Propranolol reduces the severity of experimental atheroscle¬ rosis in animal models." ß-Blockers have been shown in vitro to decrease low-density lipoprotein affinity for human arterial wall proteoglycans.7 This antiatherogenic effect may override the effects on the lipoprotein pattern. Even though Coleman et al failed to prove their theory, their recommendations to limit systemic absorption of topical ß-blockers are prudent and should be heeded by all ophthalmologists.
Blake R. Shaw, MD Robert N. Weinreb, MD La Jolla, Calif
1. Coleman AL, Diehl DLC, Jampel HD, Bachorik PS, Quigley HA. Topical timolol decreases plasma high-density lipoprotein cholesterol level. Arch
Ophthalmol. 1990;108:1260-1263.
2. Pocock SJ. Clinical Trials. New York, NY: John Wiley & Sons Inc. 1983:50-65. 3. Van Buskirk EM, Fraunfelder FT. Ocular beta-blockers and systemic effects. Am J Ophthalmol. 1984;98:623-624. 4. Wolinsky H. The effects of beta-adrenergic blocking agents on blood lipid levels. Clin Cardiol. 1987;10:561-566. 5. Byington RP, Worthy J, Craven T, Furberg CD. Propranolol-induced lipid changes and their prognostic significance after a myocardial infarction: the beta-blocker heart attack trial experience. Am J Cardiol. 1990;65:1287-1291. 6. Kaplan JR, Manuck SB, Adams MR, Weingand KW, Clarkson IB. Inhibition of coronary atherosclerosis by propranolol in behaviorally predisposed monkeys fed an atherogenic diet. Circulation. 1987;76:1364-1372. 7. Linden T, Camejo G, Wiklund O, Warnold I, Olofsson SO, Bondjers G. Effect of short-term beta blockade on serum lipid levels and on the interaction of LDL with human arterial proteoglycans. J Clin Pharmacol. 1990;30:124\x=req-\ 131.
In Reply.\p=m-\\p=m-\Wewould like to thank Drs Vogel, Shaw, and Weinreb for their observations regarding the design and conclusions of this study. Ideally, a clinical trial should be randomized and double-masked; under the circumstances, this was not feasible. Although there was no placebo control group, each subject served as his or her own control. To determine our lipid profiles at baseline and during therapy, we used mean lipid profiles calculated from two 12-hour fasting blood samples drawn at least 5 days apart before therapy and two blood samples drawn at least 5 days apart during therapy. By using mean lipid profiles, we minimized variation within volunteers. Our patients exhibited a statistically significant difference. The contention that our results may have resulted from the "passage of time" and "external factors such as diet, exercise, and inadvertent counseling by investigators" assumes that, for some reason, the HDL cholesterol level of the group worsened in a nonrandom way due to the study conditions. There is no reason to believe that this would occur. If anything, subjects who know their cholesterol levels are going to be measured might subconsciously confound the result in the other direction (that is, raising their HDL choles¬ terol levels or lowering their triglycéride levels). In our study, the triglycérides increased and the HDL cholesterol levels decreased; thus, our results are consistent. Dr Vogel calls our sample size "small," yet it yielded a statistically significant difference and is almost twice as large as the group studied by West and Longstaff,1 who, as Dr Vogel points out, found no apparent effect of timolol maléate. One wonders why Dr Vogel does not believe that the latter study had too small a population to conclude that timolol has no effect. Indeed, given the SDs and number of patients in the latter study,1 it has less than a 50% power to detect a signifi¬ cant difference of 0.06 mmol/L in HDL cholesterol levels.2 Fifty-percent power is usually considered far too low to as¬ sume that there is no effect of the experimental treatment. Furthermore, West and Longstaff analyzed their data in a manner that would obscure a difference since they apparently compared the group means (and their SD) before timolol administration with the group means after timolol rather than
paired analysis of values within subjects. Their method of analysis includes in the SD not only the intrasubject variation, but also the intersubject variation, making it more likely that an extraneous factor will confound the question at hand. The issue is not how much the subjects differ from each other in HDL cholesterol levels, but rather whether HDL cholesterol levels change nonrandomly in each subject. Our data, proper¬ ly analyzed to answer this question, showed a significant a
