1992 Archives of Ophthalmology
doi: 10.1001/archopht.1992.01080230004001
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1992 Archives of Ophthalmology
doi: 10.1001/archopht.1992.01080230015003
Abstract In Reply. —Dr Trempe seems unaware of a number of other clinical studies that have been published, at least in the popular press.1 He exaggerates by calling 200 mg of zinc acetate "toxic." Not only did we not see evidence of toxic effects in our study, but also some physicians have given similar amounts to patients for many years without evidence of "toxicity."2 Zinc sulfate is an emetic, and it is unlikely that one could ingest a truly toxic dose repeatedly. To have megaloblastic anemia, large amounts of zinc have to be ingested and retained by a patient.3Although some of the subjects in the serum ceruloplasmin study4 later participated in our clinical trial, no subject was known to be taking "large amounts of zinc" when the serum samples that we studied were obtained. References 1. Bruce RA Jr, Faulkner GD, Pomerance GN, et al. Nutritional compliance and macular degeneration: is it an untreatable disease? Ocular Surg News . 1991;9( (suppl) ):1-14. 2. Yuzbasizan-Gurkan V, Brewer GJ. The therapeutic use of zinc in macular degeneration . Arch Ophthalmol . 1989;107:1723.Crossref 3. Broun ER, Greist A, Tricot G, Hoffman R. Excessive zinc ingestion: a reversible cause of sideroblastic anemia and bone marrow depression . JAMA . 1990;264:1441-1443.Crossref 4. Newsome DA, Swartz M, Leone NC, Hewitt AT, Wolford F, Miller ED. Macular degeneration and elevated serum ceruloplasmin . Invest Ophthalmol Vis Sci . 1986;27:1675-1680.
1992 Archives of Ophthalmology
doi: 10.1001/archopht.1992.01080230015002pmid: 1444901
Abstract To the Editor. —During the past year, ophthalmologists have been subjected to an extensive publicity campaign regarding the role of micronutrients, especially zinc supplementation in the treatment of macular degeneration. The article by Newsome et al1 in the February 1988 issue of the Archives is often quoted to substantiate this advertising. In the study done by the authors, 200 mg of zinc was given daily to patients with macular degeneration. This is a toxic amount of zinc that can produce serious complications. The recommended daily allowance is 15 mg. When more than 150 mg of zinc is taken, it can produce serious copper deficiency, sideroblastic anemia, and bone marrow depression.2 Such patients must often undergo costly and unpleasant tests, such as bone marrow biopsy, to determine the cause of the anemia. It is important for clinicians to be aware of this possible complication when prescribing large amounts of References 1. Newsome DA, Swartz M, Leone ND, Elston RC, Miller E. Oral zinc in macular degeneration . Arch Ophthalmol . 1988;106:192-198.Crossref 2. Brown ER, Griest A, Tricot G, Hoffman R. Excessive zinc ingestion: a reversible cause of sideroblastic anemia and bone marrow depression . JAMA . 1990;264:1441-1443.Crossref 3. Sues FE, Klaus U. Aspects epidemiologique de la degenerescence maculaire liee a l'age . Ophthalmologie . 1992;6:3-7.
Stark, Walter J.;Stulting, R. Doyle;Maguire, Maureen G.
1992 Archives of Ophthalmology
doi: 10.1001/archopht.1992.01080230015005
Abstract In Reply. —Dr Sugar appropriately emphasizes a point that we made in the "Comment" section of our article. We also mentioned two additional factors that may have contributed to the relatively high success rate for penetrating keratoplasty in the CCTS: a vigorous educational program to assure medication compliance, and frequent, regular follow-up examinations by the transplanting surgeon. The CCTS patients were outstanding in that only 4% of all visits were missed and only 1% of patients were considered unavailable for follow-up.When we formulated the protocol for the CCTS, we were aware that high doses of postoperative steroids could mask any effect of HLA matching on corneal transplant survival. However, our goal was not to design a study that would maximize the likelihood of observing a beneficial HLA matching. Instead, we sought to determine whether HLA matching would improve graft survival when used in addition to the postoperative immunosuppressive regimen References 1. Rinne JR, Stulting RD. Current practices in the prevention and treatment of corneal graft rejection . Cornea . 1992;11:326.Crossref
1992 Archives of Ophthalmology
doi: 10.1001/archopht.1992.01080230015004pmid: 1444902
