"If you've ever been sleep-deprived, you've probably had a firsthand glimpse of the blood vessels in your eyes. But what you haven't seen—and what many eye care professionals cannot see as well as they would like—are the vessels closes"...
- Patient Information:
Details with Side Effects
Mechanism Of Action
Corticosteroids inhibit the inflammatory response to a variety of inciting agents and probably delay or slow healing. They inhibit the edema, fibrin deposition, capillary dilation, leukocyte migration, capillary proliferation, fibroblast proliferation, deposition of collagen, and scar formation associated with inflammation.
There is no generally accepted explanation for the mechanism of action of ocular corticosteroids. However, corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2. Corticosteroids are capable of producing a rise in intraocular pressure.
In a subset of patients who received the intravitreal implant, and had blood samples taken at various times (weeks 1, 4 and 34) after implantation, plasma levels of fluocinolone acetonide were below the limit of detection (0.2 ng/mL) at all times. Aqueous and vitreous humor samples were assayed for fluocinolone acetonide in a further subset of patients. While detectable concentrations of fluocinolone acetonide were seen throughout the observation interval (up to 34 months), the concentrations were highly variable, ranging from below the limit of detection (0.2 ng/mL) to 589 ng/mL.
In two randomized, double-masked, multicenter controlled clinical trials, 224 patients with chronic (a one year or greater history) non-infectious uveitis affecting the posterior segment of one or both eyes were randomized to receive a 0.59 mg RETISERT. The primary efficacy endpoint in both trials was the rate of recurrence of uveitis affecting the posterior segment of the study eye in the 34 week pre-implantation period compared to the rate of recurrence in the 34 week post-implantation period. Uveitis recurrence rates at 1, 2, and 3 year post-implantation were also compared to the 34 week preimplantation period.
Detailed results are shown in table 1 below:
Table 1: Uveitis Recurrence Rates
|Time Point||Study 1
|UVEITIS RECURRENCE RATES1,2
|34 Weeks Pre-implantation||58 (53.7)||46 (39.7)|
|34 Weeks Post-implantation||2 (1.8)||15 (12.9)|
|1 Year Post-implantation||4 (3.7)||15 (12.9)|
|2 Years Post-implantation||11 (10.2)||16 (13.8)|
|3 Years Post-implantation||22 (20.4)||20 (17.2)|
|3 Years3 Post-implantation||33 (30.6)||28 (24.1)|
|1 Recurrence of uveitis for all
post-implantation time points was compared to the 34 weeks pre-implantation
2 p-value < 0.01 from McNemar's χ2 test.
3 Results presented include imputed recurrences. Recurrences were imputed when a subject was not seen within 10 weeks of their final scheduled visit.
Last reviewed on RxList: 8/2/2011
This monograph has been modified to include the generic and brand name in many instances.
Additional Retisert Information
Report Problems to the Food and Drug Administration
You are encouraged to report negative side effects of prescription drugs to the FDA. Visit the FDA MedWatch website or call 1-800-FDA-1088.
Get breaking medical news.