Parapapillary Chorioretinal Atrophy in Patients With Ocular Hypertension: I. An Evaluation as a Predictive Factor for the Development of Glaucomatous DamageTezel, Gülgün;Kolker, Allan E.;Kass, Michael A.;Wax, Martin B.;Gordon, Mae;Siegmund, Kimberly D.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160673001pmid: 9400782
Abstract Objective: To determine whether parapapillary chorioretinal atrophy is a risk factor for the development of glaucomatous optic disc or visual field damage. Methods: The initial morphometric parameters of the optic disc and parapapillary atrophy were retrospectively investigated in 350 eyes of 175 patients with ocular hypertension. The prognostic value of parapapillary atrophy at the baseline examination and its relationship with known risk factors for the development of glaucomatous damage were analyzed by multivariate analysis. Results: Visual field loss, optic disc damage, or both were detected in 98 eyes of 53 patients during the follow-up period of at least 10 years. By univariate analysis, the presence of parapapillary atrophy, as well as higher parapapillary atrophy area—disc area, zone β area—disc area, and parapapillary atrophy length—disc circumference ratios, at the baseline examination was associated with the conversion to glaucoma. In addition, higher intraocular pressure, larger vertical cupdisc ratio, and smaller neural rim area—disc area ratio at the baseline examination were associated with subsequent glaucomatous optic nerve damage. In a multivariate regression model adjusted for other factors, intraocular pressure (relative risk, 1.19), neural rim area—disc area ratio (relative risk, 0.72), and zone β area—disc area ratio (relative risk, 1.32) were found to be associated with the development of optic disc damage, visual field damage, or both. Conclusion: The presence and the size of parapapillary atrophy are related to the development of subsequent optic disc or visual field damage in patients with ocular hypertension. References 1. Von Graefe A. Uber die Iridectomie bei Glaucom und über den Glaucomatösen Prozess . Graefes Arch Clin Exp Ophthalmol . 1857;3:456-465.Crossref 2. Fantes FE, Anderson DR. Clinical histologic correlation of human peripapillary anatomy . Ophthalmology . 1989;96:20-25.Crossref 3. Hayreh SS. Blood supply of the optic nerve head and its role in optic atrophy, glaucoma and oedema of the optic disc . Br J Ophthalmol . 1969;53:721-748.Crossref 4. Primrose J. Early signs of the glaucomatous disc . Br J Ophthalmol . 1971;55:820-825.Crossref 5. Wilensky JT, Kolker AE. Peripapillary changes in glaucoma . Am J Ophthalmol . 1976;81:341-345. 6. Heijl A, Samander C. Peripapillary atrophy and glaucomatous visual field defects . Doc Ophthalmol Proc Ser . 1985;42:403-407. 7. Nevarez J, Rockwood EJ, Anderson DR. The configuration of peripapillary tissue in unilateral glaucoma . Arch Ophthalmol . 1988;106:901-903.Crossref 8. Buus DR, Anderson DR. Peripapillary crescent and halos in normal-tension glaucoma and ocular hypertension . Ophthalmology . 1989;96:16-19.Crossref 9. Jonas JB, Nguyen XN, Gusek GC, Nauman GOH. Parapapillary chorioretinal atrophy in normal and glaucoma eyes, I: morphometric data . Invest Ophthalmol Vis Sci . 1989;30:908-918. 10. Tezel G, Kass MA, Kolker AE, Wax MB. Comparative analysis of optic disc parameters in normal pressure glaucoma, primary open angle glaucoma and ocular hypertension . Ophthalmology . 1996;103:2105-2113.Crossref 11. Tsai CS, Ritch R, Shin DH, Wan JY, Chi Y. Age related decline of disc rim area in visually normal subjects . Ophthalmology . 1992;99:29-35.Crossref 12. Wei LJ, Lin DY, Weissfeld L. Regression analysis of multivariate incomplete failure time data by modeling marginal distributions . J Am Stat Assoc . 1989;84:1065-1073.Crossref 13. Drance SM, Shulzer M, Douglas GR, Sweeney VP. Use of discriminant analysis, II: identification of persons with glaucomatous visual field defects . Arch Ophthalmol . 1978;96:57-73.Crossref 14. Hart WM, Yablonski M, Kass MA, Becker B. Multivariate analysis of the risk of glaucomatous visual field loss . Arch Ophthalmol . 1979;97:1455-1458.Crossref 15. Armaly MF, Krueger DE, Maunder L, et al. Biostatistical analysis of the collaborative glaucoma study, I: summary report of the risk factors for glaucomatous visual field defects . Arch Ophthalmol . 1980;98:2163-2171.Crossref 16. Kitazawa Y, Go F, Shirato S, Akiba Y. Use of multivariate analysis in the prognostication of ocular hypertension . In: Krieglstein GK, Leydhecker W, eds. Glaucoma Update II . New York, NY: Springer-Verlag NY Inc; 1983:145-148. 17. Kass MA, Hart WM Jr, Gordon M, Miller JP. Risk factors favoring the development of glaucomatous visual field loss in ocular hypertension . Surv Ophthalmol . 1980;25:155-162.Crossref 18. Balazsi G, Drance SM, Schulzer M, Dougles GR. Neuroretinal rim area in suspected glaucoma and early chronic open-angle glaucoma: correlations with parameters of visual function . Arch Ophthalmol . 1984;102:1011-1014.Crossref 19. Airaksinen PJ, Tuulonen A, Alanko HI. Prediction of development of glaucoma in ocular hypertensive patients . In: Krieglstein GK, ed. Glaucoma Update IV . New York, NY: Springer-Verlag NY Inc; 1991:183-186. 20. Sommer A, Pollack I, Maumenee E. Optic disc parameters and onset of glaucomatous field loss, II: static screening criteria . Arch Ophthalmol . 1979;97:1449-1454.Crossref 21. Quigley HA, Katz J, Derick RJ, Gilbert D, Sommer A. An evaluation of optic disc and nerve fiber layer examinations in monitoring progression of early glaucoma damage . Ophthalmology . 1992;99:19-28.Crossref 22. Quigley HA, Enger C, Katz J, Sommer A, Scott R, Gilbert D. Risk factors for the development of glaucomatous visual field loss in ocular hypertension . Arch Ophthalmol . 1994;112:644-649.Crossref 23. Tuulonen A, Jonas JB, Välimäki S, Alanko HI, Airaksinen PJ. Interobserver variation in the measurements of peripapillary atrophy in glaucoma . Ophthalmology . 1996;103:535-541.Crossref 24. Derick RJ, Pasquale LR, Pease ME, Quigley HA. A clinical study of peripapillary crescents of the optic disc in chronic experimental glaucoma in monkey eyes . Arch Ophthalmol . 1994;112:846-850.Crossref 25. Motolko M, Drance SM. Features of the optic disc in preglaucomatous eyes . Arch Ophthalmol . 1981;99:1992-1994.Crossref 26. Kasner O, Feuer WJ, Anderson DR. Possibly reduced prevalence of peripapillary crescents in ocular hypertension . Can J Ophthalmol . 1989;24:211-215. 27. Jonas JB, Königsreuther KA. Optic disc appearance in ocular hypertensive eyes . Am J Ophthalmol . 1994;117:732-740. 28. Stewart WC, Connor AB, Wang X. Anatomic features of the optic disc and risk of progression in ocular hypertension . Acta Ophthalmol Scand . 1995;73:237-241.Crossref 29. Zeyen TG, Caprioli J. Progression of disc and field damage in early glaucoma . Arch Ophthalmol . 1993;111:62-65.Crossref 30. Varma R, Hilton SC, Tielsch JM, Katz J, Quigley HA, Sommer A. Neural rim area declines with increased intraocular pressure in urban Americans . Arch Ophthalmol . 1995;113:1001-1005.Crossref 31. Sommer A, Tielsch JM, Katz J, et al. Relationship between intraocular pressure and primary open angle glaucoma among white and black Americans: the Baltimore Eye Survey . Arch Ophthalmol . 1991;109:1090-1095.Crossref 32. Cohen Al. Is there a potential defect in the blood-retinal barrier at the choroidal level of the optic nerve canal? Invest Ophthalmol Vis Sci . 1973;12:513-519. 33. Anderson DR. Relationship of peripapillary haloes and crescents to glaucomatous cupping . In: Krieglstein GK, Leydhecker W, eds. Glaucoma Update II . New York, NY: Springer-Verlag NY Inc; 1983:89-93.
Parapapillary Chorioretinal Atrophy in Patients With Ocular Hypertension: II. An Evaluation of Progressive ChangesTezel, Gülgün;Kolker, Allan E.;Wax, Martin B.;Kass, Michael A.;Gordon, Mae;Siegmund, Kimberly D.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160679003pmid: 9400783
Abstract Objective: To determine whether parapapillary chorioretinal atrophy in patients with ocular hypertension remained stationary or progressed along with glaucomatous optic nerve damage. Methods: The morphometric parameters and progression of parapapillary atrophy were retrospectively investigated, using serial photographs, in 350 eyes of 175 patients with ocular hypertension. The association of parapapillary atrophy progression with subsequent glaucomatous conversion and with other baseline patientand eye-specific characteristics was analyzed. Results: Progression in the area and extension of parapapillary atrophy before noticeable optic disc or visual field changes was observed in 48 (49.0%) of 98 eyes that converted to glaucoma, while parapapillary atrophy progression was noted in 25 (9.9%) of 252 ocular hypertensive eyes that did not develop glaucomatous damage (P<.001). The predictive sensitivity and specificity of this observation were 49% and 90%, respectively. In a logistic multiple regression model, the progression of parapapillary atrophy was associated with a family history of glaucoma (odds ratio, 2.7) and the initial size of zone β (odds ratio, 1.64, for an increase of 0.10 of the zone β area—disc area ratio). Conclusion: The progression of parapapillary chorioretinal atrophy may be an early glaucomatous finding in some patients with ocular hypertension. References 1. Motolko M, Drance SM. Features of the optic disc in preglaucomatous eyes . Arch Ophthalmol . 1981;99:1992-1994.Crossref 2. Kasner O, Feuer WJ, Anderson DR. Possibly reduced prevalence of peripapillary crescents in ocular hypertension . Can J Ophthalmol . 1989;24:211-215. 3. Buus DR, Anderson DR. Peripapillary crescent and halos in normal-tension glaucoma and ocular hypertension . Ophthalmology . 1989;96:16-19.Crossref 4. Airaksinen PJ, Tuulonen A, Alanko HI. Prediction of development of glaucoma in ocular hypertensive patients . In: Krieglstein GK, ed. Glaucoma Update IV . New York, NY: Springer-Verlag NY Inc; 1991:183-186. 5. Quigley HA, Enger C, Katz J, Sommer A, Scott R, Gilbert D. Risk factors for the development of glaucomatous visual field loss in ocular hypertension . Arch Ophthalmol . 1994;112:644-649.Crossref 6. Stewart WC, Connor AB, Wang X. Anatomic features of the optic disc and risk of progression in ocular hypertension . Acta Ophthalmol Scand . 1995;73:237-241.Crossref 7. Tezel G, Kass MA, Kolker AE, Wax MB. Comparative analysis of optic disc parameters in normal pressure glaucoma, primary open angle glaucoma and ocular hypertension . Ophthalmology . 1996;103:2105-2113.Crossref 8. Tsai CS, Ritch R, Shin DH, Wan JY, Chi Y. Age related decline of disc rim area in visually normal subjects . Ophthalmology . 1992;99:29-35.Crossref 9. Jonas JB, Fernandez MC, Naumann GOH. Glaucomatous parapapillary atrophy: occurence and correlations . Arch Ophthalmol . 1992;110:214-222.Crossref 10. Liang KY, Zeger SL. Longitudinal data analysis using generalized linear models . Biometrika . 1986;73:13-22.Crossref 11. Zeger SL, Liang KY. The analysis of discrete and continuous longitudinal data . Biometrics . 1986;42:121-130.Crossref 12. Kubota T, Jonas JB, Naumann GOH. Direct clinico-histological correlations of parapapillary chorioretinal atrophy . Br J Ophthamol . 1993;77:103-106.Crossref 13. Kubota T, Schlötzer-Schrehatdt UM, Naumann GOH, Kohno T, Inomata H. The ultrastructure of parapapillary chorioretinal atrophy in eyes with secondary angle-closure glaucoma . Graefes Arch Clin Exp Ophthalmol . 1996;234:351-358.Crossref 14. Korete GE, Reppucci V, Henkind P. Retinal pigment epithelium destruction causes chorioretinal atrophy . Invest Ophthalmol Vis Sci . 1984;25:1135-1145. 15. Airaksinen PJ, Juvala PA, Tuulonen A, et al. Change of peripapillary atrophy in glaucoma . In: Krieglstein GK, ed. Glaucoma Update III . New York, NY: Springer-Verlag NY Inc; 1987:97-102. 16. Rockwood EJ, Anderson DR. Acquired peripapillary changes and progression in glaucoma . Graefes Arch Clin Exp Ophthalmol . 1988;226:510-515.Crossref 17. Jonas JB, Papastathopoulos KI. Pressure-dependent changes of the optic disc in primary open-angle glaucoma . Am J Ophthalmol . 1995;119:313-317. 18. Cioffi GA, Van Buskirk M. Microvasculature of the anterior optic nerve . Surv Ophthalmol . 1994;38( (suppl) ):107-117.Crossref 19. Hayreh SS. In vivo choroidal circulation and its watershed zones . Eye . 1990;4:273-289.Crossref 20. Kellerman L, Posner A. The value of heredity in the detection and study of glaucoma . Am J Ophthalmol . 1955;40:681-685. 21. Becker B, Kolker AE, Roth FD. Glaucoma family study . Am J Ophthalmol . 1960;50:557-567. 22. Shin DH, Becker B, Kolker AE. Family history in primary open-angle glaucoma . Arch Ophthalmol . 