DOI: 10.1097/IAE.0b013e318254afda
,
Issn Print: 0275-004X
Publication Date: 2012/05/01
Facebook
Twitter
LinkedIn
Email
 |
Checking for direct PDF access through Ovid | |
Excerpt
I read with interest the article by Drs Elbendary and Shahin entitled, “Intravitreal diclofenac versus intravitreal triamcinolone acetonide in the treatment of diabetic macular edema.”1 I would like to commend the authors for conducting an important clinical trial on a topic of great personal interest to me. However, I have several comments regarding their results and conclusions. Among reported nonsteroidal anti-inflammatory drugs (NSAIDs), diclofenac has a relatively low threshold of safety within the eye, and I and others have reported toxicity at intraocular doses as low as 500 μg in rabbit eyes.2 Consequently, the lack of baseline and posttreatment electroretinography (ERG) testing in this study is concerning since incidences of diclofenac toxicity may show no overt clinical signs and could occur at lower concentrations (even after considering volume differences between human and rabbit eyes).2 Given the limited clinical experience with intravitreal administration of diclofenac, ERG testing should be strongly encouraged in future human studies as another measure of drug toxicity despite its inherent limitations. It is also difficult to attribute the sustained reduction in retinal thickness observed out to 12 weeks to diclofenac since the drug is completely eliminated from the vitreous and retina within 24 hours3,4 after intravitreal administration, and chronic diseases, such as diffuse diabetic macular edema (DME), typically require sustained treatment. In support of this, a previous study on intravitreal diclofenac using the same dose and including patients with DME found no benefit on macular thickness out to 8 weeks.5 We also performed a recent pilot study at the Vanderbilt Eye Institute (Nashville, TN) investigating the effects of intraocular 4 mg of ketorolac in patients with chronic inflammation and macular edema and observed only short-lived effects lasting no longer than 1 to 2 weeks.6 In addition, most commercial formulations of diclofenac are intended for intramuscular or intravenous use and contain preservatives, such as benzyl alcohol, which are known to be toxic within the eye. The authors should list the contents of the formulation used in their study and account for this possibility.
In sum, while I recognize and have myself reported that diclofenac is a potent NSAID with excellent activity against cyclooxygenase-27 while possessing some inhibitory activity against lipoxygenase,8 its short half-life within the eye and toxicity make it a less compelling choice for intraocular administration to treat chronic posterior segment diseases in the absence of drug modification.