Abstract To the Editor. —The results of the Collaborative Corneal Transplantation Studies (CCTS)1 provide exciting and important information that may run counter to the expectations of many. It is important, as the authors point out, to note that the use of topical corticosteroids in the study was significantly more intensive than use both by many corneal surgeons and in prior similar studies. An important conclusion from their study may well be that patients receiving high-risk corneal transplants warrant more intensive topical corticosteroid use. This intensive use of topical corticosteroids may have overwhelmed any potential beneficial effect of HLA-A, -B, and -DR matching. While all of this was well stated in the article, the casual reader reviewing only the abstract may have missed this important point. References 1. The Collaborative Corneal Transplantation Studies Research Group. The Collaborative Corneal Transplantation Studies (CCTS): effectiveness of histocompatibility matching in high-risk corneal transplantation . Arch Ophthalmol . 1992;110:1392-1403.Crossref
Avery, Robert L.;Hickingbotham, Dyson;Jaffe, Glenn;de Juan, Eugene
1992 Archives of Ophthalmology
doi: 10.1001/archopht.1992.01080230016006pmid: 1280092
Abstract To the Editor. —Recent advances in surgical techniques have made the removal of subretinal membranes and hemorrhages possible.1,2 Although preoperative fluorescein angiography is extremely useful in these cases, intraoperative fluorescein angioscopy can also be very helpful. Large subretinal hemorrhages often preoperatively obscure the source of fluorescein leakage; however, intraoperative angioscopy can be performed immediately after removal of the hemorrhage, to identify choroidal neovascularization and to allow immediate endolaser treatment. We have adapted excitation and barrier filters, made for a fluorescein angiography camera, to fit into an endoilluminator and an operating microscope, respectively. The excitation filter (Spectrotech, Saugus, Mass) is placed into the sliding tray (Fig 1, arrowheads) of a light source. When the fundus is illuminated with the filtered blue light, the fluorescein appears yellow-green. This system is similar to the one described by Charles3 that identifies sources of bleeding during vitrectomy; however, we have greatly enhanced the References 1. de Juan E Jr, Machemer R. Vitreous surgery for hemorrhagic and fibrous complications of age-related macular degeneration . Am J Ophthalmol . 1988;105:25-29. 2. Thomas MA, Kaplan HJ. Surgical removal of subretinal neovascularization in the presumed ocular histoplasmosis syndrome . Am J Ophthalmol . 1991;111:1-7. 3. Charles S. Vitreous Microsurgery . Baltimore, Md: Williams & Wilkins; 1981:89-90.
Garcia-Ferrer, Francisco J.;Murray, Patrick R.;Pepose, Jay S.
1992 Archives of Ophthalmology
doi: 10.1001/archopht.1992.01080230017007pmid: 1444903
Abstract To the Editor. —Bacterial endophthalmitis is a dreaded and often visually devastating complication of penetrating keratoplasty. Current methods to achieve antisepsis of donor corneal tissue, such as the addition of gentamicin to the corneal storage media, have had a suboptimal effect. At the storage temperature of 4°C gentamicin provides only limited coverage against gram-positive bacteria, such as Streptococcus pneumoniae.1 In comparison with antibiotics, povidoneiodine is a broad-spectrum disinfectant with rapid activity against bacteria, fungi, viruses, protozoa, and spores.2 We therefore chose to investigate the antimicrobial spectrum and corneal endothelial toxicity of povidone-iodine in DexSol corneal storage medium (Chiron, Irvine, Calif).The corneal endothelial toxicity of DexSol supplemented with gentamicin (100 μg/mL) was compared with that of DexSol supplemented with either 5%, 1%, or 0.1% povidoneiodine without gentamicin using paired human donor corneas. For each corneal pair, one cornea was placed in standard DexSol with gentamicin, and the other References 1. Garcia-Ferrer FJ, Pepose JS, Murray PR, Glaser SR, Lass JH, Green WR. Antimicrobial efficacy and corneal endothelial toxicity of DexSol corneal storage medium supplemented with vancomycin . Ophthalmology . 1991;98:863-869.Crossref 2. Zamora JL. Chemical and microbiologic characteristics and toxicity of povidone-iodine solutions . Am J Surg . 1986;151:400-406.Crossref 3. Singh G, Bohnke M, von-Domarus D, Draeger J, Lindstrom RL, Doughman DJ. Vital staining of corneal endothelium . Cornea . 1985/1986;4:80-91.Crossref 4. Hord D, Ditter W. Physical-chemical fundamentals of the microbicidal action of povidone-iodine . In: Degenes G, ed. Proceedings of the International Symposium on Povidone . Lexington: University of Kentucky; 1983:120-140. 5. Woodward FE, Hudson A. Reactions of povidone and iodine: changes in active iodine species with dilution in water . In: Degenes G, ed. Proceedings of the International Symposium on Povidone . Lexington: University of Kentucky; 1983:178-185.