detrimental effect. Drs Weinreb and Shaw asked whether there was a correla¬ tion between the amount of medication used and the change in HDL cholesterol. As we noted in the "Results" section under the heading "Plasma Lipids," there was no statistically signif¬ icant correlation with timolol dose. This study was reviewed and approved by the Johns Hop¬ kins Committee on Clinical Investigation, and both the com¬ mittee and all the volunteers, who were normal or suspected of having glaucoma, were aware of the numerous serious side effects of topical ß-blocker therapy. Therefore, we believe that this study does not provoke ethical concerns. Dr Vogel dismisses the magnitude of the change in HDL cholesterol levels by stating that it was "within the normal range." A reduction in HDL cholesterol of 0.14 mmol/L across a whole population, however, will substantially increase the population-attributable risk.3 A small reduction in HDL cho¬ lesterol levels in a large number of individuals shifts the distribution of HDL cholesterol levels for the whole popula¬ tion. This shift would be associated with increased risk of coronary heart disease in the whole population even if the reduction in HDL cholesterol is small in the individual. As physicians, we are concerned about the population-attribut¬ able risk associated with therapy that is prescribed to hun¬ dreds of thousands of persons currently using topical
ß-blockers.
We cannot address the comments of Drs Vogel, Shaw, and Weinreb that oral ß-blockers may reduce the incidence of myocardial infarction since our study was designed to exam¬ ine the effects of topical timolol only on lipoprotein concentra¬ tions and not on coronary events. We agree with Drs Vogel, Shaw, and Weinreb that further studies of the effect of topical ß-blockers on plasma lipid levels are needed. Is the effect that we found likely to be smaller or greater in a population of patients with glaucoma than in the largely normal group we tested? Is it seen with all ß-blockers? Is it affected by nasolacrimal occlusion? Does the effect in¬ crease or decrease with exposures of longer than 2 months? We were surprised that there seemed to be no available data on the effect of topical ß-blockers on cholesterol when the same group of agents taken orally were known to decrease HDL cholesterol levels. We look forward to further research into these questions. Anne L. Coleman, MD D. L. Chris Diehl, MD Henry D. Jampel, MD Paul S. Bachorik, PhD Harry A. Quigley, MD Los Angeles, Calif 1. West J, Longstaff S. Topical timolol and serum lipoproteins. Br J Oph-
thalmol. 1990;74:663-664. 2. Javitt JC. When does the failure to find a difference mean that there is none? Arch Ophthalmol. 1989;107:1034-1040. 3. Whelton PK. Essential hypertension: therapeutic implications of epidemiological risk estimation. J Hypertens. June 1984;2(suppl 2):3-8.
Photocoagulation for Threshold Retinopathy of Prematurity To the Editor. \p=m-\Thresholdstage III (TS III) has been defined as 5 contiguous clock hours of stage III retinopathy of premaLaser
Downloaded From: http://archopht.jamanetwork.com/ by a Georgetown University Medical Center User on 05/22/2015
in zone 1 or 2 in the presence of disease. The Multicenter Trial of Cryotherapy for ROP (CRYO-ROP) has shown that treatment of TS III reduces the incidence of unfavorable outcome by 46%.' Other investigators suggested that laser photocoagulation is effective in the treatment of ROP, although these studies used different delivery systems, treated at different stages, and varied in their outcome criteria.2 McNamara et al3 presented evidence of successful treatment of TS III ROP with the binocular indirect laser delivery system at the 1990 Annual Scientific Meeting of The Retina Society. Landers et al4 reported a regressive response of TS III ROP with indirect laser photocoagulation in an eye considered at risk for complications from cryotherapy. We report preliminary results on 12 eyes randomized to photocoagulation or cryotherapy for threshold ROP, followed up for 8 to 19 weeks.