1977;95:598-600.Crossref 23. Tielsch JM, Katz J, Sommer A, Quigley HA, Javitt JC. Family history and risk of primary open angle glaucoma . Arch Ophthalmol . 1994;112:69-73.Crossref 24. Best M, Toyofuku H. Ocular hemodynamics during ocular hypertension in man . Am J Ophthalmol . 1972;74:932-939. 25. Hayreh SS, Zimmerman MB, Podhajsky P, Alward WLM. Nocturnal arterial hypotension and its role in optic nerve head and ocular ischemic disorders . Am J Ophthalmol . 1994;117:603-624. 26. Hayreh SS, Walker WM. Fluorescent fundus photography in glaucoma . Am J Ophthalmol . 1967;63:982-989. 27. Raitta C, Sarmela T. Fluorescein angiography of the optic disc and the peripapillary area in chronic glaucoma . Acta Ophthalmol (Copenh) . 1970;48:303-308.Crossref 28. Ulrich A, Ulrich C, Barth T, Ulrich WD. Detection of disturbed autoregulation of the peripapillary choroid in primary open angle glaucoma . Ophthalmic Surg Lasers . 1996;27:746-757. 29. Armaly MF, Krueger DE, Maunder L, et al. Biostatistical analysis of the collaborative glaucoma study, I . Arch Ophthalmol . 1980;98:2163-2171.Crossref 30. Drance SM, Schulzer M, Thomas B, Douglas GR. Multivariate analysis in glaucoma . Arch Ophthalmol . 1981;99:1019-1022.Crossref 31. Airaksinen PJ, Tuulonen A, Alanko HI. Rate and pattern of neuroretinal rim area decrease in ocular hypertension and glaucoma . Arch Ophthalmol . 1992;110:206-210.Crossref 32. Pederson JE, Anderson DR. The mode of progressive disc cupping in ocular hypertension and glaucoma . Arch Ophthalmol . 1980;98:490-495.Crossref 33. Sommer A, Quigley HA, Robin AL, Miller NR, Katz J, Arkell S. Evaluation of nerve fiber layer assessment . Arch Ophthalmol . 1984;102:1766-1771.Crossref 34. Sommer A, Katz J, Quigley HA, et al. Clinically detectable nerve fiber atrophy precedes the onset of glaucomatous field loss . Arch Ophthalmol . 1991;109:77-83.Crossref 35. Goldman H. Some basic problems of simple glaucoma . Am J Ophthalmol . 1959;48:213-220. 36. Iwata K. Ophthalmoscopy in the detection of optic disc and retinal nerve fiber layer changes in early glaucoma . Surv Ophthalmol . 1989;33:447-448.Crossref 37. Bengtsson B. Optic disc haemorrhages preceding manifest glaucoma . Acta Ophthalmol (Copenh) . 1990;68:450-454.Crossref 38. Hart WM, Yablonski M, Kass MA, Becker B. Multivariate analysis of the risk of glaucomatous visual field loss . Arch Ophthalmol . 1979;97:1455-1458.Crossref
Effect of Cataract Extraction on the Results of Automated Perimetry in GlaucomaSmith, Scott D.;Katz, Joanne;Quigley, Harry A.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160685004pmid: 9400784
Abstract Objective: To investigate the effect of cataract extraction on the results of automated perimetry in persons with glaucomatous visual field loss. Subjects: Subjects from a retrospective study of visual field progression who underwent cataract extraction during follow-up were identified. Subjects came from the glaucoma service of a hospital-based tertiary referral center. Methods: Subjects had at least 7 Humphrey 24-2 or 30-2 visual fields over 5 years or more, with an abnormal glaucoma hemifield test result on the first 2 examinations. Visual field data were transferred to a microcomputer and comparison of the visual fields immediately before and after cataract extraction was performed. Results: Sixty-five eyes of 50 subjects (mean age, 71.8 years) were included in the analysis. A mean improvement in mean deviation (MD) of 1.68 dB (P<.001), and a mean worsening in corrected pattern SD (CPSD) of 0.54 dB (P=.09) was observed. The mean unweighted change in threshold in the 52 points of program 24-2 was 1.58 dB, corresponding to a 43.9% increase in sensitivity. A significant correlation between improvement in visual acuity and improvement in MD was also found. A mean increase in CPSD of 1.61 dB (P=.005) occurred in subjects with dense scotomas (minimum threshold value ≤5 dB) and preoperative CPSD of 8 dB or less. Conclusions: In persons with glaucomatous visual field defects, cataract extraction produces only a modest improvement in MD. After cataract surgery, the CPSD index worsened in many subjects with dense scotomas. This suggests that the development of cataract can mask progressive glaucomatous visual field loss in such persons. References 1. Guthauser U, Flammer J. Quantifying visual field damage caused by cataract . Am J Ophthalmol . 1988;106:480-484. 2. Wood JM, Wild JM, Smerdon DL, Crews SJ. Alterations in the shape of the automated perimetric profile arising from cataract . Graefes Arch Clin Exp Ophthalmol . 1989;227:157-161.Crossref 3. Lam BL, Alward WLM, Kolder HE. Effect of cataract on automated perimetry . Ophthalmology . 1991;98:1066-1070.Crossref 4. Heuer DK, Anderson DR, Knighton RW, Feuer WJ, Gressel MG. The influence of simulated light scattering on automated perimetric threshold measurements . Arch Ophthalmol . 1988;106:1247-1251.Crossref 5. Bigger JF, Becker B. Cataracts and open-angle glaucoma . Am J Ophthalmol . 1971;71:335-340. 6. Stewart WC, Rogers GM, Crinkley CMC, Carlson AN. Effect of cataract extraction on automated fields in chronic open-angle glaucoma . Arch Ophthalmol . 1995;113:875-879.Crossref 7. Smith SD, Katz J, Quigley HA. Analysis of progressive change in automated visual fields in glaucoma . Invest Ophthalmol Vis Sci . 1996;37:1419-1428. 8. Katz J. Two eyes or one? the data analyst's dilemma . Ophthalmic Surg . 1988;19:585-589. 9. Budenz DL, Feuer WJ, Anderson DR. The effect of simulated cataract on the glaucomatous visual field . Ophthalmology . 1993;100:511-517.Crossref
Factors Associated With Intraocular Pressure-Induced Acute Visual Field DepressionTrible, John R.;Anderson, Douglas R.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160693005pmid: 9400785
Abstract Objective: To determine the factors associated with visual field depression produced by artificial elevation of intraocular pressure (IOP). Methods: The visual threshold was determined at 26 locations in the central visual field at a spontaneous IOP, at 30 mm Hg, at 40 mm Hg, and at the IOP immediately following release of the suction cup used to elevate the IOP artificially in 33 subjects with and without glaucoma. The net decrease in threshold sensitivity at each IOP level relative to sensitivity obtained at the spontaneous IOP was calculated (acute visual field depression). Results: Factors potentially influencing the acute visual field depression between subjects were determined with stepwise regression. The reciprocal of ocular perfusion pressure, a clinical measure, was strongly correlated with acute visual field depression (dependent variable), particularly at 40 mm Hg (at 30 mm Hg, r=0.412, P=.02, n=32; and at 40 mm Hg, r=0.813, P<.001, n=33). When a second variable, the diagnosis of glaucoma, was included in the regression at 40 mm Hg, it contributed significantly (partial r=0.650, P<.001, n=26). The degree of glaucomatous damage (vertical cup-disc ratio or baseline Humphrey 24-2 visual field mean deviation) failed to correlate with acute field depression, with or without correction for ocular perfusion pressure. Conclusions: The elevation of IOP produces acute, reversible visual field depression. This depression is largely dependent on the subject's ocular perfusion pressure. The degree of depression is greater in those with glaucoma but is not strictly related to the degree of glaucomatous damage. References 1. Gafner F, Goldmann H. Experimentelle Untersuchungen uber den Zusammenhang von Augendrucksteigerung und Gesichtsfeldschadigung . Ophthalmologica . 1955;130:357-377.Crossref 2. Harrington DO. Pathogenesis of the glaucomatous field defects: individual variations in pressure sensitivity . In: Glaucoma, Transactions of the Fifth Conference, Chicago, Josiah Macy, Jr, Foundation . Madison, NJ: Madison Printing Co Inc; 1960:259-310. 3. Drance SM. Studies in the susceptibility of the eye to raised intraocular pressure . Arch Ophthalmol . 1962;68:478-488.Crossref 4. Tsamparlakis JC. Effects of transient induced elevation of the intraocular pressure on the visual field . Br J Ophthalmol . 1964;48:237-249.Crossref 5. Kolker AE, Becker B, Mills DW. Intraocular pressure and visual fields: effects of corticosteroids . Arch Ophthalmol . 1964;72:772-782.Crossref 6. Vandenburg D, Drance SM. Studies on the effects of artificially raised intraocular pressure on retinal differential thresholds . Can J Ophthalmol . 1966;1:92-103. 7. Vandenburg D, Drance SM. Studies of the effects of artificially raised intraocular presssure: on retinal differential thresholds of the Bjerrum area . Am J Ophthalmol . 1966;62:1049-1063. 8. Scott AB, Morris A. Visual field changes produced by artificially elevated intraocular pressure . Am J Ophthalmol . 1967;63:308-312. 9. Lobstein A. Factors affecting the susceptibility of the glaucomatous eye to raised intraocular pressure . Mod Probl Ophthalmol . 1968;6:73-93. 10. Lobstein A, Gerhard JP. Prognostic value of the visual field response to corticosteroid provocative testing in ocular hypertension: a follow-up study . In: International Glaucoma Symposium, Albi, France 1974 . Marseille, France: Diffusion Générale de Librairie; 1975:205-215. 11. Werner EB, Drance SM, Schulzer M. Trabeculectomy and the progression of glaucomatous visual field loss . Arch Ophthalmol . 1977;95:1374-1377.Crossref 12. Lundberg L, Wettrell K, Linner E. Ocular hypertension: a prospective twenty-year follow-up study . Acta Ophthalmol (Copenh) . 1987;65:705-708.Crossref 13. Shields MB. Primary open-angle glaucoma . In: Textbook of Glaucoma . 3rd ed. Baltimore, Md: Williams & Wilkins; 1992:172. 14. Bernd A, Ulrich WD, Teubel H, et al. Refraction changes during elevation of intraocular pressure by suction cup, their reflection in the pattern visual evoked potential, and their compensation . Doc Ophthalmol . 1992;83:151-162.Crossref 15. Schiefer U, Ulrich C, Ulrich WD, et al. Influence of suction cup oculopression on corneal astigmatism . Graefes Arch Clin Exp Ophthalmol . 1994;232:115-121.Crossref 16. Nordmann JP, Denis P, Nguer Y, et al. Static threshold visual field in glaucoma with the FASTPAC algorithm of the Humphrey field analyser: is the gain in examination time offset by any loss of information? Eur J Ophthalmol . 1994;4:105-110. 17. Young IM, Rait JL, Guest CS, et al. Comparison between FASTPAC and conventional Humphrey perimetry . Aust N Z J Ophthalmol . 1994;22:95-99.Crossref 18. Michaels DA. Visual Optics and Refraction: A Clinical Approach . 3rd ed. St Louis, Mo: Mosby—Year Book Inc; 1985:51-54. 19. Geijer C, Bill A. Effects of raised intraocular pressure on retinal, prelaminar, laminar, and retrolaminar optic nerve head blood flow in monkeys . Invest Ophthalmol Vis Sci . 1979;18:1030-1042. 20. Sossi N, Anderson DR. Effect of elevated intraocular pressure on blood flow: occurrence in cat optic nerve head studied with iodoantipyrine I 125 . Arch Ophthalmol . 1983;101:98-101.Crossref 21. Sperber GO, Bill A. Blood flow and glucose consumption in the optic nerve, retina, and brain: effects of high intraocular pressure . Exp Eye Res . 1985;41:639-653.Crossref 22. Hayreh SS, Bill A, Sperber GO. Effects of high intraocular pressure on the glucose metabolism in the retina and optic nerve in old atherosclerotic monkeys . Graefes Arch Clin Exp Ophthalmol . 1994;232:745-752.Crossref 23. Harrington DO. The pathogenesis of the glaucoma field: clinical evidence that circulatory insufficiency in the optic nerve is the primary cause of visual field loss in glaucoma . Am J Ophthalmol . 1959;5:177-184. 24. McLean J. Management of the primary glaucomas . Am J Ophthalmol . 1957;44:323-334. 25. Tielsch JM, Katz J, Sommer A, et al. Hypertension, perfusion pressure, and primary open-angle glaucoma: a population based assessment . Arch Ophthalmol . 1994;113:216-221.Crossref 26. Cartwright MJ, Anderson DR. Correlation of asymmetric damage with asymmetric intraocular pressure in normal-tension glaucoma (low-tension glaucoma) . Arch Ophthalmol . 1988;106:898-900.Crossref 27. Crichton A, Drance SM, Douglas GR, Schulzer M. Unequal intraocular pressure and its relation to asymmetric visual field defects in low-tension glaucoma . Ophthalmology . 1989;96:1312-1314.Crossref 28. Haefliger IO, Hitchings RA. Relationship between asymmetry of visual field defects and intraocular pressure difference in an untreated normal (low) tension glaucoma population . Acta Ophthalmol (Copenh) . 1990;68:564-567.Crossref 29. Leblanc RP, Stewart RH, Becker B. Corticosteroid provocative testing . 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MSL-109 Adjuvant Therapy for Cytomegalovirus Retinitis in Patients With Acquired Immunodeficiency Syndrome: The Monoclonal Antibody Cytomegalovirus Retinitis Trial1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160698006
