1991 Archives of Ophthalmology
doi: 10.1001/archopht.1991.01080090004001
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Folk, James C.;Blackhurst, Dawn W.;Alexander, Judith;Elman, Michael J.;Phillips, Deborah A.
1991 Archives of Ophthalmology
doi: 10.1001/archopht.1991.01080090015002pmid: 1718248
Abstract To the Editor. —The Macular Photocoagulation Study (MPS) demonstrated that argon laser treatment reduced severe visual loss in eyes with extrafoveal choroidal neovascularization (CNV) secondary to senile (age-related) macular degeneration or ocular histoplasmosis syndrome.1 However, recurrent CNV was observed in 59% of treated eyes in the senile macular degeneration study (SMDS), and in 30% of treated eyes in the Ocular Histoplasmosis Study (OHS). Recurrence was accompanied by an increased frequency of severe visual loss. We conducted a study of preoperative fundus characteristics that had not been examined in the MPS to identify clues to the pathogenesis of recurrent CNV that might lead to better treatment of patients.In collaboration with the MPS Fundus Photograph Reading Center (MPS-RC), the following six preoperative angiographic characteristics of CNV and surrounding retina were assessed: fluorescein leakage pattern (classic, smudge, or ooze), amount of fluorescein leakage (minimal to severe), contiguous peripheral blocked fluorescence, degree References 1. Macular Photocoagulation Study Group. Recurrent choroidal neovascularization after argon laser photocoagulation for neovascular maculopathy . Arch Ophthalmol . 1986;104:503-512.Crossref
Anderson, Richard L.;Holds, John B.
1991 Archives of Ophthalmology
doi: 10.1001/archopht.1991.01080090016004
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 In Reply. —We thank Small for defining ptosis and also for pointing out that his study demonstrated superior field defects in 97% of patients with a midpupil to upper lid distance of less than 2 mm.He further describes semantic problems such as the use of the term cosmetic in describing operating procedures and in ophthalmic literature. He makes an important distinction between cosmetic and reconstructive surgery. Unfortunately, our literature has referred to many problems that do not interfere with vision as "cosmetic." However, physicians should not refer to a problem as cosmetic in their charts or referral letters, for example, "I am referring you this patient with a cosmetic ptosis." If an insurance company receives such information in a second opinion or in requested records, the surgery will not be covered, regardless of what other information is provided. Therefore, it is important to avoid the term cosmetic and supplant
1991 Archives of Ophthalmology
doi: 10.1001/archopht.1991.01080090016003pmid: 1929944
Abstract To the Editor. —Bravo! The editorial by Anderson and Holds1 in the December 1990 Archives is timely and well done. However, they did not mention the importance of defining ptosis. Until a recent study at the University of Oklahoma, Oklahoma City, there was no accurate definition of this entity. We define ptosis as a midpupil to upper lid distance of less than 2 mm. Ninety-seven percent of patients with ptosis so defined will have restriction of the upper field of vision to 30° or less.2 Although this study was not intended for deciding questions of reimbursement, it is used in this part of the country as a guide for Medicare claims evaluation.Another important semantic issue not stressed in the editorial is the proper use of terms in discussing and reporting diagnoses and surgical procedures. For example, one frequently sees the word cosmetic in ophthalmic literature, especially in References 1. Anderson RL, Holds JB. Does anyone know how to differentiate a 'functional' defect from a cosmetic one? Arch Ophthalmol . 1990;108:1685-1686.Crossref 2. Small RG, Sabates NR, Burrows D. The measurement and definition of ptosis . Ophthalmic Plast Reconstr Surg . 1989;5:171-175.Crossref 3. 42 USC §1395Y. 4. IRC §213(d).