turity (ROP)
Patients and Methods.—Infants with TS III ROP were identified the screening protocol of the CRYO-ROP. Once TS III was identified in one eye, treatment was randomized to either laser photocoagulation or cryotherapy and administered within 72 hours after receiving informed consent. If both eyes developed TS III disease simultaneously, one eye was randomized and the other eye underwent the alternate treatment. If both eyes reached TS III ROP asymmetrically, the first eye was randomized and the second eye underwent the alternate treatment. All procedures were performed in the operating department with general anesthesia. Argon green laser photocoagulation was applied to avascular retinas with an HGM laser indirect delivery system (HGM, Salt Lake City, Utah). Moder¬ ate-intensity white burns were placed approximately one-half-spot apart. Photocoagulation was not applied to the neovascular ridge. Cryotherapy was applied as previously described. All infants were subjected to external ocular examinations 24 hours after therapy. Dilated funduscopic examinations to evaluate for re¬ gression of ROP were conducted 4 to 6 days after therapy on a weekly basis until the disease had been treated, then every 2 weeks there¬ after. Treatment was readministered according to CRYO-ROP crite¬ ria. If necessary, the same treatment modality was administered. All six infants in this series developed bilateral TS III ROP. There were three male and three female infants. Estimated gestational age ranged from 24 to 27 weeks. Birth weights ranged from 597 to 936 g. Age at the time of treatment ranged from 33 to 38 weeks. All infants were followed up for at least 8 weeks after treatment. Two eyes of different infants had zone 1 neovascularization; one eye was random¬ ized to cryotherapy and the other underwent laser photocoagulation. The mean number of freezing applications was 51, ranging from 46 to 61. The mean number of photocoagulation burns was 410, ranging from 138 to 655. Regression was evident within 7 to 10 days after a single treatment with either modality in 10 of 12 eyes. Two eyes of different infants, one randomized to laser therapy and the other to cryotherapy, required repeated treatment with the same modality 2 weeks after the initial therapy. The eye undergoing photocoagula¬ tion developed vitreous hemorrhage after administration of the initial therapy. This hemorrhage cleared within 2 weeks, allowing repeated treatment with subsequent regression. The eye requiring repeated treatment with cryotherapy developed a stage 4B retinal
using
detachment.
Comment. —Photocoagulation was as effective as cryother¬ apy in producing regression of TS III ROP in this small series. Photocoagulation may be less injurious to the sclera, minimiz¬ ing treatment effect on eye growth. There were no apparent complications from treatment with the binocular indirect la¬ ser delivery system. All eyes undergoing photocoagulation appeared less inflamed and had less conjunctival chemosis in the period immediately after therapy. Although longer fol¬ low-up is required, laser therapy appears at least as effective as cryotherapy in inducing regression of TS III ROP. Deborah A. Iverson, MD Michael T. Trese, MD Ira K. Orgel, MD George A. Williams, MD Royal Oak, Mich
Reprint requests to Associated Retinal Consultants, 3535 W Thirteen Mile Rd, Suite 632, Royal Oak, MI 48073 (Dr Trese). 1.
Cryotherapy for Retinopathy of Prematurity Cooperative Group.
Multi-
center trial of cryotherapy for retinopathy of prematurity: one-year outcome\p=m-\
structure and function. Arch Ophthalmol. 1990;108:1408-1416. 2. Nagata M, Yamagishi N, Ikeda S. Summarized results of treatment of acute proliferative retinopathy of prematurity during the past 15 years in Tenri Hospital. Acta Soc Ophthalmol Jpn. 1982;86:1236-1244. 3. NcNamara JA, Tasman WS, Brown GC. Laser photocoagulation for retinopathy of prematurity. Presented at the 23rd Annual Scientific Meeting of The Retina Society; October 5,1990; Key Largo, Fla. 4. Landers M III, Semple H, Ruben J, Serdahl C. Argon laser photocoagulation for advanced retinopathy of prematurity. Am J Ophthalmol. 1990;110:429\x=req-\ 430.