Abstract Objective: To evaluate the efficacy and safety of an intravenous human monoclonal antibody to cytomegalovirus (CMV), MSL-109, as adjuvant treatment for CMV retinitis. Methods: Two hundred nine patients with acquired immunodeficiency syndrome and active CMV retinitis were enrolled in a multicenter, phase 2/3, randomized, placebocontrolled clinical trial. Patients received adjuvant treatment with MSL-109, 60 mg intravenously every 2 weeks, or placebo. Randomization was stratified on the basis of whether patients had untreated or relapsed retinitis. Primary drug therapy for CMV retinitis was determined by the treating physician. Results: The rates of retinitis progression, as evaluated in a masked fashion, were 3.04/person-year in the MSL-109—treated group and 3.05/person-year in the placebo-treated group (P=.98; Wald test); the median times to progression were 67 days in the MSL-109—treated group and 65 days in the placebo-treated group. No differences between the 2 groups were noted in the rates of increase in retinal area involved by CMV, visual field loss, or visual acuity outcomes. The mortality rate in the MSL-109—treated group was 0.68/person-year, and in the placebo-treated group, 0.31/person-year (P=.01). The mortality difference was not explained by differences in baseline variables or in concurrent antiretroviral therapy. Among patients with newly diagnosed retinitis, mortality rates were similar (MSL-109, 0.41/person-year; placebo, 0.42/person-year; P=.95), whereas among patients with relapsed retinitis the MSL-109—treated group had a greater mortality rate (MSL-109, 0.83/person-year; placebo, 0.24/person-year; P=.003). However, the mortality rate in the placebo-treated patients with relapsed CMV retinitis was lower than that in the placebo-treated patients with newly diagnosed CMV retinitis and lower than that in other trials of patients with relapsed CMV retinitis. Conclusions: Intravenous MSL-109, 60 mg every 2 weeks, appeared to be ineffective adjuvant therapy for CMV retinitis. The mortality rate was higher in the MSL-109—treated group, but the reasons for this difference remain uncertain. References 1. Moore RD, Chaisson RE. Natural history of opportunistic disease in an HIV-infected urban clinical cohort . Ann Intern Med . 1996;124:633-642.Crossref 2. Hoover DR, Saah AJ, Bacellar H, et al. Clinical manifestations of AIDS in the era of Pneumocystis prophylaxis: Multicenter AIDS Cohort Study . N Engl J Med . 1993;329:1922-1926.Crossref 3. Gallant JE, Moore RD, Richman DD, Keruly J, Chaisson RE. Incidence and natural history of cytomegalovirus disease in patients with advanced human immunodeficiency virus disease treated with zidovudine: the Zidovudine Epidemiology Study Group . J Infect Dis . 1992;166:1223-1227.Crossref 4. Hoover DR, Peng Y, Saah A, et al. Occurrence of cytomegalovirus retinitis after human immunodeficiency virus immunosuppression . Arch Ophthalmol . 1996;114:821-827.Crossref 5. Jabs DA, Enger C, Bartlett JG. Cytomegalovirus retinitis and acquired immunodeficiency syndrome . Arch Ophthalmol . 1989;107:75-80.Crossref 6. Jabs DA. Ocular manifestations of HIV infection . Trans Am Ophthalmol Soc . 1995;93:623-683. 7. Pertel P, Hirschtick R, Phair J, Chmiel J, Poggensee L, Murphy R. Risk of developing cytomegalovirus retinitis in persons infected with the human immunodeficiency virus . J Acquir Immune Defic Syndr . 1992;5:1069-1074. 8. Kuppermann BD, Petty JG, Richman DD, et al. Correlation between CD4+ counts and prevalence of cytomegalovirus retinitis and human immunodeficiency virus-related noninfectious retinal vasculopathy in patients with acquired immunodeficiency syndrome . Am J Ophthalmol . 1993;115:575-582. 9. Spector SA, Weingeist T, Pollard RB, et al. A randomized, controlled study of intravenous ganciclovir therapy for cytomegalovirus peripheral retinitis in patients with AIDS: AIDS Clinical Trials Group and Cytomegalovirus Cooperative Study Group . J Infect Dis . 1993;168:557-563.Crossref 10. Studies of Ocular Complications of AIDS Research Group in collaboration with the AIDS Clinical Trials Group. Mortality in patients with the acquired immunodeficiency syndrome treated with either foscarnet or ganciclovir for cytomegalovirus retinitis . N Engl J Med . 1992;326:213-220.Crossref 11. Studies of Ocular Complications of AIDS Research Group in collaboration with the AIDS Clinical Trials Group. Foscarnet-ganciclovir cytomegalovirus retinitis trial, 4: visual outcomes . Ophthalmology . 1994;101:1250-1261.Crossref 12. The Oral Ganciclovir European and Australian Cooperative Study Group. Intravenous versus oral ganciclovir: European/Australian comparative study of efficacy and safety in the prevention of cytomegalovirus retinitis recurrence in patients with AIDS . AIDS . 1995;9:471-477.Crossref 13. Drew WL, Ives D, Lalezari JP, et al. Oral ganciclovir as maintenance treatment for cytomegalovirus retinitis in patients with AIDS: Syntex Cooperative Oral Ganciclovir Study Group . N Engl J Med . 1995;333:615-620.Crossref 14. Palestine AG, Polis MA, De Smet MD, et al. A randomized, controlled trial of foscarnet in the treatment of cytomegalovirus retinitis in patients with AIDS . Ann Intern Med . 1991;115:665-673.Crossref 15. Martin DF, Parks DJ, Mellow SD, et al. Treatment of cytomegalovirus retinitis with an intraocular sustained-release ganciclovir implant: a randomized controlled clinical trial . Arch Ophthalmol . 1994;112:1531-1539.Crossref 16. Lalezari JP, Drew WL, Glutzer E, et al. 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Pollard RB, Nokta MA, Pappas P, et al. A phase I/IIA study of a human monoclonal anti-cytomegalovirus antibody in patients with AIDS . Antiviral Res . 1992;16( (suppl 1) ):111. Abstract. 25. Tolpin M, Pollard R, Tierney M, Notka M, Wood D, Hirsch M. Combination therapy of cytomegalovirus (CMV) retinitis with a human monoclonal antibody (SDZ MSL 109) and either ganciclovir (DHPG) or foscarnet (PFA) . In: Program and abstracts of the IXth International Conference on AIDS , Berlin, Germany; 1993. Abstract WS-B11-2. 26. Studies of Ocular Complications of AIDS Research Group in collaboration with the AIDS Clinical Trials Group. Studies of ocular complications of AIDS Foscarnet-Ganciclovir Cytomegalovirus Retinitis Trial, 1: rationale, design, and methods . Control Clin Trials . 1992;13:22-39.Crossref 27. Studies of Ocular Complications of AIDS in collaboration with the AIDS Clinical Trials Group. 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Factors Predictive of Growth and Treatment of Small Choroidal Melanoma: COMS Report No. 51997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160707007pmid: 9400787
Abstract Objectives: To describe time to tumor growth of a prospectively followed group of patients with small choroidal melanoma and to determine baseline clinical and photographic characteristics associated with time to growth. Methods: The Collaborative Ocular Melanoma Study (COMS) is a set of clinical trials designed to compare radiotherapy and enucleation in the treatment of medium- and large-size choroidal melanoma. From December 1986 to August 1989, patients with small choroidal melanoma, not large enough to be eligible for the COMS clinical trials, were offered participation in a nonrandomized prospective follow-up study. Small choroidal melanomas were defined as 1.0 to 3.0mm in apical height and 5.0 to 16.0 mm in largest basal dimension. A total of 204 patients were enrolled in the study and were followed up annually through August 1989. An assessment of current size of tumor, treatment status, and vital status was conducted in 1993-1994; an additional assessment of treatment and vital status was performed in 1995-1996. Results: Of 188 small tumors not treated at the time of study enrollment, 46 grew during follow-up to a size that was large enough to be eligible for the COMS clinical trials. The Kaplan-Meier estimates of proportion of tumors that grew were 21% (95% confidence interval, 14%-27%) by 2 years and 31% (95% confidence interval, 23%-39%) by 5 years. Factors significantly associated with time to growth in a Cox proportional hazards regression model were greater initial tumor thickness and diameter, presence of orange pigment, absence of drusen, and absence of areas of retinal pigment epithelial changes adjacent to the tumor. Conclusions: Of small choroidal melanomas initially managed by observation, 21% demonstrated growth by 2 years and 31% by 5 years. The clinical and photographic features of these tumors confirm previous findings and are useful in identifying patients with small tumors at highest risk of short-term growth. References 1. Augsburger JJ. Is observation really appropriate for small choroidal melanomas? Trans Am Ophthalmol Soc . 1993;91:147-175. 2. Gass JDM. Observation of suspected choroidal and ciliary body melanomas for evidence of growth prior to enucleation . Ophthalmology . 1980;87:523-528.Crossref 3. Char DH, Heilbron DC, Juster RP, Stone RD. Choroidal melanoma growth patterns . Br J Ophthalmol . 1983;67:575-578.Crossref 4. Augsburger JJ, Schroeder RP, Territo C, Gamel JW, Shields JA. Clinical parameters predictive of enlargement of melanocytic choroidal lesions . Br J Ophthalmol . 1989;73:911-917.Crossref 5. Gass JDM. Problems in the differential diagnosis of malignant melanomas of the choroid and ciliary body . Am J Ophthalmol . 1977;83:299-323. 6. Zimmerman L, McLean I. Do growth and onset of symptoms of uveal melanomas indicate subclinical metastasis? Ophthalmology . 1984;91:685-691.Crossref 7. Macllwaine WA, Anderson B, Klintworth GK. Enlargement of a histologically documented choroidal nevus . Am J Ophthalmol . 1979;87:480-486. 8. Diener-West M, Hawkins, BS, Markowitz JM, Schachat AP. A review of mortality from choroidal melanoma, II: a meta-analysis of 5-year mortality rates following enucleation, 1966 through 1988 . Arch Ophthalmol . 1992;110:245-250.Crossref 9. Augsburger JJ, Vrabec TR. Impact of delayed treatment in growing posterior uveal melanomas . Arch Ophthalmol . 1993;111:1382-1386.Crossref 10. Shields JA, Shields CL, Kiratli H, dePotter P, Cater JR. Risk factors for growth and metastasis of small choroidal melanocytic lesions . Ophthalmology . 1995;102:1351-1361.Crossref 11. Schachat AP. In discussion: Butler P, Char DH, Zarvin M, Kroll S. Natural history of indeterminate pigmented choroidal tumors . Ophthalmology . 1994;101:717. 12. McLean IW. In discussion: Shields JA, Shields CL, Kiratli H, dePotter P, Cater JR. Risk factors for growth and metastasis of small choroidal melanocytic lesions . Ophthalmology . 1995;102:1361.Crossref 13. Coleman JD. In discussion: Shields CL, Shields JA, Kiratli H, dePotter P, Cater JR. Risk factors for growth and metastasis of small choroidal melanocytic lesions . Trans Am Ophthalmol Soc . 1995;93:275. 14. Butler P, Char DH, Zarvin M, Kroll S. Natural history of indeterminate pigmented choroidal tumors . Ophthalmology . 1994;101:710-716.Crossref 15. Erie JC, Robertson DM. Serous detachments of the macula associated with presumed small choroidal melanomas . Am J Ophthalmol . 1986;102:176-178.Crossref 16. Erie JC, Robertson DM, Mieler WF. Presumed small choroidal melanomas with serous macular detachments with and without surface laser photocoagulation treatment . Am J Ophthalmol . 1990;109:259-264. 17. Collaborative Ocular Melanoma Study Group. Design and methods of a clinical trial for a rare condition: The Collaborative Ocular Melanoma Study, COMS Report No.3 . Control Clin Trials . 1993;14:362-391.Crossref 18. Collaborative Ocular Melanoma Study. COMS Manual of Procedures . Springfield, Va: National Technical Information Service; January 1995. PB95-179693. 19. Collaborative Ocular Melanoma Study. COMS Study Forms Book . Springfield, Va: National Technical Information Service: May 1991. Publication PB91-217315. 20. Kaplan EL, Meier P. Nonparametric estimation from incomplete observations . J Am Stat Assoc . 1958;53:457-481.Crossref 21. Cox DR. Regression models and life tables (with discussion) . J R Stat Soc B . 1972;34:187-200. 22. Collaborative Ocular Melanoma Study Group. Mortality in patients with small choroidal melanoma: COMS Report No. 4 . Arch Ophthalmol . 1997;115:886-893.Crossref 23. Char DH, Hogan M. Management of small elevated pigmented choroidal lesions . Br J Ophthalmol . 1977;61:54-58.Crossref 24. Byrne SF, Green RL. Intraocular Tumors: Ultrasound of the Eye and Orbit . St Louis, Mo: CV Mosby Co; 1992:140-149. 25. Kupfer C. In discussion: Shields CL, Shields JA, Kiratli H, dePotter P, Cater JR. Risk factors for growth and metastasis of small choroidal melanocytic lesions . Trans Am Ophthalmol Soc . 1995;93:277.
