Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism of uveitis following cataract surgery, which is mediated in part by the cyclooxygenase pathway, is complex, the complexity of which is likely to be due to several factors. We investigated the possible local involvement of interleukin 6 (IL-6) in this response. Using a specific bioassay, we showed a dramatic increase of IL-6 levels (> 4 x 10(3) times) in all of the aqueous humors of 12 patients following cataract surgery. The IL-6 levels in serum samples were below detection limits, indicating a local production of this cytokine. In addition, the injection of highly purified recombinant interleukin 6 in the anterior chamber of the eye in rabbits resulted in an inflammatory response. These observations suggest that IL-6 may play a crucial role in the occurrence of inflammation after cataract surgery, and it may lead to new therapeutic approaches to this problem.
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PMID:Role of interleukin 6 in the inflammatory response after cataract surgery. An experimental and clinical study. 184 75

Ocular tissues, like those of other organs, exhibit limited morphologic reactions to trauma, i.e., hyperemia, abrupt vasodilation, increased blood flow; increased permeability of blood vessels, edema and increased tissue pressure (disrupted blood-ocular barrier); and later, a cellular inflammatory response. The cystoid macular edema (CME) that occurs after surgery for cataract has a considerably higher incidence in more severely traumatized eyes. It is characterized by increased perifoveal capillary permeability that may be related either to prior vasoconstriction or to vasodilation, and it may be accompanied by a cellular inflammatory response either in the (uvea) ciliary body, vitreous, or retina, or in combination thereof. Virtually all the physiologic, metabolic, and morphologic responses to trauma can be assigned to liberation of endogenous mediators. The lesions that occur after ocular trauma may be related to the synthesis and release of prostaglandins. There is moderate support for this hypothesis, but other or additional endogenous mediators must also be considered as contributing to the production of retinal edema as a nociceptive response to trauma. The various factors that may contribute to development of CME, and their mechanisms of action, are discussed. The speculations and hypotheses contained in this review need to be confirmed or denied by applications to the eye of techniques that have been used successfully in other organ systems. Adequate prophylaxis may be provided by cyclooxygenase inhibitors, but it is more likely accomplished with corticosteroids. However, definitive clinical tests have not been done, and it should be noted that excellent surgery with minimal disruption of the blood-ocular barrier is the best prophylaxis for this iatrogenic disease. When the lesion is established and does not respond to large doses of corticosteroids, a careful study is needed to decide whether vitreous inflammation and/or strand formation accounts for the irreversibility.
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PMID:Aphakic cystoid macular edema. The pharmacology of ocular trauma. 637 50

Lens cells can synthesize, degrade, and remodel lipids. Endogenous lipid synthesis, in conjunction with uptake of exogenous cholesterol and certain fatty acids, leads to the formation of a plasma membrane that is especially rich in sphingomyelin, cholesterol, and long-chain saturated fatty acids. As a result of this unusual lipid composition, lens membranes have very low fluidity, which is restricted even further by lipid-protein interactions. The composition and metabolism of membrane lipids may affect the formation of various types of cataracts. Diets rich in vegetable oils offer some protection against the formation of osmotic cataracts and the hereditary cataract of the RCS rat, although the mechanism of this effect is not clear. Vitamin E also protects against the formation of several types of cataract in vivo and in vitro, suggesting that lipid peroxidation may play a role in cataractogenesis. Certain drugs which inhibit lipid synthesis or degradation are cataractogenic, and a deficiency in cataractogenic, and a deficiency in phosphatidylserine is associated with a loss of Na+/K+ ATPase activity in several types of cataract. Human senile cataracts show a marked loss of protein-lipid interactions, although the overall lipid composition is normal. This loss of protein-lipid interactions may be related to oxidative damage to membrane-associated proteins. Interestingly, the decrease in the fluidity of lens membranes with age would counteract the formation of aqueous pores in the membrane, which can result from the oxidative cross-linking of membrane-associated proteins. Certain pathways of lipid metabolism seem to have regulatory functions. Among these are phosphatidylinositol turnover, phosphatidylethanolamine methylation, and arachidonic acid metabolism. All of these pathways function in the lens. Phosphatidylinositol turnover is correlated with the rate of lens epithelial cell division, while phosphatidylethanolamine methylation seems to be related to the initiation of lens fiber cell formation. Both pathways are associated with the release and metabolism of arachidonic acid in other cell types. While it is not known whether phosphatidylinositol turnover or phosphatidylethanolamine methylation result in the release of arachidonic acid in the lens, recent work has shown that lens cells from a variety of species can metabolize arachidonic acid by both the cyclooxygenase and lipoxygenase pathways. The possible physiological significance of these metabolites to the lens is yet to be determined.
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PMID:Lens lipids. 639 28