Medication-induced Bilateral Anterior Uveitis
To the Editor.\p=m-\I was interested to see the recent article by Tilden et al1 reporting 13 cases of bilateral anterior uveitis caused by systemic use of sulfonamides. It was surprising to learn that, as mentioned in the article, only one case of this cause-effect relationship had been previously reported.2 It reminded me of a patient I saw in 1974 whom I believed had two episodes of medication-induced anterior uveitis; the first as a response to methenamine hippurate, and the second caused by sulfamethoxazole and trimethoprim.
Report of a Case.\p=m-\On November 26, 1974, a 28-year-old black presented with a symmetric, moderately severe, bilateral, anterior uveitis and presumed trabeculitis 2 days after beginning methenamine hippurate for a bladder infection. She had a history of congenital bladder problems that resulted in frequent bladder infections requiring antibiotic treatment. On presentation she had elevated intraocular pressure (27 mm Hg OD and 32 mm Hg OS), corneal bedewing, and decreased visual acuity (20/30 OD and 20/30 OS). All of her signs and symptoms cleared nicely as a result of topical steroids and mydriatic treatment. Ten months later, the patient presented again complaining of photophobia, redness, and aching eyes, which she noted 2 hours after beginning treatment with sulfamethoxazole and trimethoprim and phenazopyridine hydrochloride for another bladder infection. Exami¬ nation revealed bilateral, symmetric, moderate, anterior chamber cell and flare, 360° limbal corneal infiltrates, and mild episcleral hyperemia. Visual acuity and intraocular pressures were normal. Her inflammation again resolved as a result of topical steroids and mydriatic treatment. While avoiding systemic use of the above medications, she had had woman
no recurrence
of anterior uveitis when last seen in 1988.
Comment.—The authors mention that systemic use of sul¬ fonamides as a cause of anterior uveitis is a rarely diagnosed clinical event. This is probably so, but possibly this associa¬ tion has been seen more than is currently appreciated. I encourage others who may have seen such a case, and like me, did not realize that this association was not well documented in the literature, to make their cases known. Richard J. Kolker, MD Baltimore, Md 1. Tilden ME, Rosenbaum JT, Fraunfelder FT. Systemic sulfonamides as a of bilateral, anterior uveitis. Arch Ophthalmol. 1991;109:67-69. 2. Fujardo RV. Acute bilateral anterior uveitis caused by sulfa drugs. In: Saari KM, ed. Uveitis Update. Princeton, NJ: Excerpta Medica; 1984:115-118. cause
A Multilens Case
To the Editor\p=m-\Ophthalmologistscarry several lenses and a scleral depressor for use in eye examinations. Most lenses are kept in individual protective cases that add bulk to laboratory coat pockets (Fig 1). A scleral depressor can easily fall out of a pocket. A wooden case designed to contain three lenses (ie, 20 diopter (D), 28 D, and 90 D) was recently described.1 We describe an easy modification of an existing multilens case that holds a 20-D or panretinal lens, a 28-D or 30-D lens, a 90-D lens, a four-mirror gonioscopic lens, and a scleral
depressor.
Downloaded From: http://archopht.jamanetwork.com/ by a Georgetown University Medical Center User on 05/22/2015
Blake R. Shaw, MD Robert N. Weinreb, MD La Jolla, Calif
1. Coleman AL, Diehl DLC, Jampel HD, Bachorik PS, Quigley HA. Topical timolol decreases plasma high-density lipoprotein cholesterol level. Arch
Ophthalmol. 1990;108:1260-1263.