Visual Function 5 Years After Optic Neuritis: Experience of the Optic Neuritis Treatment Trial1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160715008
Abstract Objective: To assess the 5-year visual course, including the incidence of recurrent optic neuritis, in 454 patients enrolled in the Optic Neuritis Treatment Trial. Methods: Five-year follow-up vision testing, which included measures of visual acuity, contrast sensitivity, visual field, and color vision, was completed for 397 (87%) of the 454 patients. Results: Visual function test results in the eyes that experienced optic neuritis at study enrollment (affected eyes) were normal or only slightly abnormal after 5 years in most patients; the results did not significantly differ by treatment group (P=.37 for visual acuity). The visual acuity in the affected eyes was 20/25 or better in 87%, 20/25 to 20/40 in 7%, 20/50 to 20/190 in 3%, and 20/200 or worse in 3%. The recurrence of optic neuritis in either eye occurred in 28% of the patients and was more frequent in patients with multiple sclerosis (P=.001) and in patients without multiple sclerosis who were in the prednisone treatment group (P=.004). Most eyes with a recurrence retained normal or almost normal visual function. Conclusions: Most patients retained good to excellent vision in the 5 years following an attack of optic neuritis, even if the optic neuritis recurred. Recurrences were more frequent in patients with multiple sclerosis and in those treated with oral prednisone alone. The completion of the 5-year follow-up by the Optic Neuritis Treatment Trial cohort has not altered our management recommendations based on the results we reported earlier. References 1. Beck RW, Cleary PA, Anderson MM, et al. A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis . N Engl J Med . 1992;326:581-588.Crossref 2. 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Trans Ophthalmol Soc U K . 1959;79:701-716. 20. Hutchinson WM. Acute optic neuritis and the prognosis for multiple sclerosis . J Neurol Neurosurg Psychiatry . 1976;39:283-289.Crossref 21. Rodriguez M, Siva A, Cross SA, O'Brien PC, Kurland LT. Optic neuritis: a populationbased study in Olmsted County, Minnesota . Neurology . 1995;45:244-250.Crossref 22. Kupersmith MJ, Nelson JI, Seiple WH, Carr RE, Weiss PA. The 20/20 eye in multiple sclerosis . Neurology . 1983;33:1015-1020.Crossref 23. Kupersmith MJ, Seiple WH, Nelson JI, Carr RE. Contrast sensitivity loss in multiple sclerosis . Invest Ophthalmol Vis Sci . 1984;25:632-639. 24. Engell T, Trojaborg W, Raun NE. Subclinical optic neuropathy in multiple sclerosis: a neuro-ophthalmological investigation by means of visually evoked response, Farnworth-Munsell 100 hue test and Ishihara test and their diagnostic value . Acta Ophthalmol (Copenh) . 1987;65:735-740.Crossref 25. Ashworth B, Aspinall PA, Mitchell JD. 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Systemic Hyperoxia Decreases Vascular Endothelial Growth Factor Gene Expression in Ischemic Primate RetinaPournaras, Constantin J.;Miller, Joan W.;Gragoudas, Evangelos S.;Husain, Deeba;Munoz, Jean L.;Tolentino, Michael J.;Kuroki, Masatoshi;Adamis, Anthony P.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160723009pmid: 9400789
Abstract Objectives: To determine whether systemic hyperoxia can reverse retinal hypoxia and decrease vascular endothelial growth factor (VEGF) gene expression in ischemic nonhuman primate retina. Methods: Six eyes of 3 cynomolgus monkeys were studied. Retinal ischemia was induced via laser vein occlusion and confirmed with fluorescein angiography. Animals were randomly assigned to treatment with either 21% or 100% inhaled oxygen. Arterial Po2 was monitored while systemic acid-base status was maintained. An oxygen microelectrode on a micromanipulator was used to measure preretinal oxygen concentrations in ischemic and nonischemic retina in situ. RNA was isolated from fresh whole retinas, and VEGF messenger RNA levels were quantified with Northern blotting. Results: The preretinal Po2 in ischemic retina was less than the Po2 in nonischemic retina in animals breathing 21% oxygen (intervascular zone Po2, 14.3±0.53 vs 21.8±0.55 mm Hg; P=.002). After 8 hours of systemic hyperoxia (arterial P02, 512±18 mm Hg), the preretinal Po2 in ischemic retina increased to 166.2±15.6 mm Hg (21.8% oxygen) and retinal VEGF messenger RNA levels were reduced by an average of 55%. Conclusions: These data demonstrate that systemic hyperoxia can lower retinal VEGF gene expression and reoxygenate ischemic adult primate retina. References 1. Leung DW, Cachianes G, Kuang WJ, Goeddel DV, Ferrara N. Vascular endothelial growth factor is a secreted angiogenic mitogen . Science . 1989;246:1306-1309.Crossref 2. Keck PJ, Hauser SD, Krivi G, et al. Vascular permeability factor, an endothelial cell mitogen related to PDGF . Science . 1989;246:1309-1312.Crossref 3. Senger DR, Galli SJ, Dvorak AM, Perruzzi CA, Harvey VS, Dvorak HF. Tumor cells secrete a vascular permeability factor that promotes accumulation of ascites fluid . Science . 1983;219:983-985.Crossref 4. Carmeliet P, Ferreira V, Breir G, et al. 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Hypoxic induction of endothelial cell growth factors in retinal cells: identification and characterization of vascular endothelial growth factor (VEGF) as the sole mitogen . Mol Med . 1995;2:182-193. 17. Miller J, Adamis AP, Shima DT, et al. Vascular endothelial growth factor/vascular permeability factor is temporally and spatially correlated with ocular angiogenesis in a primate model . Am J Pathol . 1994;145:574-584. 18. Pierce EA, Avery RL, Foley ED, Aiello LP, Smith LEH. Vascular endothelial growth factor/vascular permeability factor expression in a mouse model of retinal neovascularization . Proc Natl Acad Sci U S A . 1995;92:905-909.Crossref 19. Pe'er J, Shweiki D, Itin A, Hemo I, Gnessin H, Keshet E. Hypoxia-induced expression of vascular endothelial growth factor by retinal cells is a common factor in neovascularizing ocular diseases . Lab Invest . 1995;72:638-645. 20. Dorey CK, Aouididi S, Reynaud X, Dvorak HF, Brown LF. Correlation of vascular permeability factor/vascular endothelial growth factor with extraretinal neovascularization in the rat . Arch Ophthalmol . 1996;114:1210-1217.Crossref 21. Adamis AP, Miller J, Bernal M, et al. Increased vascular endothelial growth factor levels in the vitreous of eyes with proliferative diabetic retinopathy . Am J Ophthalmol . 1994;118:445-450. 22. Malecaze F, Clamens S, Simorre-Pinatel V, et al. Detection of vascular endothelial growth factor messenger RNA and vascular endothelial growth factor-like activity in proliferative diabetic retinopathy . Arch Ophthalmol . 1994;112:1476-1482.Crossref 23. Aiello LP, Avery RL, Arrigg PG, et al. Vascular endothelial growth factor in ocular fluid of patients wth diabetic retinopathy and other retinal disorders . N Engl J Med . 1994;331:1480-1487.Crossref 24. Aiello LP, Pierce EA, Foley ED, et al. Suppression of retinal neovascularization in vivo by inhibition of vascular endothelial growth factor (VEGF) using soluble VEGF-receptor chimeric proteins . Proc Natl Acad Sci U S A . 1995;92:10457-10461.Crossref 25. Tolentino MJ, Miller JW, Gragoudas ES, Chatzistefanou K, Ferrara N, Adamis AP. Vascular endothelial growth factor is sufficient to produce iris neovascularization and neovascular glaucoma in a non-human primate . Arch Ophthalmol . 1996;114:964-970.Crossref 26. Tolentino MJ, Miller JW, Gragoudas ES, et al. Intravitreal injections of vascular endothelial growth factor produce retinal ischemia and microangiopathy in an adult primate . Ophthalmology . 1996;103:1820-1828.Crossref 27. Shweiki D, Itin A, Softer D, Keshet E. Vascular endothelial growth factor induced by hypoxia may mediate hypoxia-initiated angiogenesis . Nature . 1992;359:843-845.Crossref 28. Plate KH, Breier G, Weich HA, Risau W. 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Vascular endothelial growth factor acts as a survival factor for newly formed retinal vessels and has implications for retinopathy of prematurity . Nat Med . 1995;1:1024-1028.Crossref 34. Pierce EA, Foley ED, Smith LE. Regulation of vascular endothelial growth factor by oxygen in a model of retinopathy of prematurity [see comments] . Arch Ophthalmol . 1996;114:1219-1228.Crossref 35. Pournaras CJ, Tsacopoulos M, Strommer K, Gilodi N, Leuenberger PM. Experimental retinal branch vein occlusion in miniature pigs induces local tissue hypoxia and vasoproliferative microangiopathy . Ophthalmology . 1990;97:1321-1328.Crossref 36. Pournaras CJ, Tsacopoulos M, Riva CE, Roth E. Diffusion of O2 in normal and ischemic retinas of anesthetized miniature pigs in normoxia and hyperoxia . Graefes Arch Clin Exp Ophthalmol . 1990;228:138-142.Crossref 37. Pournaras CJ. Retinal oxygen distribution: its role in the physiopathology of vasoproliferative microangiopathies . Retina . 1995;15:332-347.Crossref 38. Pournaras CJ, Shonat RD, Munoz JL, Petrig BL. New ocular micromanipulator for measurements of retinal and vitreous physiologic parameters in the mammalian eye . Exp Eye Res . 1991;53:723-727.Crossref 39. Tsacopoulos M, Lehmenkuhler A. A double-barrelled pt-microelectrode for simultaneous measurement of Po2 and bioelectrical activity in excitable tissues . Experientia . 1977;33:1337-1338.Crossref 40. Tsacopoulos M, Poitry S, Borsellino A. Diffusion and consumption of oxygen in the superfused retina of the drone (Apis mellifera) in darkness . J Gen Physiol . 1981;77:601-628.Crossref 41. Dollery CT, Bulpitt CJ, Kohner EM. Oxygen supply to the retina from the retinal and choroidal circulations at normal and increased arterial oxygen tensions . Invest Ophthalmol . 1969;8:588-594. 42. Linsenmeier RA, Yancey CM. Effects of hyperoxia on the oxygen distribution in the intact cat retina . Invest Ophthalmol Vis Sci . 1989;30:612-618. 43. Pournaras CJ, Riva CE, Tsacopoulos M, Strommer K. Diffusion of O2 in the retina of anesthetized miniature pigs in normoxia and hyperoxia . Exp Eye Res . 1989;49:347-360.Crossref 44. Lutty GA, McLeod DS, Merges C, Diggs A, Plouet J. Localization of vascular endothelial growth factor in human retina and choroid . Arch Ophthalmol . 1996;114:971-977.Crossref 45. Linsenmeier RA, Braun RD. Oxygen distribution and consumption in the cat retina during normoxia and hypoxemia . JGen Physiol . 1992;88:521-530. 46. Alder VA, Cringle SJ, Constable IJ. The retinal oxygen profile in cats . Invest Ophthalmol Vis Sci . 1983;24:30-37. 47. Ahmed J, Braun RD, Dunn RJ, Linsenmeier RA. Oxygen distribution in the macaque retina . Invest Ophthalmol Vis Sci . 1993;34:516-521. 48. Husain D, Ryan AM, Cuthberton RA, et al. Vascular endothelial growth factor (VEGF) expression is correlated with choroidal neovascularization in a monkey model . Invest Ophthalmol Vis Sci . 1997;38:2310. Abstract. 49. Shima DT, Deutsch U, D'Amore PA. Hypoxic induction of vascular endothelial growth factor (VEGF) in human epithelial cells is mediated by increases in mRNA stability . FEBS Lett . 1995;370:203-208.Crossref
Apoptosis in Patients With Posterior UveitisChan, Chi-Chao;Matteson, Dawn M.;Li, Qian;Whitcup, Scott M.;Nussenblatt, Robert B.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160729010pmid: 9400790
Abstract Background: Apoptosis plays a part in the pathogenesis of autoimmune diseases. Objective: To investigate the expression of apoptotic markers in the eyes of patients with uveitis. Methods: With the use of immunohistochemical and in situ apoptotic detection techniques, apoptotic molecules (Fas or Fas ligand [FasL]) and nuclear DNA fragmentation were examined in 8 enucleated eyes with Behçet's disease (1), sarcoidosis (1), subretinal fibrosis and uveitis (1), sympathetic ophthalmia (4), and the Vogt-Koyanagi-Harada syndrome (1); in 5 chorioretinal biopsy specimens with acute retinal necrosis (2), multifocal choroiditis (1), sarcoidosis (1), and subretinal fibrosis and uveitis (1); and in 3 normal control eyes. Results: Fas and FasL were constitutively expressed in the normal human retina, but they were expressed much less in the choroid. Increased expression of Fas and FasL was found in the retina, chorioretinal scar, and choroidal granulomas in uveitic eyes. However, Fas and FasL expression was absent in the biopsy specimens with acute retinal necrosis, and little Fas or FasL was noted on infiltrating lymphocytes. DNA fragmentation was also identified in eyes with chorioretinal scar and gliosis. Conclusions: Apoptosis occurs in uveitic eyes and may play a regulatory role in limiting ocular inflammation. In uveitic eyes, a dysregulation of the Fas-FasL apoptotic pathway may lead to gliosis and fibrosis. References 1. Pepose JS, Holland GN, Wilhelmus KR. Ocular Infection & Immunity . St Louis, Mo: Mosby-Year Book Inc; 1996. 2. Nussenblatt RB, Whitcup WM, Palestine AG. Uveitis: Fundamentals and Clinical Practice . 2nd ed. St Louis, Mo: Mosby-Year Book Inc; 1996. 3. Chan CC, Li Q. The immunopathology of uveitis. Br J Ophthalmol. In press. 4. Whitcup SM, Chan CC, Li Q, Nussenblatt RB. Expression of cell adhesion molecules in posterior uveitis . Arch Ophthalmol . 1992;110:662-666.Crossref 5. Chan CC, Detrick B, Nussenblatt RB, Palestine AG, Fujikawa LS, Hooks JJ. HLA-DR antigens on retinal pigment epithelial cells from patients with uveitis . Arch Ophthalmol . 1986;104:725-729.Crossref 6. Cohen J. Apoptosis . Immunol Today . 1993;14:126-130.Crossref 7. Savill J, Fadok V, Henson P, Haslett C. Phagocyte recognition of cells undergoing apoptosis . Immunol Today . 1993;14:131-136.Crossref 8. Carson D, Ribeiro JM. Apoptosis and disease . Lancet . 1993;341:1251-1254.Crossref 9. Nagata S. Fas and Fas ligand: a death factor and its receptor . Adv Immunol . 1994;57:129-144. 10. Nagata S, Golstein P. The Fas death factor . Science . 1995;267:1449-1456.Crossref 11. Lynch DH, Ramsdell F, Alderson MR. Fas and FasL in the homeostatic regulation of immune responses . Immunol Today . 1995;16:569-574.Crossref 12. D'Souza SD, Bonetti B, Balasingam V, et al. Multiple sclerosis: Fas signaling in oligodendrocyte cell death . J Exp Med . 1996;184:2361-2370.Crossref 13. Giordanoc C, Stassi G, Galluzzo A. Potential involvement of Fas and its ligand in the pathogenesis of Hashimoto's thyroiditis . Science . 1997;275:960-964. 