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Ocular Inflammation and Nsaids: an Overview with Selective and Non-Selective Cox Inhibitors

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Ocular Inflammation and Nsaids: an Overview with Selective and Non-Selective Cox Inhibitors OCULAR INFLAMMATION AND NSAIDS: AN OVERVIEW WITH SELECTIVE AND NON-SELECTIVE COX INHIBITORS Rajesh Rao, Rakesh Kumar, Amita Sarwal, V. R. Sinha* University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160014, India E-mail: [email protected] Abstract: Inflammation is a complex biological response and like other parts of the body, ocular inflammation could have untoward effects on vision if not detected and/or diagnosed early. NSAIDs are the major ocular therapeutics for treating such eye inflammations and preferred over corticosteroids. NSAIDs are given orally as well as topically to treat ocular inflammations, however topical route is preferred over systemic route for treating such conditions. To further decrease the adverse effects caused by NSAIDs due to their non-selective nature, preferential cyclooxygenase-2 (COX-2) inhibitors are preferred over non-selective cyclooxygenase (COX) inhibitors. The present review covers various facets of NSAIDs in ocular drug delivery for treating ocular inflammatory condition. Keywords: Ocular inflammation, NSAIDs, Cyclooxygenase, Topical ocular delivery 1. INTRODUCTION lead to visual impairment and blindness. Hence, the Inflammation is an immediate complex treatments of ocular inflammatory conditions are biological response of the body that occurs often quite necessary for protection of vitality of vision. due to invading parasite or tissue injury triggered Nonsteroidal anti-inflammatory drugs (NSAIDs) by chemicals, or physical stress [1-2]. Hence, a have been reckoned as an efficient modulators of defensive response wherein altered physiological ocular inflammatory reactions as they inhibit reactions limit tissue damage and expelled out prostaglandin biosynthesis, the major product of pathogenic substances or abnormally generated COX pathway [7]. This review solely focuses on self-compounds produced during tissue injury [3-4]. NSAIDS mechanism and regulation as selective Acute inflammation is a short-term response and non-selective COX inhibitors for various characterized by vasodilation, infiltration of ocular inflammatory conditions. leukocytes at infected region with a rapid resolution phase and repair of the damaged tissue. 2. OCULAR INFLAMMATION AND Therefore, inflammation executed beneficial PHARMACOTHERAPEUTICS activities against acute infection and injury. In Majorly depending on the tissues, the contrast, chronic inflammation is the state of inflammation of eye can be divided in these parts prolonged and uncontrolled inflammatory (Figure 1). reactions. As inflammatory mediators are not specific to particular tissue targets, chronic 2.1. Conjunctiva inflammation could be a common etiological and It is a translucent mucous membrane that physiological factor for various chronic conditions delineates the posterior surface of the eyelids and like allergy, atherosclerosis, arthritis, cancer and anterior of eyeball. Inflammation of conjunctiva several autoimmune diseases [2-3, 5]. (conjunctivitis) [8] includes infective conjunctivitis Eye is a delicate organ supplied with (bacterial, chlamydial or viral), allergic highly responsive nerves. The inflammation conjunctivitis and granulomatous conjunctivitis [8]. process in eyes is similar to rest of body organs and usually encounter in postoperative incidences 2.2. Cornea especially after cataract surgery. Post-operative Cornea is a transparent, avascular, watch inflammation includes disrupted blood-aqueous glass like structure that forms anterior one-sixth of barrier, conjunctival hyperaemia, miosis, increased the outer fibrous coat of the eyeball. Inflammation intra-ocular pressure (IOP), mediated by COX of the cornea (keratitis) includes ulcerative keratitis pathways [6]. These conditions, if left untreated, can and non-ulcerative keratitis [8]. 74 Fig. 1. Various ocular inflammatory diseases 2.3. Sclera swelling which finally results into blurred and Sclera forms the posterior 5/6th part of the external distorted vision [11-12]. fibrous tunic of the eyeball. Inflammation of sclera is known as scleritis. It is a systemic inflammatory The various ocular inflammatory or infectious disorder. Symptoms of scleritis conditions have been effectively treated with anti- include red eye, blurred vision, eye discomfort, eye inflammatory drugs like corticosteroids and non pain, red patches on the whites of the eyes, tearing steroidal anti-inflammatory (NSAIDs). of the eye, and photophobia. It is further divided into epicscleritis, anterior Scleritis (diffuse, nodular Corticosteroids and necrotizing with/without inflammation) and Corticosteroids are one of the important posterior scleritis [9]. therapeutics