Baudouin, Christophe;Brignole, Françoise;Gastaud, Pierre
1991 Archives of Ophthalmology
doi: 10.1001/archopht.1991.01080090017007pmid: 1929946
Abstract To the Editor. —We were interested in the study by Jaffe and associates,1 disclosing the potential use of immunotoxins to inhibit the growth of retinal pigment epithelial cells in patients with proliferative vitreoretinopathy (PVR). Exposing the proliferating retinal pigment epithelial cells to an immunotoxin composed of a monoclonal antibody directed against transferrin receptor and conjugated to ricin A chain, caused a significant decrease in the number of cells and affected their morphologic appearance. This study was based on the hypothesis that transferrin receptors, which are expressed at high density on various types of proliferating cells, could constitute a useful target for immunotoxins, whereby proliferating retinal pigment epithelial cells would be inhibited during PVR.This hypothesis, however, was investigated by studying the cells in vitro, not in vivo, so that it could be determined whether such antiproliferative agents might be used in patients with PVR. We have been studying PVR References 1. Jaffe GJ, Earnest K, Fulcher S, Lui GM, Houston LL. Antitransferrin receptor immunotoxin inhibits proliferating human retinal pigment epithelial cells . Arch Ophthalmol . 1990;108:1163-1168.Crossref 2. Baudouin C, Fredj-Reygrobellet D, Baudouin F, Lapalus P, Gastaud P. Immunopathological study on proliferative vitreoretinopathy . Am J Ophthalmol . 1989;108:387-394. 3. Baudouin C, Fredj-Reygrobellet D, Gordon WC, et al. Immunohistologic study of epiretinal membranes in proliferative vitreoretinopathy . Am J Ophthalmol . 1990;110:593-598.
1991 Archives of Ophthalmology
doi: 10.1001/archopht.1991.01080090017005pmid: 1929945
Abstract To the Editor. —In the article by Kuriyama et al1 in the November 1990 issue of the Archives, the authors report an unusually high number of retinal detachments due to macular holes. In fact, the largest series in the literature, to our knowledge, reports a 0.6% incidence of macular break as a cause of retinal detachment.2 In our institution, it is rare to see a retinal detachment secondary to a macular hole. On first impression, many detachments in patients with high myopia appear to have a hole in the macula. The detached macula in these patients is extremely thin at the fovea and gives the appearance of a full-thickness hole. Myopic retinal detachments frequently have very small peripheral tears that are difficult to see. The majority of the patients in the article by Kuriyama et al1 underwent scleral buckling procedures. The repair of the detachments could be References 1. Kuriyama S, Matsumura M, Harada T, Ishigooka H, Ogino N. Surgical techniques and reattachment rates in retinal detachment due to macular hole . Arch Ophthalmol . 1990;108:1559-1561.Crossref 2. Margherio RR, Schepens CL. Macular breaks, I: diagnosis, etiology and observations . Am J Ophthalmol . 1969;4:24.
Kuriyama, Shoji;Matsumura, Miyo;Harada, Takafumi;Ishigooka, Hitoshi;Ogino, Nobuchiki
1991 Archives of Ophthalmology
doi: 10.1001/archopht.1991.01080090017006
Abstract In Reply. —We appreciate Dr Davidorf's interest in our article and his comments regarding the initial operation in a patient with high myopia who has a retinal detachment presumably due to a macular hole. In Japan, it is not rare to see a patient with a retinal detachment due to macular hole. In fact, some Japanese ophthalmologists report a 10% incidence of macular hole causing a retinal detachment, which is much higher than the incidence reported by Margherio and Schepens.1 The difference in the incidence of retinal detachment secondary to a macular hole between Japan and the United States may be attributed to the difference between the races. Our coauthor, Dr Ogino, reported a 27% incidence of associated frequencies of peripheral retinal tears with macular hole and a 13.1% incidence in patients with degenerative myopia.2 These data are in agreement with Dr Davidorf's comments.We evaluated retinal detachment References 1. Margherio RR, Schepens CL. Macular breaks, I: diagnosis, etiology and observations . Am J Ophthalmol . 1969;4:24. 2. Ogino N. Retinal detachment with macular hole: statistical study of some characteristics . Acta Soc Ophthalmol Jpn . 1979;83:275-278.
Finger, Paul T.;Gougelman, Henry P.