14. Griffith TS, Herndon JM, Green DR, Ferguson TA. CD95-induced apoptosis of lymphocytes in an immune privileged site induces immunological tolerance . Immunity . 1996;5:7-16.Crossref 15. Griffith T, Brunner T, Fletcher S, Green D, Ferguson T. Fas ligand-induced apoptosis as a mechanism of immune privilege . Science . 1995;270:1189-1192.Crossref 16. Chan CC, BenEzra D, Rodrigues MM, et al. Immunohistochemistry and electron microscopy of choroidal infiltrates and Dalen-Fuchs nodules in sympathetic ophthalmia . Ophthalmology . 1985;92:580-590.Crossref 17. Chan CC, Nussenblatt RB, Fujikawa LS, et al. Sympathetic ophthalmia: immunopathological findings . Ophthalmology . 1986;93:690-695.Crossref 18. Chan CC, Wetzig RP, Palestine AG, Kuwabara T, Nussenblatt RB. Immunohistopathology of ocular sarcoidosis . Arch Ophthalmol . 1987;105:1398-1402.Crossref 19. George RK, Chan CC, Whitcup SM, Nussenblatt RB. Ocular immunopathology of Behçet's disease . Surv Ophthalmol . 1997;42:157-162.Crossref 20. Chan C, Palestine A, Kuwabara T, Nussenblatt R. Immunopathologic study of Vogt-Koyanagi-Harada syndrome . Am J Ophthalmol . 1988;105:607-611. 21. Kim MK, Chan CC, Belfort RJ, et al. Histopathologic and immunohistopathologic features of subretinal fibrosis and uveitis syndrome . Am J Ophthalmol . 1987;104:15-23. 22. Martin D, Chan C, de Smet M, et al. The role of chorioretinal biopsy in the management of posterior uveitis . Ophthalmology . 1993;100:705-714.Crossref 23. Chan C, Palestine A, Davis J, et al. Role of chorioretinal biopsy in inflammatory eye disease . Ophthalmology . 1991;98:1281-1286.Crossref 24. Palestine A, Nussenblatt R, Chan C, Hooks J, Friedman L, Kuwabara T. Histopathology of the subretinal fibrosis and uveitis syndrome . Ophthalmology . 1985;92:834-844.Crossref 25. Gavrieli Y, Sherman Y, Ben-Sasson SA. Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation . J Cell Biol . 1992;119:493-501.Crossref 26. Suda T, Okazaki T, Naito Y, et al. Expression of the Fas ligand in cells of T cell lineage . J Immunol . 1995;154:3806-3813. 27. Trauth EC, Klas C, Peters AM, et al. Monoclonal antibody-mediated tumor regression by induction of apoptosis . Science . 1989;245:301-305.Crossref 28. Suda T, Nagata S. Purification and characterization of the Fas-ligand that induces apoptosis . J Exp Med . 1994;179:873-879.Crossref 29. Suda T, Takahashi T, Golstein P, Nagata S. Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family . Cell . 1993;75:1169-1178.Crossref 30. Cohen PL, Eisenberg RA. Lpr and gld: single gene models of systemic autoimmunity and lymphoproliferative disease . Annu Rev Immunol . 1991;9:243-262.Crossref 31. Berlin J, Armstrong RC, Ottilie S, et al. Death effector domin-containing herpesvirus and poxvirus proteins inhibit both Fas- and TNFR1-induced apoptosis . Proc Natl Acad Sci U S A . 1997;94:1172-1176.Crossref 32. Liu C-C, Young LHY, Young JD-E. Lymphocyte-mediated cytolysis and disease . N Engl J Med . 1996;335:1651-1659.Crossref 33. Cohen P, Eisenberg P. The Ipr and gld genes in systemic autoimmunity: life and death in the Fas lane . Immunol Today . 1992;13:427-428.Crossref 34. Watanabe-Fukunaga R, Brannon C, Copeland N, Jenkins N, Nagata S. Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis . Nature . 1992;356:314-317.Crossref 35. Lynch DH, Watson ML, Alderson MR, et al. The mouse Fas-ligand gene is mutated in gld mice and is part of a TNF family gene cluster . Immunity . 1994;1:131-136.Crossref 36. Aliprantis AO, Diez-Roux G, Mulder LCF, Zychlinsky A, Lang RA. Do macrophages kill through apoptosis? Immunol Today . 1996;17:573-576.Crossref 37. Zembala M, Asherson GL. Human Monocytes . New York, NY: Academic Press Inc; 1989. 38. Gold R, Schmied M, Giegerich G, et al. Differentiation between cellular apoptosis and necrosis by the combined use of in situ tailing and nick translation techniques . Lab Invest . 1994;71:219-225. 39. Shimizu A, Masuda Y, Kitamura H, Ishizaki M, Sugisaki Y, Yamanaka N. Apoptosis in progressive crescentic glomerulonephritis . Lab Invest . 1996;74:941-951. 40. Haslett C, Savill JS, Whyte MK, Stern M, Dransfield I, Meagher LC. Granulocyte apoptosis and the control of inflammation . Philos Trans R Soc Lond B Biol Sci . 1994;345:327-333.Crossref
Sorsby Fundus Dystrophy: Reevaluation of Variable Expressivity in Patients Carrying a TIMP3 Founder MutationFelbor, Ute;Benkwitz, Claudia;Klein, Michael L.;Greenberg, Jacquie;Gregory, Cheryl Y.;Weber, Bernhard H. F.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160739011pmid: 9400791
Abstract Interfamilial phenotypic variations in Sorsby fundus dystrophy (SFD) have given rise to controversy as to whether SFD constitutes more than 1 nosologic entity. The recent identification of the tissue inhibitor of metalloproteinases-3 (TIMP3) as the gene causing SFD has made it possible to readdress the question of genetic and clinical heterogeneity. In this study, we have extended previous findings on a Ser181Cys founder mutation in SFD families from the British Isles and show that carriers of this mutation residing in Canada, the United States, and South Africa likewise are descendants of the British ancestor. In addition, we have reevaluated the question of variable SFD phenotypes by analyzing the available clinical data on carriers of the Ser181Cys mutation. References 1. Sorsby A, Mason MEJ. Gardener N. A fundus dystrophy with unusual features . Br J Ophthalmol . 1949;33:67-97.Crossref 2. Weber BHF, Vogt G, Pruett RC, Stöhr H, Felbor U. Mutations in the tissue inhibitor of metalloproteinases-3 (TIMP3) in patients with Sorsby's fundus dystrophy . Nat Genet . 1994;8:352-356.Crossref 3. Felbor U, Suvanto EA, Forsius HR, Eriksson AW, Weber BHF. Autosomal recessive Sorsby fundus dystrophy revisited: molecular evidence for dominant inheritance . Am J Hum Genet . 1997;60:57-62. 4. Felbor U, Stöhr H, Amann Th, et al. A second independent Tyr168Cys mutation in the tissue inhibitor of metalloproteinases-3 (TIMP3) in Sorsby's fundus dystrophy . J Med Genet . 1996;33:233-236.Crossref 5. Wijesuriya SD, Evans K, Jay MR, et al. Sorsby's fundus dystrophy in the British Isles: demonstration of a striking founder effect by microsatellite-generated haplotyes . Genome Res . 1996;6:92-101.Crossref 6. Carrero-Valenzuela RD, Klein ML, Weleber RG, Murphey WH, Litt M. Sorsby's fundus dystrophy: a family with the Ser181Cys mutation of TIMP3 . Arch Ophthalmol . 1996;114:737-738.Crossref 7. Peters AL, Greenberg J. Sorsby's fundus dystrophy: a South African family with a point mutation on the tissue inhibitor of metalloproteinases-3 gene on chromosome 22 . Retina . 1995;15:480-485.Crossref
Associations With Intraocular Pressure in the Barbados Eye StudyWu, Suh-Yuh;Leske, M. Cristina
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160742012pmid: 9400792
Abstract Objective: To evaluate the demographic, medical, ocular, familial, and other factors possibly associated with intraocular pressure (IOP) in a black population, after excluding persons with any type of glaucoma. Design: The Barbados Eye Study was a populationbased study of a random sample of residents of Barbados, West Indies, aged 40 to 84 years. Participants: A subset of the Barbados Eye Study population consisting of 3752 black Barbados Eye Study participants without glaucoma. Data Collection: A standardized protocol included applanation tonometry and other ocular data, blood pressure measurements, anthropometry, complexion pigmentation gradings, and a comprehensive interview. Main Outcome Measure: Intraocular pressure was based on the average of 3 measurements at the Barbados Eye Study visit. Multiple linear regression was used to evaluate factors associated with IOP. Results: Systolic blood pressure (or hypertension), diabetes history, and age were the major factors positively associated with IOP (P<.01). Other positively related factors were female gender, darker complexion, pulse rate, higher body mass, seasonality, family history of glaucoma, current alcohol use, and current smoking. These factors explained 10% of the variation in IOP. Conclusions: By identifying risk factors, these results define specific subgroups most likely to have an elevated IOP. The high IOP in this population may be linked to the high prevalence of hypertension and diabetes. Aside from age and a family history of glaucoma, none of the risk factors for high IOP evaluated in this study was similar to those associated with open-angle glaucoma. References 1. Leske MC. The epidemiology of open-angle glaucoma: a review . Am J Epidemiol . 1983;118:166-191. 2. Bengtsson B. Some factors affecting the distribution of intraocular pressure in a population . Acta Ophthalmol (Copenh) . 1972;50:33-46.Crossref 3. Leske MC, Podgor MJ. Intraocular pressure, cardiovascular risk variables and visual field defects . Am J Epidemiol . 1983;118:280-287. 4. Hollows FC, Graham PA. Intraocular pressure, glaucoma and glaucoma suspects in a defined population . Br J Ophthalmol . 1966;50:570-586.Crossref 5. Klein BEK, Klein R, Linton KLP. Intraocular pressure in an American community: the Beaver Dam Eye Study . Invest Ophthalmol Vis Sci . 1992;33:2224-2228. 6. Graham P. Epidemiology of simple glaucoma and ocular hypertension . Br J Ophthalmol . 1972;56:223-229.Crossref 7. Shiose Y. The aging effect on intraocular pressure in an apparently normal population . Arch Ophthalmol . 1984;102:883.Crossref 8. Shiose Y, Kawase Y. A new approach to stratified normal intraocular pressure in a general population . Am J Ophthalmol . 1986;101:714-721. 9. Mason RP, Kosoko O, Wilson MR, et al. National survey of the prevalence and risk factors of glaucoma in St Lucia, West Indies, part I: prevalence findings . Ophthalmology . 1989;96:1363-1368.Crossref 10. Tielsch JM, Sommer A, Katz J, et al. Racial variations in the prevalence of primary open-angle glaucoma: the Baltimore Eye Survey . JAMA . 1991;266:369-374.Crossref 11. Leske MC, Connell AMS, Schachat AP, et al. The Barbados Eye Study: prevalence of open angle glaucoma . Arch Ophthalmol . 1994;112:821-829.Crossref 12. Burt VL, Whelton P, Roccella EJ, et al. Prevalence of hypertension in the US adult population: results from the third National Health and Nutrition Examination Survey, 1988-91 . Hypertension . 1995;25:305-313.Crossref 13. Freeman V, Fraser H, Forrester T, et al. A comparative study of hypertension prevalence, awareness, treatment and control rates in St Lucia, Jamaica and Barbados . J Hypertens . 1996;14:495-501.Crossref 14. Carter JS, Pugh JA, Monterrosa A. Non-insulin dependent diabetes mellitus in minorities in the United States . Ann Intern Med . 1996;125:221-232.Crossref 15. Leske MC, Connell AMS, Wu SY, et al. Risk factors for open-angle glaucoma: the Barbados Eye Study . Arch Ophthalmol . 1995;113:918-924.Crossref 16. Leske MC, Nemesure B, He Q, et al. Open-angle glaucoma and blood groups: the Barbados Eye Study . Arch Ophthalmol . 1996;114:205-210.Crossref 17. Nemesure B, Leske MC, He Q, et al. Analyses of reported family history of glaucoma: a preliminary investigation . Ophthalmic Epidemiol . 1996;3:135-141.Crossref 18. Leske MC, Connell AMS, Wu S-y, Hyman L, Schachat AP, for the Barbados Eye Study Group. Distribution of intraocular pressure: the Barbados Eye Study . Arch Ophthalmol . 1997;115:1051-1057.Crossref 19. Rose GA. The diagnosis of ischemic heart pain and intermittent claudication in field surveys . WHO Bull . 1962;27:645-658. 20. Ganley JP. Epidemiological aspects of ocular hypertension . Surv Ophthalmol . 1980;25:130-135.Crossref 21. Tielsch JM, Katz J, Sommer A, et al. Hypertension, perfusion pressure, and primary open-angle glaucoma: a population-based assessment . Arch Ophthalmol . 1995;113:216-221.Crossref 22. Tielsch JM, Katz J, Quigley HA, et al. Diabetes, intraocular pressure, and primary open-angle glaucoma in the Baltimore Eye Survey . Ophthalmology . 1995;102:48-53.Crossref 23. Hiller R, Sperduto RD, Krueger DE. Race, iris pigmentation, and intraocular pressure . Am J Epidemiol . 1982;115:674-683. 24. Klein BEK, Klein R. Intraocular pressure and cardiovascular risk variables . Arch Ophthalmol . 1981;99:837-839.Crossref 25. Carel RS, Korczyn AD, Rock M, et al. Association between ocular pressures and health parameters . Ophthalmology . 1984;91:311-314.Crossref 26. Bulpitt CJ, Hodes C, Everitt MG. Intraocular pressure and systemic blood pressure in the elderly . Br J Ophthalmol . 1975;59:717-720.Crossref 27. Morgan RW, Drance SM. Chronic open-angle glaucoma and ocular hypertension: an epidemiological study . Br J Ophthalmol . 1975;59:211-215.Crossref 28. Armaly MF. The genetic determination of ocular pressure in the normal eye . Arch Ophthalmol . 1967;78:187-192.Crossref 29. Bouzas AG, Gragoudas ES, Balodimos MCC, et al. Intraocular pressure in diabetes . Arch Ophthalmol . 1971;85:423-427.Crossref 30. Pan-American Health Organization. Health Conditions in the Americas . Washington, DC: PAHO; 1990:2. Scientific publication 524. 31. Katz J, Sommer A. Risk factors for open angle glaucoma . Am J Prev Med . 1988;4:110-114. 32. Kahn HA, Milton RC. Alternative definitions of open-angle glaucoma: effect on prevalence and associations in the Framingham Eye Study . Arch Ophthalmol . 1980;98:2172-2177.Crossref 33. Wilson MR, Hertzmark E, Walker AM, et al. A case-control study of risk factors in open angle glaucoma . Arch Ophthalmol . 1987;105:1066-1071.Crossref 34. Blumenthal M, Blumenthal R, Peritz E, et al. Seasonal variation in intraocular pressure . Am J Ophthalmol . 1970;69:608-610. 35. Sveinsson K. Glaucoma and heredity in Iceland . Acta Ophthalmol . 1959;37:192. 36. Tielsch JM, Katz J, Sommer A, et al. Family history and risk of primary openangle glaucoma: the Baltimore Eye Survey . Arch Ophthalmol . 1994;112:69-73.Crossref
Small Choroidal MelanomaMurray, Timothy G.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160747013pmid: 9400793