1992 Archives of Ophthalmology
doi: 10.1001/archopht.1992.01080230027008pmid: 1444904
Abstract A 54-year-old man with −10.00 to −11.00 diopters (D) of myopia in both eyes underwent uncomplicated radial keratotomy (RK) in his left eye in December 1986 and in his right eye in May 1987. Within several months after the second RK he experienced gradually declining visual acuity. The patient was treated with topical steroids with no effect. Within 18 months after surgery his condition had stabilized. Report of a Case. —We first examined the patient 38 months after the second RK. Best corrected visual acuity was 20/30+ OD with −3.00 sphere and 20/60− OS with −2.00 sphere. No decrease in visual acuity was noted in bright light. Keratometry measured 38.50/39.50 at 170 OD and 38.25/38.62 at 180 OS with mild distortion in both eyes. Biomicroscopy revealed bilateral eight-incision RK with 2-mm central clear zones. Incisions did not extend into the central optical zones. Mild superficial peripheral corneal vascularization was References 1. Waring GO, Lynn MJ, Nizam A, et al. Results of the prospective evaluation of radial keratotomy (PERK) study five years after surgery . Ophthalmology . 1991;98:1164-1176.Crossref 2. Nirankari VS, Katzen LE, Richards RD, Karesh JW, Lakhanpal V, Billings E. Prospective clinical study of radial keratotomy . Ophthalmology . 1982;89:677-683.Crossref 3. Bechara SJ, Grossniklaus HE, Waring GO. Subepithelial fibrosis after myopic epikeratoplasty . Arch Ophthalmol . 1992;110:228-232.Crossref
Bechara, Samir J.;Grossniklaus, Hans E.;Waring, George O.
1992 Archives of Ophthalmology
doi: 10.1001/archopht.1992.01080230028009pmid: 1444905
Abstract A variety of postoperative complications can occur after epikeratoplasty. Poor reepithelization of the lenticule surface has been a major clinical problem and may lead to aseptic stromal necrosis (corneal melting). We describe a patient who received a nonfreeze epikeratoplasty followed by aseptic necrosis of the lenticule in the absence of a preexisting epithelial defect. Report of a Case. —A 70-year-old man was referred to the Emory Eye Center, Atlanta, Ga, in September 1989 for evaluation of his left eye, which had undergone extracapsular cataract extraction with an intraocular lens implant in 1982. The intraocular lens had been removed in 1984 because of inflammation and dislocation. The patient had previously undergone panretinal photocoagulation for diabetic retinopathy. His best spectacle-corrected visual acuity was 20/25 OD and 20/400 OS. Since he was intolerant of contact lenses, a nonfreeze, aphakic epikeratoplasty was performed on the patient's left eye.Two weeks after the procedure the References 1. Frangieh GT, Kenyon KR, Wagoner MD, Hanninen L, John T, Steinert RF. Epithelial abnormalities and sterile ulceration of epikeratoplasty grafts . Ophthalmology . 1988;95:213-227.Crossref 2. Binder PS, Zavala EY. Why do some epikeratoplasties fail? Arch Ophthalmol . 1987;105:63-69.Crossref 3. Pepose JS, Benevento WJ. Detection of HLA antigens in human epikeratoplasty lenticules . Cornea . 1991;10:105-109.Crossref
Kok, Jan H. C.;Dunnebier, Erwin A.;Nieuwendaal, Carla P.;Kijlstra, Aize
1992 Archives of Ophthalmology
doi: 10.1001/archopht.1992.01080230029010pmid: 1444906
Abstract Because the corneal endothelium is the primary site for the metabolic pump that maintains corneal deturgescence, any change in the morphologic characteristics of endothelial cells is of considerable interest. It has been suggested that the functional reserve of the endothelium may be compromised with more severe cases of polymegethism. Adverse effects of contact lens wear on physiologic features of the cornea were recently emphasized by the discovery that polymegethism and pleomorphism occurred with contact lens wear.1 These changes could be ascribed to oxygen shortage, carbon dioxide buildup, and pH changes under the lens.1 The same phenomena could be induced in the corneal endothelium of patients suffering from long-standing ptosis, which results in a decreased oxygen tension of approximately one third of the oxygen available under open-eye conditions.2 Report of a Case. —We report the case of an 85-year-old woman with ptosis of the left eye for more than References 1. Bruce AS, Brennan NA. Corneal pathophysiology with contact lens wear . Surv Ophthalmol . 1990;35:25-58.Crossref 2. Schoessler JP, Orsborn GN. A theory of corneal endothelial polymegathism and aging . Curr Eye Res . 1987;6:301-306.Crossref 3. Nieuwendaal CP, Kok JHC, de Moor EAM, Oosting J, Venema HW. Corneal endothelial cell morphology under permanent wear of contact lenses . Int Ophthalmol . 1991;15:313-319.Crossref
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