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)

Since the start of photorefractive keratectomy (PRK) Seiler has recommended the use of topical corticosteroids during the first 3 months after surgery. The rationale for this treatment was to diminish the inflammatory reaction as well as to control the keratocytes from producing collagen and creating scars. Our knowledge of corneal wound healing in general, and after PRK in particular, is very limited and the action of corticosteroids is still unclear. Corticosteroids, when given in comparatively large topical doses, create problems. Between 15 and 30% of patients are corticosteroid responders with increased intraocular pressure. This is a threat to the eye, and also a burden for the doctor as intraocular pressure has to be checked during the treatment. The risk for cataract formation after longer periods of topically administered corticosteroids also has been discussed. In order to decrease the rise in intraocular pressure, FML has been used in place of dexamethasone. During the 4 years follow up after PRK it has been reported that a number of patients do not regress or get a scar formation if they have not used corticosteroids in the postoperative period. The reasons to avoid topical corticosteroids in some patients are a misunderstanding of their instructions, or those who have had a history of herpes infection or glaucoma. A double-masked study of the effects of corticosteroids after PRK was performed by Gartry, et al in a small group of patients. After 6 months, the results revealed that there were no differences between the corticosteroid and the non-corticosteroid group. However, the standard deviation was high.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of corticosteroids in postoperative care following photorefractive keratectomies. 849 81

We performed this prospective, randomised, investigator-masked, parallel-group study to compare Fluorometholone-Gentamicin eye drops with Maxitrol (dexamethasone, neomycin, polymyxin B) eye drops in the reduction of ocular bacterial flora and control of ocular inflammation after cataract surgery. One hundred and twelve (FML-Genta 54, Maxitrol 58) patients of both sexes undergoing cataract and posterior chamber lens implant surgery for visually disabling cataract were enrolled in the study and examined pre-operatively and post-operatively on days 1, 6-8 and 24-34. The baseline parameters were similar in the two study groups. The conjunctival bacterial colony count on day 6-8 post-operatively was significantly less on FML-Genta compared with Maxitrol (p = 0.033). There was no statistically significant difference between the two treatments in the degree of intra-ocular inflammation as assessed by flare and cells in the anterior chamber. Both treatments were judged to be equal in the global assessment of the success of therapy and local tolerance by the study patients and doctors. Fluorometholone-gentamicin eye drops were more effective than Maxitrol eye drops in the reduction of ocular bacterial flora while being as well-tolerated and as effective as Maxitrol in the control of ocular inflammation after cataract surgery.
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PMID:A comparison of two ophthalmic steroid-antibiotic combinations after cataract surgery. 924 17

The prevailing view regarding the mechanism of steroid cataract formation holds that glucocorticoids are covalently bound to lens proteins resulting in destabilization of the protein structure allowing further modification (i.e. oxidation) leading to cataract. Alternative hypotheses (e.g. that cataracts result from glucocorticoid receptor mediated effects) have been difficult to test since protein binding does in fact occur for many cataractogenic steroids. A glucocorticoid lacking the typical glucocorticoid hydroxy group at C21 (fluorometholone, FML), other steroids which can bind to proteins but lack glucocorticoid activity, and a glucocorticoid antagonist (RU486) have been utilized to discriminate between these two hypotheses. Purified bovine beta-crystallin incubated with three different 3H-steroids, dexamethasone (Dex), aldosterone or progesterone demonstrated that the C-21 hydroxyl group is not essential for steroid binding. Progesterone (with no C-21 OH) bound to the greatest extent. Pretreatment of the protein with aspirin to acetylate the free protein amino groups blocked this binding, demonstrating the probability of a Schiff base mechanism. Lens culture studies with the same three radiolabeled steroids demonstrated much the same result. Rat lenses cultured for 48 hr-11 days, demonstrated that loss of GSH is an early and significant effect of several glucocorticoids (Dex, prednisolone and FML) but is not seen with other non-glucocorticoid steroids. However, none of the steroids tested consistently produced lenticular opacification (i.e. cataracts) in this in vitro system, nor did they alter rubidium transport. We suggest that a mechanism other than covalent binding of steroids to lens proteins is responsible for glucocorticoid induced cataracts because: (1) non-glucocorticoids were demonstrated to bind lens proteins as well or better than the glucocorticoid Dex and (2) only glucocorticoids, and not other steroids, lowered lens reduced glutathione content which has been demonstrated to be associated with other forms of cataract.
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PMID:Steroid-induced cataract: new perspective from in vitro and lens culture studies. 946 84