Abstract In this issue of the Archives, the Collaborative Ocular Melanoma Study (COMS) Group reports on factors that are predictive of growth and treatment of small choroidal melanomas based on data generated from their small-tumor observational study.1 Their article sets the stage for an ongoing debate in the evaluation and management of patients with presumed small choroidal melanomas. Uveal melanoma is the most common primary intraocular malignant neoplasm in adults. The management of patients with this malignancy has been a topic of controversy for decades. In 1985 the National Eye Institute,joined by the National Cancer Institute in 1991, funded the COMS Group to evaluate the treatment of choroidal melanoma.2 The COMS was structured in 3 protocols: 2 randomized clinical trials to evaluate treatment of medium and large choroidal melanomas and a third, nonrandomized study of small choroidal melanomas.3 The large-tumor treatment trial compared fractionated external beam radiotherapy prior References 1. Collaborative Ocular Melanoma Study Group. Factors predictive of growth and treatment of small choroidal melanoma: COMS Report No. 5 . Arch Ophthalmol . 1997;115:1537-1544.Crossref 2. Collaborative Ocular Melanoma Study Group. COMS Manual of Procedures . Springfield, Va: National Technical Information Service; 1995. Publication PB95-179693. 3. Collaborative Ocular Melanoma Study Group. Design and methods of a clinical trial for a rare condition: the Collaborative Ocular Melanoma Study: COMS Report No.3 . Control Clin Trials . 1993;14:362-391.Crossref 4. Zimmerman L, McLean IW, Foster WD. Does enucleation of the eye containing a malignant melanoma prevent or accelerate the dissemination of tumour cells? Br J Ophthalmol . 1978;62:420-425.Crossref 5. Collaborative Ocular Melanoma Study Group. Accuracy of diagnosis of posterior uveal melanomas . Arch Ophthalmol . 1990;108:1268-1273.Crossref 6. Diener-West M, Hawkins BS, Markowitz JA, Schachat AP. Review of mortality from choroidal melanoma, II: a meta-analysis of 5-year mortality rates following enucleation, 1966 through 1988 . Arch Ophthalmol . 1992;110:245-250.Crossref 7. Augsburger JJ. Is observation really appropriate for small choroidal melanomas? Trans Am Ophthalmol Soc . 1993;91:147-174. 8. Zimmerman L, McLean I. Do growth and onset of symptoms of uveal melanomas indicate subclinical metastasis? Ophthalmology . 1984;91:685-691.Crossref 9. Thomas J, Green W, Maumenee A. Small choroidal melanomas: a long-term follow-up study . Arch Ophthalmol . 1979;97:861-864.Crossref 10. Shields CL, Shields JA, Kiratli H, De Potter R, Cater JR. Risk factors for growth and metastases of small choroidal melanocytic lesions . Ophthalmology . 1995;102:1351-1361.Crossref 11. Shammas HF, Blodi FC. Prognostic factors in choroidal and ciliary body melanomas . Arch Ophthalmol . 1977;95:63-69.Crossref 12. Seddon JM, Albert DM, Lavin PT. A prognostic factor study of disease-free interval and survival following enucleation for uveal melanoma . Arch Ophthalmol . 1983;101:1894-1899.Crossref 13. Packard R. Pattern of mortality in choroidal malignant melanoma . Br J Ophthalmol . 1980;64:565-575.Crossref 14. Pach J, Robertson D. Metastasis from untreated uveal melanomas . Arch Ophthalmol . 1986;104:1624-1625.Crossref 15. McLean I, Zimmerman L, Evans R. Uveal melanoma: location, size, cell type, and enucleation as risk factors in metastasis . Hum Pathol . 1982;13:123-132.Crossref 16. McLean I, Foster WD, Zimmerman LE. Prognostic factors in small malignant melanomas of choroid and ciliary body . Arch Ophthalmol . 1977;95:48-58.Crossref 17. Gass JDM. Observation of suspected choroidal and ciliary body melanomas for evidence of growth prior to enucleation . Ophthalmology . 1980;87:523-528.Crossref 18. Davidorf FH, Lang JR. The natural history of malignant melanoma of the choroid: small vs large tumors . Trans Am Acad Opthalmol Otolaryngol . 1975;79:310-320. 19. Butler P, Char DH, Zarvin M, Kroll S. Natural history of indeterminate pigmented choroidal tumors . Ophthalmology . 1994;101:710-716.Crossref 20. Barr CC, Sipperley JO, Nicholson DH. Small melanomas of the choroid . Arch Ophthalmol . 1978;96:1580-1582.Crossref 21. Augsburger JJ, Schroeder RP, Territo C, Gamel JW, Shields JA. Clinical parameters predictive of enlargement of melanocytic choroidal lesions . Br J Ophthalmol . 1989;73:911-917.Crossref 22. Zimmerman L, McLean I. The natural course of untreated uveal melanomas . Doc Ophthalmol . 1980;50:75-82.Crossref 23. Collaborative Ocular Melanoma Study Group. Mortality in patients with small choroidal melanoma: COMS Report No.4 . Arch Ophthalmol . 1997;115:886-893.Crossref 24. Kupfer C. In discussion: Risk factors for growth and metastasis of small choroidal melanocytic lesions . Trans Am Ophthalmol Soc . 1995;93:277.
Maximal Medical Therapy for GlaucomaZimmerman, Thom J.;Fechtner, Robert D.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160749014pmid: 9400794
Abstract Not too LONG AGO, maximal tolerated medical therapy (MTMT) for glaucoma usually meant a β-blocker, a cholinergic agent (usually pilocarpine or carbachol), and an oral carbonic anhydrase inhibitor (CAI) (usually diamox or neptazane). Sometimes epinephrine or dipivefrin was added to the regimen. Prescribing MTMT for an individual patient depended on whether or not that patient could tolerate any or all of this regimen. With MTMT compliance was always suspect, not just because of the side effects of these drugs, especially the cholinergic agents and the CAIs, but also because of the difficult dosing schedules. At worst, a patient would be taking 4 pills and 6 to 8 drops in each eye daily. The morning and evening dosing could take 15 minutes under the best conditions (the patient applying bilateral nasolacrimal occlusion while a family member administered drops to both eyes every 5 minutes). This would be difficult to tolerate even References 1. Yaldo MK, Shin DH, Parrow KA, Lee SH, Lee SY, et al. Additive effect of 1% apraclonidine hydrochloride to nonselective beta-blockers . Ophthalmology . 1991;98:1075-1078.Crossref 2. Blasini M, Shields MB. Apraclonidine hydrochloride as an adjunct to timolol maleate therapy . J Glaucoma . 1992;1:148-152.Crossref 3. Strahlman E, Tipping R, Vogel R. A double-masked, randomized 1-year study comparing dorzolamide (Trusopt), timolol, and betaxolol . Arch Ophthalmol . 1995;113:1009-1016.Crossref 4. Racz P, Ruzsonyi MR, Nagy ZT, Gaygi Z, Bito LZ. Around-the-clock intraocular pressure reduction with once-daily application of latanoprost by itself or in combination with timolol . Arch Ophthalmol . 1996;114:268-273.Crossref 5. Watson P, Stjemschantz J. A six-month, randomized, double-masked study comparing latanoprost with timolol in open-angle glaucoma and ocular hypertension . Ophthalmology . 1996;103:126-37.Crossref 6. Camras CB. Comparison of latanoprost and timolol in patients with ocular hypertension and glaucoma: a six-month masked, multicenter trial in the United States . Ophthalmology . 1996;103:138-47.Crossref 7. Nordlund JR, Pasquale LR, Robin AL, et al. The cardiovascular, pulmonary, and ocular hypotensive effects of 0.2% brimonidine . Arch Ophthalmol . 1995;113:77-83.Crossref 8. Allen RC, Epstein DL. Additive effect of betaxolol and epinephrine in primary open angle glaucoma . Arch Ophthalmol . 1986;104:1178-1184.Crossref 9. Parrow KA, Hong YJ, Shin DH, Shi DX, McCarty B. Is it worthwhile to add dipivefrin HCI 0.1% to topical beta 1 -,beta 2-blocker therapy? Ophthalmology . 1989;96:1338-1342.Crossref 10. Millar JC, Kaufman PL. PGF2a/pilocarpine interactions on IOP and accommodation in monkeys . Exp Eye Res . 1995;61:677-683.Crossref 11. Clineschmidt CM, Strahlman ER, Anderson K. Comparison of a fixed combination of darzolamide and timolol (bid) to concomitant administration of dorzolamide (tid) plus timolol (bid) in patients with open-angle glaucoma for three months . Invest Ophthalmol Vis Sci . 1995;36( (suppl) ):S736. Abstract. 12. Strohmaier K, Snyder E, Adamsons I. Long-term safety and efficacy of Cosopt, a fixed combination of dorzolamide and timolol . Invest Ophthal Vis Sci . 1996;37( (suppl) ):S1102. Abstract. 13. Gamero GE, Robison MY, Harmon H, Goldsmith LJ, Fechtner RD, Zimmerman TJ. The duration of action of dorzolamide 2% with concomitant use of a topical beta adrenergic antagonist . Invest Ophthalmol Vis Sci . 1996;37( (suppl) ):S1102.
Melanogenic Neuroectodermal Tumor of the Retina (Primary Malignant Melanoma of the Retina)Freitag, Suzanne K.;Eagle, Ralph C.;Shields, Jerry A.;Duker, Jay S.;Font, Ramon L.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160751015pmid: 9400795
Abstract A 35-month-old girl with leukocoria was clinically diagnosed with unilateral sporadic retinoblastoma. Macroscopic examination of her enucleated eye disclosed a white retinal tumor that appeared to be a retinoblastoma. Histopathologic examination, however, revealed that the tumor was composed of poorly differentiated neuroblastic cells, larger spindle-shaped cells, and anaplastic epithelioid cells, which is inconsistent with retinoblastoma. Immunohistochemical testing disclosed that the tumor cells were immunoreactive for melanoma-specific antigen HMB-45, while electron microscopy showed premelanosomes in the tumor cells, both of which are consistent with melanogenesis. To our knowledge, such an ocular tumor has not been reported previously. References 1. Shields JA, Shields CL. Retinoblastoma: clinical and pathologic features . In: Shields JA, Shields CL, eds. Intraocular Tumors: A Text and Atlas . Philadelphia, Pa: WB Saunders Co; 1992:306. 2. Broughton WL, Zimmerman LE. A clinicopathologic study of 56 cases of intraocular medulloepithelioma . Am J Ophthalmol . 1978;85:407-418. 3. Wilson ME, McClatchey SK, Zimmerman LE. Rhabdomyosarcoma of the ciliary body . Ophthalmology . 1990;97:1484-1488.Crossref 4. Shields CL, Shields JA, Milite J, et al. Uveal melanoma in teenagers and children: a report of 40 cases . Ophthalmology . 1991;98:1662-1666.Crossref 5. Shields JA, Eagle RC Jr, Shields CL, De Potter P. Congenital neoplasms of the nonpigmented ciliary epithelium (medulloepithelioma) . Ophthalmology . 1996;103:1998-2006.Crossref 6. Shields JA, Eagle RC Jr, Shields CL, De Potter P. Acquired neoplasms of the nonpigmented ciliary epithelium (adenoma and adenocarcinoma) . Ophthalmology . 1996;103:2007-2016.Crossref 7. Soffer D, Lach B, Constantini S. Melanotic cerebral ganglioglioma: evidence for melanogenesis in neoplastic astrocytes . Acta Neuropathol . 1992;83:315-323.Crossref 8. Boesel CP, Suhan JP, Sayers MP. Melanotic medulloblastoma: report of a case with ultrastructural findings . J Neuropathol Exp Neurol . 1978;37:531-543.Crossref 9. Kapur RP, Bigler SA, Skelly M, Gown AM. Antimelanoma monoclonal antibody HMB-45 identifies an oncofetal glycoconjugate associated with immature melanosomes . J Histochem Cytochem . 1995;40:207-212.Crossref
Primary Basal Cell Carcinoma of the CarunclePoon, Alexander;Sloan, Brian;McKelvie, Penelope;Davies, Rodger
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160755016pmid: 9400796
Abstract Basal cell carcinomas (BCCs) of the caruncle are rare. We report a case of a primary BCC of the caruncle in a 74-year-old man who was seen with a medial interpalpebral lesion. He had a history of sun exposure and multiple malignant neoplasms of the skin. The lesion was excised and histological examination showed a BCC of the caruncle. The clinical history, examination findings, and histological features are given. References 1. Shields CL, Shields JA, White D, Augsburger JJ. Types and frequency of lesions of the caruncle . Am J Ophthalmol . 1986;102:771-778. 2. Luthra CL, Doxanan MT, Green WR. Lesions of the caruncle: a clinicohistopathologic study . Surv Ophthalmol . 1978;23:183-195.Crossref 3. Margo CE, Waltz K. Basal cell carcinoma of the eyelid and periocular skin . Surv Ophthalmol . 1993;38:169-187.Crossref 4. Ash JE. Epibulbar tumors . Am J Ophthalmol . 1950;33:1203-1219. 5. Husain SE, Patrinely JR, Zimmerman LE, Font RL. Primary basal cell carcinoma of the limbal conjunctiva . Ophthalmology . 1993;100:1720-1722.Crossref
Myoepithelioma of the Lacrimal GlandGrossniklaus, Hans E.;Wojno, Ted H.;Wilson, Matthew W.;Someren, Ayten O.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160758017pmid: 9400797
Abstract A right orbital tumor was excised from a 76-year-old woman. Pathological examination showed that the tumor was composed of spindle to cuboidal cells arranged in a solid to trabecular pattern. Immunohistochemical stains were positive for S-100 protein, muscle-specific actin, cytokeratins MAK6 and AE1,3, and glial fibrillary acid protein and negative for CD34 in tumor cells. Ultrastructural features of tumor cells included microvillous processes, intercellular junctions, and intracytoplasmic filaments with electron densities. To our knowledge, this is the first non-spindle cell myoepithelioma noted to arise in the lacrimal gland. This tumor likely has a similar biological behavior to pleomorphic adenoma (benign mixed tumor). References 1. Jakobiec FA, Bilyk JR, Font RL. Orbit . In: Spencer WH, ed. Ophthalmic Pathology. An Atlas and Textbook . Philadelphia, Pa: WB Saunders Co; 1996:2485-2518. 2. Grossniklaus HE, Abbuhl MF, McLean IW. Immunohistologic properties of benign and malignant mixed tumor of the lacrimal gland . Am J Ophthalmol . 1990;110:540-549. 3. Dardick I, Thomas MJ, van Nostrand AWP. Myoepithelioma-new concepts of histology and classification: a light and electron microscopic study . Ultrastruct Pathol . 1989;13:187-224.Crossref 4. Rosenbaum PS, Hahadevia PS, Goodman LA, Kress Y. Acinic cell carcinoma of the lacrimal gland . Arch Ophthalmol . 1995;113:781-785.Crossref 5. Heathcote JG, Hurwitz JJ, Dardick I. A spindlecell myoepithelioma of the lacrimal gland . Arch Ophthalmol . 1990;108:1135-1139.Crossref 6. Font RL, Garner A. Myoepithelioma of the lacrimal gland: report of a case with spindle cell morphology . Br J Ophthalmol . 1992;76:634-636.Crossref 7. Biggs SL, Font RL. Oncocytic lesions of the lacrimal gland . Arch Ophthalmol . 1977;95:474-478.Crossref 8. Proia A. Basal cell adenocarcinoma of the lacrimal gland. Presented at the Annual Verhoeff Society Meeting; May 14,1994; Rochester, Minn. 9. Rootman J. Diseases of the Orbit: A Multidisciplinary Approach . Philadelphia, Pa: JB Lippincott; 1988;119-139; 384-405. 10. Ostrawski ML, Font RL, Halpern J, Nicolitz E, Barnes R. Clear cell epithelial-myoepithelial carcinoma arising in pleomorphic adenoma of the lacrimal gland . Ophthalmology . 1994;101:925-930.Crossref 11. Traweek ST, Kandalaft PL, Mehta P, Battifora H. The human hematopoietic progenitor cell antigen (CD34) in vascular neoplasia . Am J Clin Pathol . 1991;96:25-31. 12. Boniuk M. Spindle cell myoepithelioma of the lacrimal gland. Presented at the Annual Verhoeff Society Meeting; April 18,1996; Houston, Tex.
