in the retina and alters the vascular integrity of the blood retinal barrier (BRB), leading to retinal edema.2
Diabetic patients are no strangers to frequent doctor appointments. However, in real-world practice, DME patients received far fewer injections than those in major clinical trials. The result can be that patients are being undertreated and experiencing lesser outcomes.3 Short-duration treatments can allow edema to recur resulting in fluctuations in retinal thickness of DME patients, which can lead to retinal damage over time.4
In a large retrospective claims analysis, patients in clinical practice were found to be monitored less frequently and receive far fewer injections than patients in major clinical trials. The mean number of visits with an anti-VEGF injection for all DME cohorts was 3.0 per year. Less than 6% of patients received ≥ 10 injections in 12 months in actual clinical practice.5 In the PALADIN Study, during the 36-months pre-FAc, visual acuity declined by a mean of 6.4 letters, and 75.3% of the eyes received ≤ 5 yearly treatments (mean 3.5). Through 36 months post-FAc, BCVA significantly improved by a mean of 4.5 letters, and the mean number of yearly supplemental treatments was reduced to 1.7 with 68.3% of eyes requiring ≤ 2 yearly supplemental treatments.6
Corticosteroids are widely recognized as an effective treatment for inflammation throughout the body. An ideal treatment for DME would be a durable therapeutic agent that can directly target the retinal tissue and effectively suppress the inflammatory response.6,7 By suppressing this inflammatory response and the resulting edema, retinal damage and permanent vision loss may be prevented.1,8
ILUVIEN® (fluocinolone acetonide intravitreal implant) 0.19 mg is indicated for the treatment of diabetic macular edema (DME) in patients who have been previously treated with a course of corticosteroids and did not have a clinically significant rise in intraocular pressure.
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1-844-445-8843. US-ILV-MMM-0538
Consider ILUVIEN for phakic patients with DME, particularly those aged > 50 years and/or with developing cataracts
Patients with diabetes are 2 to 5 times more prone to cataract development2
In the ILUVIEN Phase 3 clinical trials:
Observations from a small, real-world cohort of vitrectomized patients with DME treated with ILUVIEN
Authors of this study received compensation from Alimera. Two authors received speaker honoraria from Alimera, and two authors were consultants. One author received reimbursement of travel expenses and study support from Alimera.
FAME A and B were randomized, double-masked, sham injection-controlled, parallel-group, multicenter studies conducted under a single protocol over 36 months.
Study arms:
956 subjects randomized 2:2:1
Primary endpoint:
Proportion of subjects with improvement in BCVA ≥ 15 letters at 24 months
Inclusion criteria:
Foveal thickness ≥ 250 μm despite ≥ 1 prior focal/grid macular laser photocoagulation treatment and BCVA in ETDRS letter score between 19 and 68 (20/50–20/400).
Exclusion criteria:
Glaucoma, ocular hypertension, IOP > 21 mm Hg, or using IOP-lowering drops.
References:
1. ILUVIEN® [package insert]. Alpharetta, GA: Alimera Sciences, Inc.
1. ILUVIEN® [package insert]. Alpharetta, GA: Alimera Sciences, Inc.
2. Parrish RK, Campochiaro PA, Pearson PA, Green K, Traverso CE, FAME Study Group. Characterization of intraocular pressure increases and management strategies following treatment with fluocinolone acetonide intravitreal implants in the FAME trials. Ophthalmic Surg Lasers Imaging Retina. 2016;47:426-435.
1. Meireles A, Goldsmith C, El-Ghrably I, et al. Efficacy of 0.2 µg/day fluocinolone acetonide implant (ILUVIEN) in eyes with diabetic macular edema and prior vitrectomy. Eye (Lond). 2017;31(5):684-690.
1. ILUVIEN® [package insert]. Alpharetta, GA: Alimera Sciences, Inc.
2. Javadi MA, Zari-Ghanavati S. Cataracts in diabetic patients: A review article. J Ophthalmic Vis Rec. 2008;3(1):52-65.
3. Data on file. Alimera Sciences, Inc.
4. Mordi JA, Ciuffreda KJ. Statis aspects of accommodation: age and presbyopia. Vision Res. 1998;38:1643-1653.
5. Campochiaro PA, Brown DM, Pearson A, et al. Long-term benefit of sustained-delivery fluocinolone acetonide vitreous inserts for diabetic macular edema. Ophthalmology. 2011;118:626-635.
6. Yang Y, Bailey C, Holz FG, et al. Long-term outcomes of phakic patients with diabetic macular oedema treated with intravitreal fluocinolone acetonide (FAc) implants. Eye (Lond). 2015;29:1173-1180.
1. Data on file. Alimera Sciences, Inc.
1. Data on file. Alimera Sciences, Inc.