for inflammation suppression though possess serious side effects like alteration of lipid, 2.4. Uveal tract protein and carbohydrate metabolism and other Uveal tissue constitutes middle vascular enzymatic reactions, susceptibility to infection, coat of the eyeball and divided into iris, ciliary hypertension, muscle weakness. Hence, use of body and choroid. Uvea provides nutrition to steroid is indicated for short term treatment only various part of eye such as cornea, lens, retina, and and for specific inflammatory process [13]. In vitreous. Symptoms of uveitis (uveal inflammation) market various corticosteroids such as cortisone include light sensitivity, pain, blurring of vision acetate (0.5% suspension and 1.5% ointment), and redness. The major inflammations are anterior hydrocortisone (0.5% suspension and 0.2% uveitis (inflammation of the iris alone), solution), dexamethasone sodium phosphate (0.1% intermediate uvietis (Ciliary body), posterior solution and 0.5% ointment), medrysone (1% uveitis (Choroid) and it may be diffuse involving suspension) etc. are available [14]. However, all parts of uvea (panuveitis/endophthalmitis). administration of these steroids for therapy of Additionally there is degeneration of iris and ocular inflammation usually associated with choroid with some tumors of choroid, ciliary body various adverse effects. Ocular side effects of and iris [10]. steroid therapy are generally observed with its systemic administration. For example, subcapsular 2.5. Retina cataracts and papilledema occured after prolonged Cystoid macular edema (CME) is a systemic administration of prednisolone and painless condition affecting macula (central retina). triamcinolone respectively [13]. Apart from systemic This condition is characterized by multiple cyst like administration, topical delivery of steroids too areas of fluid that appears in the macula leading to affect eye adversely. Incidence of keratitis 75 (bacterial, fungal and/or viral) was observed with over corticosteroids, still posses certain side effects the use of topical or sub-conjunctival like blurred vision, dry eye, diplopia, retinopathy corticosteroids. Similarly, galucoma, pupil dilation, etc (Table I) [22-30]. These could be attributed to blurred vision, occasional refractive changes, lens their low solubility which makes them difficult to opacities, and ptosis were noted following topical dispense in aqueous solution. However various corticosteroid administration. In few cases, relapse formulation technologies such as solubilization, of ocular inflammation was observed on rapid or cyclodextrin complexation, nanoemulsion, abrupt discontinuation of topical ocular steroid use. liposomes, niosomes, ocular inserts, hydrogels etc. These side effects often become prominent on have been emerged as a solution for such prolonged administration but could be avoided with difficulties. short-term use (less than 3-4 weeks) [13-15]. 3. NSAIDs Non-steroidal anti-inflammatory drugs For management of ocular inflammatory 3.1. Ophthalmic indications conditions, NSAIDs are preferred over NSAIDs act by irreversibly blocking cyclo- corticosteroids due to improved safety profile as oxygenage (COX) enzyme. COX enzyme is they are deprived of steroid related adverse affects essential for the synthesis of prostaglandin [6, 16-19]. Moreover, these anti-inflammatory drugs (conversion of arachidonic acid to prostaglandins). are imperative in pre and post operative Additionally they also block lysosomal enzymes, inflammation. [20-21]. Though NSAIDs have an edge TABLE I Characteristics of various NSAIDs with topical side effects [22-30] NSAID Solubility Protein Topical side effects Novel systems improving drug binding (%) characteristics Aspirin 1.46 1.43 80 Periorbital angioedema Iontophoresis, Polymeric nanoparticle Indomethacin 0.0024 3.4 97 Stromal opacities, Polymeric nanoparticle, hydrogel Retinopathy inserts, microemulsion Ibuprofen 0.0068 3.5 99 Blurred vision, Nanostuctured lipid carrier, Polymric diplopia, dry eye nanosuspension Naproxen 0.05 3.29 99 Intracranial Bioerodible implant, polymeric hypertension nanoparticle Ketoprofen 0.02 3.29 99 Blurred vision Sloid lipid nanoparticles Flurbiprofen 0.025 3.57 99 Exacerbated ocular Nanoemulsion, polymeric tissue bleeding nanosuspension Diclofenac 0.0045 4.98 99 Corneal erosion Polymeric nanoparticle, Solid lipid nanoparticle Piroxicam 0.06 1.81 99 Eye pain, blurred Microsphere, nanosuspension vision Ketorolac 0.051 2.66 99 Transient stinging and In-situ gel, hydrogel inserts, burning polymeric suspension & micelles Nimesulide 0.019 2.56 >90 Transient ocular Polymeric nanoparticle irritation Meloxicam 0.016 2.15 99.4 Corneal opacification Thermogel Celecoxib 0.005 3.99 97 Corneal opacification Polymeric microsphere Aceclofenac 0.015 2.17 99 Transient stinging and Polymeric insert & polymeric burning nanoparticle
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