2. Pocock SJ. Clinical Trials. New York, NY: John Wiley & Sons Inc. 1983:50-65. 3. Van Buskirk EM, Fraunfelder FT. Ocular beta-blockers and systemic effects. Am J Ophthalmol. 1984;98:623-624. 4. Wolinsky H. The effects of beta-adrenergic blocking agents on blood lipid levels. Clin Cardiol. 1987;10:561-566. 5. Byington RP, Worthy J, Craven T, Furberg CD. Propranolol-induced lipid changes and their prognostic significance after a myocardial infarction: the beta-blocker heart attack trial experience. Am J Cardiol. 1990;65:1287-1291. 6. Kaplan JR, Manuck SB, Adams MR, Weingand KW, Clarkson IB. Inhibition of coronary atherosclerosis by propranolol in behaviorally predisposed monkeys fed an atherogenic diet. Circulation. 1987;76:1364-1372. 7. Linden T, Camejo G, Wiklund O, Warnold I, Olofsson SO, Bondjers G. Effect of short-term beta blockade on serum lipid levels and on the interaction of LDL with human arterial proteoglycans. J Clin Pharmacol. 1990;30:124\x=req-\ 131.
In Reply.\p=m-\\p=m-\Wewould like to thank Drs Vogel, Shaw, and Weinreb for their observations regarding the design and conclusions of this study. Ideally, a clinical trial should be randomized and double-masked; under the circumstances, this was not feasible. Although there was no placebo control group, each subject served as his or her own control. To determine our lipid profiles at baseline and during therapy, we used mean lipid profiles calculated from two 12-hour fasting blood samples drawn at least 5 days apart before therapy and two blood samples drawn at least 5 days apart during therapy. By using mean lipid profiles, we minimized variation within volunteers. Our patients exhibited a statistically significant difference. The contention that our results may have resulted from the "passage of time" and "external factors such as diet, exercise, and inadvertent counseling by investigators" assumes that, for some reason, the HDL cholesterol level of the group worsened in a nonrandom way due to the study conditions. There is no reason to believe that this would occur. If anything, subjects who know their cholesterol levels are going to be measured might subconsciously confound the result in the other direction (that is, raising their HDL choles¬ terol levels or lowering their triglycéride levels). In our study, the triglycérides increased and the HDL cholesterol levels decreased; thus, our results are consistent. Dr Vogel calls our sample size "small," yet it yielded a statistically significant difference and is almost twice as large as the group studied by West and Longstaff,1 who, as Dr Vogel points out, found no apparent effect of timolol maléate. One wonders why Dr Vogel does not believe that the latter study had too small a population to conclude that timolol has no effect. Indeed, given the SDs and number of patients in the latter study,1 it has less than a 50% power to detect a signifi¬ cant difference of 0.06 mmol/L in HDL cholesterol levels.2 Fifty-percent power is usually considered far too low to as¬ sume that there is no effect of the experimental treatment. Furthermore, West and Longstaff analyzed their data in a manner that would obscure a difference since they apparently compared the group means (and their SD) before timolol administration with the group means after timolol rather than
paired analysis of values within subjects. Their method of analysis includes in the SD not only the intrasubject variation, but also the intersubject variation, making it more likely that an extraneous factor will confound the question at hand. The issue is not how much the subjects differ from each other in HDL cholesterol levels, but rather whether HDL cholesterol levels change nonrandomly in each subject. Our data, proper¬ ly analyzed to answer this question, showed a significant a
detrimental effect. Drs Weinreb and Shaw asked whether there was a correla¬ tion between the amount of medication used and the change in HDL cholesterol. As we noted in the "Results" section under the heading "Plasma Lipids," there was no statistically signif¬ icant correlation with timolol dose. This study was reviewed and approved by the Johns Hop¬ kins Committee on Clinical Investigation, and both the com¬ mittee and all the volunteers, who were normal or suspected of having glaucoma, were aware of the numerous serious side effects of topical ß-blocker therapy. Therefore, we believe that this study does not provoke ethical concerns. Dr Vogel dismisses the magnitude of the change in HDL cholesterol levels by stating that it was "within the normal range." A reduction in HDL cholesterol of 0.14 mmol/L across a whole population, however, will substantially increase the population-attributable risk.3 A small reduction in HDL cho¬ lesterol levels in a large number of individuals shifts the distribution of HDL cholesterol levels for the whole popula¬ tion. This shift would be associated with increased risk of coronary heart disease in the whole population even if the reduction in HDL cholesterol is small in the individual. As physicians, we are concerned about the population-attribut¬ able risk associated with therapy that is prescribed to hun¬ dreds of thousands of persons currently using topical
ß-blockers.