Pseudomembranous Conjunctivitis Following Topical Gentamicin TherapyBullard, Steven R.;O'Day, Denis M.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160761018pmid: 9400798
Abstract Topical gentamicin sulfate is known to have adverse effects on the cornea and external segment of the eye that include contact dermatoconjunctivitis, punctate keratopathy, and papillary conjunctivitis.1 Focal conjunctival hyperemia with fluorescein staining has also been described.2 We report 2 cases of pseudomembranous conjunctivitis following use of topical gentamicin. To our knowledge, pseudomembranes have not been previously reported as a manifestation of an ocular toxic reaction for topical gentamicin. Report of Cases. Case 1. A 71-year-old white woman had begun treatment with 0.3% (3 mg/mL) gentamicin sulfate drops, 4 times daily, in the left eye following removal of 2 penetrating keratoplasty sutures from a healthy graft that had been placed 18 months previously. Four days later she was seen with a complaint of burning in and redness of her left eye. Her other ocular medications included 1% pilocarpine hydrochloride, twice daily, in both eyes (for 17 months) and References 1. Wilson FM. Adverse external ocular effects of topical ophthalmic medications . Surv Ophthalmol . 1979;24:57-58.Crossref 2. Nauheim R, Nauheim J. Bulbar conjunctival defects associated with gentamicin . Arch Ophthalmol . 1987;105:1321.Crossref 3. Ostler HB. Conjunctival infections and inflammations . In: Diseases of the External Eye and Adnexa: A Text and Atlas . Baltimore, Md: Williams & Wilkins; 1993:chap 3. 4. Wilson FM. Adverse external ocular effects of topical ophthalmic therapy: an epidemiologic, laboratory, and clinical study . Trans Am Ophthalmol Soc . 1983;81:854-965. 5. Abbott RL, Kremer PA, Abrams MA. Bacterial corneal ulcers . In: Tasman W, ed. Duane's Clinical Ophthalmology . Philadelphia, Pa: Lippincott-Raven Publishers; 1995;4:chap 18.
Bilateral Corneal Infection as a Complication of Laser In Situ KeratomileusisWatanabe, Hitoshi;Sato, Shigeru;Maeda, Naoyuki;Inoue, Yoshitsugu;Shimomura, Yoshikazu;Tano, Yasuo
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160763019pmid: 9400799
Abstract Laser in situ keratomileusis (LASIK) as described by Pallikaris et al1 has been shown to be effective in treating a wide range of myopia. Laser in situ keratomileusis has the advantage over excimer photorefractive keratectomy(PRK), that with LASIK there is less stromal wound healing response.2-4 However, LASIK requires the use of a sophisticated microkeratome and greater surgical skill than PRK. Intraoperative and postoperative complications of LASIK but not of PRK include severing of the flap, epithelial ingrowth under the flap, flap wrinkling, and corneal astigmatism.3,4 To our knowledge, however, corneal infection as a complication of LASIK has not been published in the literature. Corneal infection following PRK has been reported in 3 cases, but in each case, the infection was observed in only one eye.5,6 We herein report a case of bilateral severe corneal infection affecting visual acuity in a patient who underwent simultaneous bilateral LASIK. References 1. Pallikaris IG, Papatzanaki ME, Siganos DS, Tsilimbaris MK. A corneal flap technique for laser in situ keratomileusis: human studies . Arch Ophthalmol . 1991;109:1699-1702.Crossref 2. Pallikaris IG, Siganos DS. Excimer laser in situ keratomileusis and photorefractive keratectomy for correction of high myopia . J Refract Corneal Surg . 1994;10:498-510. 3. Marinho A, Pinto MC, Pinto R, Vaz F, Neves MC. LASIK for high myopia: one year experience . Ophthalmic Surg Lasers . 1996;27( (suppl) ):S517-S520. 4. Fiander DC, Tayfour F. Excimer laser in situ keratomileusis in 124 myopic eyes . J Refract Surg . 1995;22( (suppl) ):S234-S236. 5. Sampath R, Ridgeway AEA, Leatherbarrow B. Bacterial keratitis following excimer laser photorefractive keratectomy: a case report . Eye . 1994;8:481-482.Crossref 6. Amayem A, Ali AT,Waring GO III, Ibrahim O. Bacterial keratitis after photorefractive keratectomy . J Refract Surg . 1996;12:642-644. 7. Seiler T, McDonnell PJ. Excimer laser photorefractive keratectomy . Surv Ophthalmol . 1995;40:89-118.Crossref
Hypertensive Retinopathy Simulating Leber Idiopathic Stellate NeuroretinitisNoble, Kenneth G.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160764020pmid: 9400800
Abstract Leber idiopathic stellate neuroretinitis, first described in 1916, may be considered a clinical syndrome complex characterized by (1) sudden onset of visual loss (usually monocular), (2) partial or complete macula star exudate (preceded by a peripapillary exudative neurosensory retinal detachment), and (3) optic nerve swelling with disc capillary leakage. In most cases the origin is unknown although various infectious agents (eg, cat scratch disease, mumps, leptospira, or syphilis) or vascular disorders (eg, acute systemic hypertension, increased intracranial pressure, or ischemic optic neuropathy) have been associated with this syndrome.1-3 The following patient was initially seen with a central serous detachment of the macula without obvious optic disc edema. Findings from subsequent studies and follow-up examinations indicated the typical syndrome complex, probably as a result of systemic hypertension. Report of a Case. A 45-year-old black woman had the sudden onset of blurred vision in the left eye (documented visual acuity was References 1. Dreyer RF, Hopen G, Gass JDM, Smith JL. Leber's idiopathic stellate neuroretinitis . Arch Ophthalmol . 1984;102:1140-1145.Crossref 2. Maitland CG, Miller NR. Neuroretinitis . Arch Ophthalmol . 1984;102:1146-1150.Crossref 3. Gass JDM: Stereoscopic Atlas of Macular Diseases . 4th ed. St Louis, Mo: Mosby—Year Book Inc; 1997:467, 998.
Inflammatory Mass of the Optic Nerve Head Associated With Systemic Bartonella henselae InfectionCunningham, Emmett T.;McDonald, H. Richard;Schatz, Howard;Johnson, Robert N.;Ai, Everett;Grand, M. Gilbert
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160766021pmid: 9400801
Abstract Cat-scratch disease is caused by Bartonella henselae, a pleomorphic gram-negative rod formerly referred to as Rochalimaea henselae. Common ocular sequelae include Parinaud oculoglandular syndrome and neuroretinitis.1 Acute multifocal retinitis with or without optic nerve edema may also occur,2 occasionally causing a branch retinal artery occlusion3 or serous detachment of the neurosensory retina.4 We describe the use of a recently developed indirect fluorescent antibody test5 to document systemic B henselae infection in 2 patients with an unusual inflammatory mass of the optic nerve head after a flulike illness and exposure to cats. Report of Cases. Case 1. A 7-year-old girl was seen with profound loss of vision in her left eye 2 months after an acute febrile illness. Her medical history was notable for multiple recent cat scratches. Best-corrected visual acuity was 20/20 OD and no light perception OS. An afferent pupillary defect was present in References 1. Jones DB. Cat-scratch disease . In: Pepose JS, Holland GN, Wilhelmus KR, eds. Ocular Infection and Immunity . St Louis, Mo: Mosby-Year Book Inc; 1996:1389-1397. 2. Golnik KC, Marotto ME, Fanous MM, et al. Ophthalmic manifestations of Rochalimaea species . Am J Ophthalmol . 1994;118:145-151. 3. Cohen SM, Davis JL, Gass DM. Branch retinal arterial occlusions in multifocal retinitis with optic nerve edema . Arch Ophthalmol . 1995;113:1271-1276.Crossref 4. Zacchei AC, Newman NJ, Sternberg P. Serous retinal detachment of the macula associated with cat scratch disease . Am J Ophthalmol . 1995;120:796-797. 5. Dalton MJ, Robinson LE, Cooper J, Regnery RL, Olson JG, Childs JE. Use of Bartonella antigens for serologic diagnosis of cat-scratch disease at a national referral center . Arch Intern Med . 1995;155:1670-1676.Crossref 6. Fish RH, Hogan RN, Nightingale SD, Anand R. Peripapillary angiomatosis associated with catscratch neuroretinitis . Arch Ophthalmol . 1992;110:323.Crossref 7. Ulrich GG, Waecker NJ Jr, Meister SJ, Peterson TJ, Hooper DG. Cat scratch disease associated with neuroretinitis in a 6-year-old girl . Ophthalmology . 1992;99:246-249.Crossref
Epiretinal Membrane Delamination With a Diamond KnifeMeredith, Travis A.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160768022pmid: 9400802
Abstract Removal of membranes from the retinal surface is an integral part of many vitreoretinal surgical procedures. Two-handed tissue delamination with a knife allows precise and accurate control of dissection planes. A newly designed diamond knife provides the consistently sharp cutting edge required for this technique. References 1. Meredith TA, Kaplan HJ, Aaberg TM. Pars plana vitrectomy techniques for relief of epiretinal traction by membrane segmentation . Am J Ophthalmol . 1980;89:408-413. 2. Charles S. Delamination . In: Vitreous Microsurgery . Baltimore, Md: Williams & Wilkins; 1981:115. 3. Abrams GW, Williams GA. 'En bloc' excision of diabetic membranes . Am J Ophthalmol . 1987;103:302-308.
Conjunctival Squamous Cell Carcinoma Treated With Topical 5-FluorouracilMidena, Edoardo;Boccato, Paolo;Angeli, Claudia Degli
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160770023pmid: 9400803
References 1. Boccato P, Blandamura S, Midena E. Citodiagnostica in Oftalmologia . Rome, Italy: Edizioni Mediche Scientifiche Internazionali; 1994;169-192. 2. Erie JC, Campbell RG, Liesegang TJ. Conjunctival and corneal intraepithelial and invasive neoplasia . Ophthalmology . 1986;93:176-183.Crossref 3. Fraunfelder FT, Wingfield D. Management of intraepithelial conjunctival tumors and squamous cell carcinomas . Am J Ophthalmol . 1 983;95:359-363. 4. de Keizer RJW, de Wolff-Rouendaal D, Van Delft JL. Topical application of 5-fluorouracil in premalignant lesions of cornea, conjunctiva and eyelid . Doc Ophthalmol . 1986;64:31-42.Crossref 5. Yeatts RP, Ford JG, Stanton CA, Reed JW. Topical 5-fluorouracil in treating epithelial neoplasia of the conjunctiva and cornea . Ophthalmology . 1995;102:1338-1344.Crossref
Familial TrichomegalyHarrison, Devin A.;Mullaney, Paul B.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160772024pmid: 9400804
References 1. Rubin PAD. Disorders of the eyelashes and eyebrows . In: Albert DM, Jakobiec FA, eds. Principles and Practice of Ophthalmology . Philadelphia, Pa: WB Saunders Co; 1994:1852. 2. Casanova JM, Puig T, Rubio M. Hypertrichosis of the eyelashes in acquired immunodeficiency syndrome . Arch Dermatol . 1987;123:1599-1601.Crossref 3. Graham DA, Sires BS. Acquired trichomegaly associated with acquired immunodeficiency syndrome . Arch Ophthalmology . 1997;115:557-558.Crossref 4. Gorlin RJ, Cohen MM, Levin LS. de Lange syndrome (Brachmann-de Lange syndrome) . In: Gorlin RJ. Syndromes of the Head and Neck . New York, NY: Oxford University Press; 1990:300-304.