Proliferative vitreoretinopathy is a severe reactive process which leads to the formation of cellular membranes on the surface of the retina and in the vitreous. We determined the fibroblast growth-promoting activity of intraocular fluid from patients suffering from proliferative vitreoretinopathy, retinal detachment or cataract and further evaluated the effect of acetylsalicylic acid on growth-stimulated fibroblasts. The results demonstrated a significant enhancement of growth-promoting activity of intraocular fluid in proliferative vitreoretinopathy as compared to that of control samples. We showed that the augmented growth-promoting activity of intraocular fluid in proliferative vitreoretinopathy was significantly antagonized by inhibition of cyclooxygenase with acetylsalicylic acid (ID50 approximately 5 microM). In contrast, no significant effect was seen in corresponding control experiments. The findings suggest that metabolites of the cyclooxygenase pathway are involved in the regulation of enhanced intraocular fluid-induced fibroblast proliferation in proliferative vitreoretinopathy and that acetylsalicylic acid might be useful as an antiproliferative agent in intraocular fibrogenesis.
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PMID:Fibroblast growth-promoting activity in proliferative vitreoretinopathy: antagonism by acetylsalicylic acid. 781 91

In a prospective, randomized, double-blind study the effect of different anti-inflammatories (diclofenac 0.1%, flurbiprofen 0.03%) versus placebo on the intra- and postoperative inflammation in 65 eyes was examined. Prednisolone acetate 0.5% eye drops were the basic therapy in all three groups. As criteria served the difference between pre- and postoperative flare and cell concentration in the anterior chamber, measured using the laser flare cell meter, the clinical course, and the level of the inflammatory mediator 6-oxo-PGF1 alpha (prostacyclin) in the aqueous humor after intraoperative paracentesis, determined by means of enzyme-linked immunosorbent assay. The level of prostacyclin was not influenced in any of the three groups. The numbers of cells decreased continuously, but without marked differences among the groups. On the basis of the concentration of protein measured in the aqueous humor and the clinical course, diclofenac 0.1% proved to be a more potent additive anti-inflammatory therapy than flurbiprofen 0.03% immediately after the surgical procedure (P = 0.039 at 1 day after operation), but the final results (4 weeks after operation) revealed no detectable difference. By application of placebo, an obvious higher concentration of protein was measured during all the observations (P = 0.0002). Therefore in the case of cataract extraction the local steroidal therapy should be combined with nonsteroidal anti-inflammatory drugs (cyclooxygenase inhibitors).
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PMID:[Effect of diclofenac and flurbiprofen on the course of inflammation after cataract extraction]. 795 Jan 19

Recent clinical studies indicate that flurbiprofen, a cyclooxygenase inhibitor, prevents miosis and breakdown of the blood-aqueous barrier during cataract surgery. Yet based on clinical and experimental data, some researchers do not agree that flurbiprofen prevents miosis. We conducted a double-blind clinical study of the effects of topical 0.03% flurbiprofen sodium on intraoperative pupillary diameter and iris fluorescein leakage after extracapsular cataract surgery. In the first phase of the study, 120 patients who had extracapsular cataract extraction with posterior chamber intraocular lens implantation were randomly assigned to receive preoperative topical flurbiprofen or a placebo, with or without intraoperative epinephrine, in addition to the standard regimen. In the second phase, 60 of the 120 patients continued the topical flurbiprofen or placebo for one month postoperatively. Iris fluorescein angiography was performed at the end of the first and the fourth weeks. The results indicate that flurbiprofen was significantly more effective (P < .0001) in maintaining mydriasis during surgery than the placebo. This action was enhanced by intraoperative epinephrine. Flurbiprofen also significantly reduced (P < .001) postoperative iris fluorescein leakage.
J Cataract Refract Surg 1993 Sep
PMID:Topical flurbiprofen in extracapsular cataract surgery: effect on pupillary diameter and iris fluorescein leakage. 822 20

