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Nanomedicines for Ocular NSAIDs: State-of-the-Art Update of the Safety on Drug Delivery
Published in Lajos P. Balogh, Nano-Enabled Medical Applications, 2020
Joana R. Campos, Joana Araújo, Elisabet Gonzalez-Mira, Maria A. Egea, Elena Sanchez-Lopez, Marta Espina, Selma B. Souto, Maria L. Garcia, Eliana B. Souto
NSAIDs are effective drugs compared to placebos for the relief of anterior chamber inflammation [34]. The goals of topical prophylactic NSAIDs treatment include the prevention of intraoperative miosis [35], management of postoperative inflammation, prevention or treatment of CME [36] and reduction of ocular pain [37]. There are four NSAIDs currently approved by the U.S. Food and Drug Administration (FDA) for the treatment of post operative inflammation after cataract surgery [38], namely kerotolac, bromfenac, diclofenac, and nepafenac. This latter is the only prodrug NSAID and thus requires conversion to its more active state, amfenac, through intraocular enzymatic hydrolysis [39]. A study compared aqueous humour concentrations of these four NSAIDs after administration in patients having cataract surgery and the cyclooxigenase-1 (COX-1) and COX-2 inhibitory activity was also determined, via in vitro measurement of PG inhibition to rank order the potency of the molecules, showing nepafenac significantly greater ocular bioavailability than the others and amfenac greater potency at COX-2 inhibition [38]. Furthermore, diclofenac, nepafenac, ketorolac, and bromfenac have relatively greater significant effects than other topical NSAIDs. NSAIDs were first approved by the FDA to prevent surgically induced miosis [40]. Newer NSAIDs are being investigated for their ability to reduce the incidence of CME after cataract surgery. CME is a major complication after cataract surgery and remains the primary cause of surgical visual disorders [41]. Whether NSAIDs can effectively prevent the development of CME is still controversial. Recent comprehensive analyses investigated the ability of NSAIDs to reduce the incidence of CME after cataract surgery, but a positive effect was not observed [40]. Although ambiguity surrounds NSAIDs regarding CME prevention, NSAIDs play an important role in cataract surgery.
Efficacy and safety of bromfenac 0.075% formulated in DuraSite for pain and inflammation in cataract surgery
Published in Expert Opinion on Pharmacotherapy, 2019
Scott M Wentz, Francis Price, Alon Harris, Brent Siesky, Thomas Ciulla
Bromfenac sodium (sodium 2-amino-3-(4-bromobenzoyl)phenylacetate sesquihydrate) (Box 1) is a topical ophthalmic non-steroidal anti-inflammatory drug (NSAID) used especially for mitigating post-operative pain and inflammation associated with cataract surgery [6]. NSAIDs inhibit prostaglandin production via blockade of cyclooxygenase (COX)-1 and COX-2 enzymes, but with much more affinity to COX-2 [7]. COX-2 predominantly mediates inflammation, whereas COX-1 sustains homeostasis in the kidneys, platelets, and stomach [8,9]. Inhibition of COX-2 reduces local levels of specific prostaglandins, prostaglandin E2 and prostacyclin, which normally incite local vasodilation, pain, and increased vasopermeability [10]. Other factors that are affected by prostaglandins include altering intraocular pressure and producing miosis [11–14]. By inhibiting prostaglandin synthesis, topical ophthalmic NSAIDs are used frequently in the peri-operative cataract surgery setting to facilitate control and prevention of pain, inflammation, and post-operative inflammation-mediated pseudophakic CME [3–5]. Additionally, topical ophthalmic NSAIDs may also be used as adjunctive treatment for episcleritis or scleritis. However, the mainstay treatment for scleritis is oral NSAIDs, and, in episcleritis, cool compresses, artificial tears or observation is usually all that is required. A topical ophthalmic NSAID or topical corticosteroid may be used if the patient has some discomfort [15].
Optimization of hyaluronan-enriched cubosomes for bromfenac delivery enhancing corneal permeation: characterization, ex vivo, and in vivo evaluation
Published in Drug Delivery, 2023
Nabil A. Shoman, Rana M. Gebreel, Mohamed A. El-Nabarawi, Alshaimaa Attia
Non-steroidal anti-inflammatory drugs (NSAIDs) are used clinically to reduce the inflammatory process owing to the manipulation of ocular structures like, surgery, trauma, infections, among others. As a cyclooxygenase (COX-1 & COX-2) inhibitor, NSAIDs have been widely considered as an effective alternative to ocular corticosteroids for the relief of ocular inflammation and post-operative pain. Bromfenac sodium (BS) is the first and only topical ophthalmic NSAID with a once-daily dosing regimen approved by the US Food and Drug Administration for the management of pain and inflammation associated with cataract surgery (Cable 2012). It has good ocular penetration with insignificant systemic reactions following topical administration. Bromfenac, like other NSAIDs, is a weakly acidic drug. Reducing the pH formulation increases the unionized fraction of the drug, which, in turn, improves its ocular penetration (Hoffman et al., 2016). It is a very potent (COX-2) inhibitor of prostaglandin production that improves the inflammation signs induced by eye dryness in patients with of Dry eye syndrome (DES) (Fujishima et al., 2015). DES is a multifactorial disorder of the preocular tear film and ocular surface characterized by pain, visual disturbance, and tear film instability. DES affects between 5% and 34% of people, with additional symptoms including redness, burning, itching, sensation of foreign objects, pruritus, stinging and light sensitivity (Huynh and Priefer 2020). In recent decades, the most commonly used therapy is the use of artificial tears made up of sodium hyaluronate, polyvinyl alcohol, povidone, and cellulose derivatives (Fezza 2018).
Comparison of the Effect of Bromfenac versus Betamethasone Ophthalmic Solutions in Patients with Diabetic Macular Edema
Published in Current Eye Research, 2023
Yui Tobimatsu, Rie Ogihara, Naoko Endo, Akira Hirose, Ryuji Takeda, Tetsuya Babazono, Shigehiko Kitano
Chronic inflammation of retinal microvessels causes an increase in inflammatory mediators, including PGs and VEGFs, weakening the blood-retinal barrier and resulting in macular edema.14,15 Corticosteroids can reduce macular edema through several mechanisms. One mechanism involves inhibition of the COX-1 and COX-2 inflammatory pathways. NSAIDs act mainly through potent inhibition of prostaglandin E2 (PGE2) synthesis by suppression of arachidonic acid transformation catalyzed by COX-1 and COX-2. Topical NSAIDs do not appreciably reach the posterior segment, whereas intravitreal injection allows greater bioavailability and efficacy of the drug. However, it has been reported that sodium bromfenac reaches the retina sufficiently with topical administration.11 A study using rabbits has confirmed that the instillation of BF twice a day can maintain an IC50 for COX in choroid tissues;11 it has been shown that the instillation of NSAIDs reduced the concentration of PGE2 in the vitreous body.16 It is believed that BF demonstrated sufficient migration even in ophthalmic solution treatment, and exhibited anti-inflammatory action via PGE2 inhibition in the vitreous body, improving diabetic macular edema. Furthermore, the effects of bromfenac on nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor,17 and VEGF,18 apart from COX-2, have been reported. Bromfenac exerts an anti-inflammatory effect on substances other than PGE2 similar to sodium diclofenac, which, in addition to inhibition of cyclooxygenase, regulates leukotriene production by inflammatory cells via a mechanism mediated in part through the redistribution of arachidonic acid in lipid pools.19 In DME, in addition to increased vascular permeability, retinal inflammation is also an important factor, and these anti-inflammatory actions may be associated with and involved in the improvement of DME.