What Is the Evidence Supporting Chemotherapy for Intraocular Retinoblastoma?Hernandez, J. Carlos
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160774025pmid: 9400805
Abstract I read with interest the article by Gallie et al1 in the November 1996 issue of the Archives regarding the use of chemotherapy in eyes with intraocular retinoblastoma. Gallie et al describe a series of 40 eyes treated with focal therapy and chemotherapy—eyes that "conventionally should be enucleated or receive radiotherapy."1 However, 16 (40%) of these 40 eyes contained tumors that measured 10 disc diameters or less (Reese-Ellsworth [RE] classification I-II), which in other institutions would have been treated with focal treatment modalities alone (laser therapy, cryotherapy, and plaque brachytherapy) if the macula was uninvolved. These patients would not have required external beam radiotherapy [EBR], much less enucleation. This discrepancy could be due to the unavailability of plaque brachytherapy in their institution, but this is not mentioned in the text; it is also not explained why the authors did not make this focal modality available to their patients References 1. Gallie BL, Budning A, DeBoer G, et al. Chemotherapy with focal therapy can cure intraocular retinoblastoma without radiotherapy . Arch Ophthalmol . 1996;114:1321-1328.Crossref 2. Murphree AL, Villabianca JG, Deegan WF III, et al. Chemotherapy plus local treatment in the management of intraocular retinoblastoma . Arch Ophthalmol . 1996;114:1348-1356.Crossref 3. Hernandez JC, Brady LW. Conservative treatment of retinoblastoma: the use of plaque brachytherapy . Am J Clin Oncol . 1993;16:397-401.Crossref 4. Eng C, Li FP, Abramson DH, et al. Mortality from second tumors among long-term survivors of retinoblastoma . J Nati Cancer Inst . 1993;85:1121-1128.Crossref
What Is the Evidence Supporting Chemotherapy for Intraocular Retinoblastoma?-ReplyGallie, Brenda L.;Chan, Helen S. L.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160774026
Abstract In reply Dr Hernandez raises 3 questions about our report on the treatment of intraocular retinoblastoma with chemotherapy, cyclosporine, and focal therapy1; however, in each instance he has failed to notice that the answers to his questions are in the published article. First, the 16 eyes with RE group I to II tumors either contained tumors threatening the macula, where brachytherapy or focal therapy alone would have destroyed central vision, or the other eye had a group V tumor that was treated with chemotherapy, as indicated in our publication (in the Table, in Figure 2 [patient 3], and in the first paragraph of the "Patients and Methods" section).1 We agree that group I to II tumors that do not threaten vision should not be treated with chemotherapy. Dr Hernandez did not notice that brachytherapy was used to treat progressive tumor at the ora serrata after chemotherapy in one References 1. Gallie BL, Budning A, DeBoer G, et al. Chemotherapy with focal therapy can cure intraocular retinoblastoma without radiotherapy . Arch Ophthalmol . 1996;114:1321-1328.Crossref 2. Pui CH, Ribeiro RC, Hancock ML, et al. Acute myeloid leukemia in children treated with epipodophyllotoxins for acute lymphoblastic leukemia . N Engl J Med . 1991;325:1682-1687.Crossref 3. Phillips RA, Gill RM, Zacksenhaus E, et al. Why don't germline mutations in RB1 predispose to leukemia? Curr Top Microbiol Immunol . 1992;182:485-491. 4. Winick NJ, McKenna RW, Shuster JJ, et al. Secondary acute myeloid leukemia in children with acute lymphoblastic leukemia treated with etoposide . J Clin Oncol . 1993;11:209-217. 5. Eng C, Li FP, Abramson DH, et al. Mortality from second tumors among longterm survivors of retinoblastoma . J Natl Cancer Inst . 1993;85:1121-1128.Crossref
What Is the Evidence Supporting Chemotherapy for Intraocular Retinoblastoma?-ReplyMurphree, A. Linn;Villablanca, Judith
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160774027
Abstract In reply Dr Hernandez addresses several issues we appreciate the opportunity to clarify. There are several clear reasons for using chemotherapy in addition to local modalities for RE group I and II tumors.1. In the RE classification, group I tumors are less than 4 disc diameters (6 mm) in greatest diameter and are located posterior to the equator. Cryotherapy is not recommended for tumors posterior to the equator.1 Traditional photocoagulation is recommended only for tumors no greater than 3 to 4 mm in diameter2 away from visually important retina. Most group I tumors occur in the posterior pole of young infants with a family history of retinoblastoma. Because of their posterior location, EBR, not cryotherapy or laser photocoagulation, has been the most common treatment.2 The risk of radiationinduced second malignant neoplasms in children younger than 1 year3,4 led us to search for an alternative to References 1. Shields JA, Shields CL. Treatment of retinoblastoma with cryotherapy . Trans Pa Acad Ophthalmol Otolaryngol . 1990;42:977-980. 2. Shields JA, Augsburger JJ. Current approaches to the diagnosis and management of retinoblastoma . Surv Ophthalmol . 1981;25:347-371.Crossref 3. Eng C, Li FP, Abramson DH, et al. Mortality from second tumors among longterm survivors of retinoblastoma . J Natl Cancer Inst . 1993;85:1121-1128.Crossref 4. Frank CM, Abramson DH. Second non-ocular tumors in retinoblastoma survivors: something new you need to know . In: Program and abstracts of the International Symposium on Ocular Tumors ; April 6-10, 1997;Jerusalum, Israel. Abstract. 5. Shields CL, Shields JA, DePotter P, et al. Plaque radiotherapy in the management of retinoblastoma . Ophthalmology . 1993;100:216-224.Crossref 6. Winick NJ, McKenna RW, Shuster JJ, et al. Secondary acute myeloid leukemia in children with acute lymphoblastic leukemia treated with etoposide . J Clin Oncol . 1993;11:209-217.
A Case of Primary Choroidal Melanoma in a Patient With Previous Cutaneous MelanomaAbramson, David H.;Servodidio, Camille A.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160776028pmid: 9400806
Abstract I enjoyed reading the article by Scull et al1 in the June 1997 issue of the Archives. Seventeen years earlier, we had reported a case of simultaneous cutaneous and ocular melanoma.2 It is generally accepted that multifocal malignant melanomas have genetic bases, and I think the suggestion of the authors that there is no predisposition misses the important point that it is exactly the type of patient that we and they describe who does have a predisposition for malignant melanomas. Recent research has suggested that the gene for this condition is on chromosome 9, but that still needs to be completely investigated. References 1. Scull JJ, Alcocer CE, Deschênes J, Burnier MN Jr. Primary choroidal melanoma in a patient with previous cutaneous melanoma . Arch Ophthalmol . 1997;115:796-798.Crossref 2. Abramson DH, Rodriguez-Sains RS, Rubman R. B-K mole syndrome: cutaneous and ocular malignant melanoma . Arch Ophthalmol . 1980;98:1397-1399.Crossref
A Case of Primary Choroidal Melanoma in a Patient With Previous Cutaneous Melanoma-ReplyBurnier, Miguel N.;Peschlow, Alexandra
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160776029
Abstract In reply We thank Dr Abramson and Ms Servodidio for their interest in our article.1 We had several reasons for describing this patient with a history of cutaneous melanoma that was excised 7 years prior to the development of a choroidal melanoma. The main reason was to analyze the difficulties that arise in the differential diagnosis between 2 primary tumors vs metastatic disease. We discussed the fact that the ocular tumor was seen as a single choroidal nodule 7 years after the cutaneous melanoma had been removed. In addition to the absence of systemic disease, this strongly suggests that this patient had 2 primary tumors. We also discussed the value of immunohistochemical markers, particularly S100-β, as a possible tool to aid in the histopathological differential diagnosis between primary and metastatic choroidal melanomas.Abramson and coworkers2 described a 51 -year-old man who had dysplastic nevus syndrome or B-K mole References 1. Scull JJ, Alcocer CE, Deschênes J, Burnier MN. Primary choroidal melanoma in a patient with previous cutaneous melanoma . Arch Ophthalmol . 1997;115:796-798.Crossref 2. Abramson DH, Rodriguez-Sains RS, Rubman R. B-K mole syndrome: cutaneous and ocular malignant melanoma . Arch Ophthalmol . 1980;98:1397-1399.Crossref 3. Vink J, Crijns MB, Mooy CM, et al. Ocular melanoma in families with dysplastic nevus syndrome . J Am Acad Dermatol . 1984;23:858-862.Crossref 4. Holly E, Aston DA, Ahn DK, et al. No excess prior cancer in patients with uveal melanoma . Ophthalmology . 1991;98:608-611.Crossref 5. McLean. Uveal nevi and malignant melanomas . In: Spencer's Ophthalmic Pathology, A Text and Atlas . 4th ed. Philadelphia, Pa:: WB Saunders Co; 1996;3:2121-2168.
Women in OphthalmologyZubcov-Iwantscheff, A. A;Schnaudigel, O. E.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160777032pmid: 9400808
Abstract We read with interest the editorial by Ross1 regarding women in ophthalmology, which appeared in the April 1997 issue of the Archives. The contributions of these scientists inspire women to pursue careers in ophthalmology and vision research. Clearly, the numbers regarding the current representation of women in American academic ophthalmology indicate that improvement is necessary. This trend, of course, is not unique to America. In Europe, we also seek parity. In Frankfurt, in 1842, Maria Francisca Charlotta Gehringin was the first female ophthalmologist approved by Karl VII of Bayern as "operatricin, Leib- und Wundaerztin" (physician and operating surgeon). Gehringin fought to have her privileges accepted by the city of Frankfurt.2 Today, of the 36 ophthalmology chairs in Germany, only one is occupied by a woman—Professor Ingrid Kreissig, at Tübingen. In Austria, in the late 1860s, Isabel Barrows was the first woman admitted to study ophthalmology at the References 1. Ross RD. The emergence of women in ophthalmology . Arch Ophthalmol . 1997;115:544-546.Crossref 2. Hel J. Die Geschichte der Augenheikunde in Frankfurt am Main bis zum Beginn des 19:Jahrhunderts . Frankfurt, Germany: University of Frankfurt; 1965. Dissertation. 3. Tracy Wilkinson. Cultural shock as the Vienna Philharmonic admits women . The Philadelphia Inquirer . (April 20) , 1997:A7. 4. Mülgassner AM. Strabologie im Wiener . Aerztezeitung ½ . (January 25) , 1997:19-20. 5. Treacher-Collins ET. The History and Traditions of the Moorfields Eye Hospital: One Hundred Years of Ophthalmic Discovery and Development . London, England: Lewis; 1929.
Should We Patch Corneal Erosions?-ReplyBrunette, Isabelle;Boisjoly, Hélène Marie
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160777031
Abstract In reply It is true that patients with traumatic corneal abrasions and patients with recurrent erosion syndrome were enrolled in this study. The pathophysiological features of the 2 entities are indeed different. However, despite variable degrees of involvement of the epithelial basement membrane, this group was homogeneous in that in none of the eyes was the involvement posterior to the Bowman layer surface. Moreover, it is often not possible at the time of the emergency visit to identify to what extent the traumatized epithelium was predisposed to erosion. Often the mate of an eye known for a recurrent erosion syndrome will only show minor irregularities1 at the slit lamp, consisting of a few intraepithelial microcysts that can well be missed at the time of this first visit. Furthermore, the presence of microcysts and fingerprint patterns can fluctuate notably from one visit to another.Therefore, we decided to enroll all References 1. Waring GO III, Rodrigues MM, Laibson PR. Corneal dystrophies, 1: dystrophies of the epithelium, Bowman's layer and stroma . Surv Ophthalmol . 1978;23:71-122.Crossref 2. Arbour JD, Brunette I, Boisjoly HM, Shi ZH, Dumas J, Guertin MC. Should we patch corneal erosions? Arch Ophthalmol . 1997;115:313-317.Crossref
An Introduction to the Biology of VisionWeinstein, Joel
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160778033
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract Anyone who has attended a meeting of the Association for Research in Vision and Ophthalmology has probably felt overwhelmed by the explosion of knowledge in the visual neurosciences. The pace of things began to accelerate some time in the early 1960s, when Hubel and Weisel began to unravel the neuronal events that encode complex visual stimuli. This was the beginning of our understanding of parallel processing in the visual system—the concept that various characteristics of visual stimuli, including shape, size, orientation, and color, are extracted by independent neural pathways and recombined at a higher level. It was also the beginning of our understanding of plasticity in the developing visual system, and of the effects of visual deprivation. The breadth and depth of knowledge in these new areas is now so great that it is difficult for a newcomer to know where to start. Many clinical texts unfortunately only impart
Clinical Decisions in Medical Retinal DiseaseBlodi, Christopher F.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160779035
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract This multiauthored text is not quite adequately described by its title. Rather than emphasizing various controversies and situations in which difficult clinical decisions need to be made, this book reviews many of the more common macular diseases. A brief review of fluorescein angiography (but not indocyanine green angiography) is included at the beginning of the book. This is followed by the longest and most extensively referenced chapter, in which Alan Bird, MD, succinctly reviews various retinal dystrophies that can be generally thought of as occurring at the level of the photoreceptors. Many of the chapters cover common conditions such as agerelated macular degeneration and diabetic retinopathy. Especially useful summaries include chapters on myopic macular degeneration, macular holes, radiation retinopathy, and pars planitis. Much useful information is presented here that is often difficult to find in 1 location in other texts. The chapter by J. Arch McNamara, MD, on retinopathy of
Clinical Cases in OphthalmologySabb, Patricia C.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100160779034
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract This concise and easy-to-read book will be useful to all ophthalmology residents. It succinctly covers both rare and common diseases of the eye. Each case begins with an illustrative color clinical photograph, followed by a discussion of the pertinent findings, a differential diagnosis, diagnostic workup, management options, and the prognosis. The case usually concludes with a few tips and 1 or 2 references. This is an excellent quick review for the Ophthalmic Knowledge Assessment Program examination. However, the title is somewhat misleading. The reader is not provided with a clinical history associated with the photograph. Fortunately, the photographs are classic enough that the history of the case can usually be inferred. Future editions might be improved by presenting the photographs as "unknowns" and not revealing the disease process until the applicable findings have been described and discussed.