This 6-week, partially masked, three-arm, multicenter study was conducted to evaluate the postoperative anti-inflammatory efficacy of ketorolac, a cyclooxygenase inhibitor. The study setting was the clinical practice of six ophthalmic surgeons. The study enrolled 157 candidates for routine extracapsular cataract extraction or phaco-emulsification and posterior-chamber intraocular lens implantation. Patients who received any glucocorticoid or cyclooxygenase inhibitor within 1 week of surgery were excluded. All patients were treated with solutions of 0.5% ketorolac, 1% prednisolone acetate, or 0.1% dexamethasone instilled into the operative eye three times daily from 1 day before surgery to 4 weeks after surgery. Efficacy variables included the signs of anterior-segment inflammation, primarily cells and flare in the anterior chamber, as observed by slit-lamp biomicroscopy; fluorescein leakage across the blood-aqueous barrier as measured by fluorophotometry; and the rating of efficacy by the investigator. No significant differences were seen between ketorolac and either glucocorticoid in cells and flare. No significant differences were found in other signs of inflammation, except conjunctival hyperemia and Descemet's folds at week 2. Ketorolac showed significantly greater efficacy than the glucocorticoids against blood-aqueous barrier breakdown at day 5 and week 2, as demonstrated by the difference in fluorescein concentration between the operated and nonoperated eyes. Investigators did not detect any significant difference in rating for overall effectiveness and acceptability. These findings support the use of ketorolac as an alternative to glucocorticoids for the treatment of postoperative inflammation.
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PMID:Ketorolac, prednisolone, and dexamethasone for postoperative inflammation. 915 65

has been described in humans and many animal species. Traumatic rupture of the lens capsule may result in vision-threatening intraocular inflammation that is poorly responsive to medical management. Phthisis bulbi, persistent uveitis or glaucoma often occurs in these eyes. Surgical removal of the lens material is generally indicated shortly after the injury in an effort to preserve vision. Leaking of lens proteins through an intact lens capsule may result in a lympho-plasmacytic anterior uveitis. This is most commonly associated with the presence of a hypermature cataract. The presence of lens-induced uveitis prior to cataract surgery significantly reduces the success rate of cataract surgery. Small amounts of circulating lens proteins maintain a normal T-cell tolerance for lens proteins. Lens-induced uveitis develops when a breakdown occurs of this normal T-cell tolerance. Immune complexes play an important role in the tissue damage associated with the ensuing inflammation. Other factors associated with the tissue damage include hydroxyl radicals, nitroxide radicals, and hydrogen peroxide and arachidonic acid metabolites. Treatment consists of topical and systemic anti-inflammatory medications, mydriatic agents, and glaucoma medications when indicated. Experimental pharmacological agents include dual cyclooxygenase/lipoxygenase inhibitors, interleukin-1 blockers, antioxidants and hydroxyl radical scavengers.
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PMID:Lens-induced uveitis. 1139 8

Topically applied nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used in the management and prevention of ocular inflammation and cystoid macular edema related to cataract surgery and the maintenance of mydriasis during cataract surgery. Other common uses are the reduction of discomfort after refractive surgery or in allergic conjunctivitis. NSAIDs primarily act as cyclooxygenase inhibitors and thus reduce the formation of endogenous PGs. Today, several NSAIDs are commercially available: diclofenac, flurbiprofen, indomethacin, ketorolac and suprofen. At present the ophthalmologist has to make a decision between the use of topical corticosteroids, with their potential adverse effects, or of topical NSAIDs, with their possibly increased benefit, unknown effect on ocular pressure, wound healing and corneal tissue, higher costs and limited track record. However, the improvement of surgical techniques might support an increasing use of NSAIDs in the future. Preoperative anti-inflammatory treatment should be considered in eyes at a higher risk of developing severe postoperative inflammatory reactions. This decision has to be made carefully and has to be guided by the clinical circumstances, the spectrum of diagnosis and the individual benefit-risk ratio of each patient.
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PMID:Topical nonsteroidal anti-inflammatory therapy in ophthalmology. 1259 44

Ophthalmic bromfenac sodium sesquihydrate is a topically applied selective cyclooxygenase (COX)-2 inhibitor. It is similar to amfenac, except for a bromine atom at the C(4) of the benzoyl ring position, which markedly affects its in vitro and in vivo potency, extends the duration of anti-inflammatory activity, and enhances its inhibitory effect on COX-2 absorption across the cornea and penetration into ocular tissues. The United States Food and Drug Administration approved bromfenac in 2005 for the treatment of postoperative inflammation and the reduction of ocular pain in patients who have undergone cataract surgery. Nonsteroidal anti-inflammatory drugs (NSAIDs), and among them bromfenac, could be even more effective than steroids at reestablishing the blood-aqueous barrier, as revealed by flare on slit-lamp examination and as quantitatively measured using ocular fluorophotometry. Similar to other NSAIDs, it has a role in inhibiting intraoperative miosis during cataract surgery. However, bromfenac also seems to be useful in other situations, such as refractive surgery, allergic conjunctivitis (not useful in dry eye), choroidal neovascularization, and even ocular oncology. No reports of systemic toxicity have been published and bromfenac has good topical tolerance with a low incidence of adverse effects.
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PMID:Update on twice-daily bromfenac sodium sesquihydrate to treat postoperative ocular inflammation following cataract extraction. 2257 May 44


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