Editor’s Note: Welcome to “Eye Catching: Let's Chat,” a blog series featuring contributions from members of the ophthalmic community. These blogs are an opportunity for ophthalmic bloggers to engage with readers with about a topic that is top of mind, whether it is practice management, experiences with patients, the industry, medicine in general, or healthcare reform. The series continues with this blog by Joshua Mali, MD, a board certified vitreoretinal surgeon at The Eye Associates, a private multi-specialty ophthalmology practice in Sarasota, FL. The views expressed in these blogs are those of their respective contributors and do not represent the views of Ophthalmology Times or UBM Medica.
As retinal specialists, we are truly fortunate to live in a time where we have several treatment options for patients with diabetic macular edema (DME). A fluocinolone acetonide (FAc) intravitreal implant 0.19 mg (Iluvien, Alimera Sciences) is indicated for the treatment of DME in patients who have been previously treated with a course of corticosteroids and did not have a clinically significant rise in IOP.1,2
Once the selection of the FAc implant as the treatment modality has been confirmed, the next step in the clinical decision making process is crucial. What is the best predictor of a clinically significant rise in IOP with the implant?
Traditionally, retinal specialists utilize dexamethasone intravitreal implant (Ozurdex, Allergan) to provide the best simulation of the effects of what an FAc implant administration may provide. This is done for several reasons: to help determine clinical efficacy of intravitreal steroids with an individual patient’s DME, predict an unacceptable IOP rise from steroids, and confirm a patient does not report a “floater” symptom from the implant. However, these reasons need to be closely analyzed and evaluated.
The clinical efficacy of the FAc implant has been proven with extensive clinical trials, particularly the FAME trials, which demonstrated significant clinical efficacy with the implant in patients with DME.
In regards to the floater symptom, is dexamethasone really a fair comparison to fluocinolone acetonide? The FAc implant (3.5 mm in length and 0.37 mm in diameter)2 is much smaller than the dexamethasone implant (6 mm in length and 0.46 mm in diameter)3 and typically the FAc implant settles in the inferior vitreous base/ora serrata region which essentially eliminates the chance of a floater symptom.
Finally, predicting the rise of IOP with corticosteroid treatment is key when considering the FAc implant, but is the dexamethasone implant truly the best predictor? If not, which steroid should be the most predictive of the IOP response associated with FAc? Let us take a closer look.
There are three important factors to consider when choosing the agent best suited to simulate the effects of FAc: water solubility, tissue penetration, and chemical structure. Having a low water solubility is a critical factor in determining whether or not compounds can penetrate intraocular tissues, particularly the retina and trabecular meshwork. Lower water solubility (lipophilic) equates to better tissue penetration and higher levels of clinical effect at target sites.
We know from previous studies which analyzed the corticosteroid family that dexamethasone is over 180 times more water soluble than FAc, whereas FAc has similar water solubility rates compared to other steroids such as difluprednate (Durezol, Alcon Laboratories), prednisolone acetate (Pred Forte, Allergan), and triamcinolone acetonide.4-8 The way dexamethasone achieves its clinical efficacy is due to the initial burst of high drug concentration intraocularly to overcome the high water solubility factor. Previous clinical studies have also used topical prednisolone acetate successfully to identify patients who had the potential to demonstrate an uncontrolled IOP response associated with intravitreal triamcinolone (IVTA).9