1991 Archives of Ophthalmology
doi: 10.1001/archopht.1991.01080090018010
Abstract In Reply. —Several barrier devices have been used in an effort to prevent conjunctival adhesions after chemical burns or cryotherapy or for ocular pemphigoid.1-4 It was not within the scope or format of our letter to the editor to provide a review of similar devices.There are characteristics that differentiate the barrier plaque from the dome-shaped corneal-scleral contact lens described by Ridley.2 In this case, the barrier plaque was manufactured to mold to half of the bulbar conjunctiva with an opening for the cornea. In contrast to the scleral contact lens, we could examine the anterior and posterior segments of the eye and measure intraocular pressure without disturbing the plaque or its function. We found that the suture-fixed barrier plaque was immobile and relatively comfortable.4 We hope Dr Girard will prospectively evaluate the barrier plaque with his patients so as to appreciate its unique qualities in comparison References 1. Cooper WW. On Wounds and Injuries of the Eye . London, England: J Churchill; 1859:285-288. 2. Ridley F. The contact lens in investigation and treatment . Trans Ophthalmol Soc U K . 1954;74:377-410. 3. Girard LJ, Alford WE, Feldman GL, Williams B. Severe alkali burns . Trans Am Acad Ophthalmol Otolaryngol . 1970;74:788-803. 4. Finger PT, Gougelman HP. A barrier plaque designed to prevent conjunctival adhesions . Arch Ophthalmol . 1990;108:1669-1670.Crossref
1991 Archives of Ophthalmology
doi: 10.1001/archopht.1991.01080090018009pmid: 1929947
Abstract To the Editor. —In a recent article in the Archives, Finger and Gougelman1 describe a barrier device used for prevention of symblepharon after cryotherapy as treatment for conjunctival melanosis. Such a device was described by Ridley2 in 1967 and others.3The symblepharon ring will work in the prevention of mild adhesions, but will not prevent symblepharon in severely pathologic conjunctiva, such as chemical burns or ocular pemphigoid. References 1. Finger PT, Gougelman HP. A barrier plaque designed to prevent conjunctival adhesions . Arch Ophthalmol . 1990;108:1669-1670.Crossref 2. Ridley F. Therapeutic lenses . In: Girard LJ, ed. Corneal and Scleral Contact Lenses. Proceedings of the International Congress . St Louis, Mo: CV Mosby Co; 1967:483. 3. Girard LJ, Alford WE, Feldman GL, Williams B. Severe alkali burns . Trans Am Acad Ophthalmol Otolaryngol . 1970;74:788-803.
Jaffe, Glenn J.;Fulcher, Sam;Houston, L. L.
1991 Archives of Ophthalmology
doi: 10.1001/archopht.1991.01080090017008
Abstract In Reply. —We were pleased to see that the data collected by Baudouin et al show transferrin receptors on retinal pigment epithelial cells from subretinal and vitreous fluids in patients with proliferative vitreoretinopathy; thus, these cells are targets for transferrin receptor-specific immunotoxin. Weller et al1 have similarly shown that transferrin receptors are present on cells in PVR membranes, which are additional targets for this agent. These data support the idea that immunotoxins directed against markers of cell proliferation will be useful in treating patients with PVR. Normal, nonproliferating ocular tissues are likely to contain transferrin receptors; therefore, the immunotoxin should selectively inhibit actively dividing cells. We found that the immunotoxin selectively inhibited proliferating, and not quiescent, cells in vitro.2,3 Recently, Davis et al4 reported that transferrin receptors were present in increased numbers on proliferating retinal pigment epithelial cells compared with nonproliferating cells; these data suggest that the References 1. Weller M, Wiedemann P, Motor H, Heimann K. Transferrin and transferrin receptor expression in intraocular proliferative disease: APAAP-immunolabeling of retinal membranes and ELISA for vitreal transferrin . Graefes Arch Clin Exp Ophthalmol . 1989;227:281-286.Crossref 2. Jaffe GJ, Earnest K, Fulcher S, Lui GM, Houston LL. Antitransferrin receptor immunotoxin inhibits proliferating human retinal pigment epithelial cells . Arch Ophthalmol . 1990;108:1163-1168.Crossref 3. Fulcher S, Lui GM, Houston LL, et al. Use of immunotoxin to inhibit proliferating human corneal endothelium . Invest Ophthalmol Vis Sci . 1988;29:755-759. 4. Davis AA, Whidby DE, Privette T, Houston LL, Hunt RC. Selective inhibition of growing pigment epithelial cells by a receptor-directed immunotoxin . Invest Ophthalmol Vis Sci . 1990;31:2514-2519. 5. Hermson VM, Fulcher SFA, Spiekerman AM, Phinizy JL, Di Tullio NW. Long-term inhibition of cellular proliferation by immunotoxins . Arch Ophthalmol . 1990;108:1009-1011.Crossref
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