We cannot address the comments of Drs Vogel, Shaw, and Weinreb that oral ß-blockers may reduce the incidence of myocardial infarction since our study was designed to exam¬ ine the effects of topical timolol only on lipoprotein concentra¬ tions and not on coronary events. We agree with Drs Vogel, Shaw, and Weinreb that further studies of the effect of topical ß-blockers on plasma lipid levels are needed. Is the effect that we found likely to be smaller or greater in a population of patients with glaucoma than in the largely normal group we tested? Is it seen with all ß-blockers? Is it affected by nasolacrimal occlusion? Does the effect in¬ crease or decrease with exposures of longer than 2 months? We were surprised that there seemed to be no available data on the effect of topical ß-blockers on cholesterol when the same group of agents taken orally were known to decrease HDL cholesterol levels. We look forward to further research into these questions. Anne L. Coleman, MD D. L. Chris Diehl, MD Henry D. Jampel, MD Paul S. Bachorik, PhD Harry A. Quigley, MD Los Angeles, Calif 1. West J, Longstaff S. Topical timolol and serum lipoproteins. Br J Oph-
thalmol. 1990;74:663-664. 2. Javitt JC. When does the failure to find a difference mean that there is none? Arch Ophthalmol. 1989;107:1034-1040. 3. Whelton PK. Essential hypertension: therapeutic implications of epidemiological risk estimation. J Hypertens. June 1984;2(suppl 2):3-8.
Photocoagulation for Threshold Retinopathy of Prematurity To the Editor. \p=m-\Thresholdstage III (TS III) has been defined as 5 contiguous clock hours of stage III retinopathy of premaLaser
Downloaded From: http://archopht.jamanetwork.com/ by a Georgetown University Medical Center User on 05/22/2015
in zone 1 or 2 in the presence of disease. The Multicenter Trial of Cryotherapy for ROP (CRYO-ROP) has shown that treatment of TS III reduces the incidence of unfavorable outcome by 46%.' Other investigators suggested that laser photocoagulation is effective in the treatment of ROP, although these studies used different delivery systems, treated at different stages, and varied in their outcome criteria.2 McNamara et al3 presented evidence of successful treatment of TS III ROP with the binocular indirect laser delivery system at the 1990 Annual Scientific Meeting of The Retina Society. Landers et al4 reported a regressive response of TS III ROP with indirect laser photocoagulation in an eye considered at risk for complications from cryotherapy. We report preliminary results on 12 eyes randomized to photocoagulation or cryotherapy for threshold ROP, followed up for 8 to 19 weeks.
turity (ROP)
Patients and Methods.—Infants with TS III ROP were identified the screening protocol of the CRYO-ROP. Once TS III was identified in one eye, treatment was randomized to either laser photocoagulation or cryotherapy and administered within 72 hours after receiving informed consent. If both eyes developed TS III disease simultaneously, one eye was randomized and the other eye underwent the alternate treatment. If both eyes reached TS III ROP asymmetrically, the first eye was randomized and the second eye underwent the alternate treatment. All procedures were performed in the operating department with general anesthesia. Argon green laser photocoagulation was applied to avascular retinas with an HGM laser indirect delivery system (HGM, Salt Lake City, Utah). Moder¬ ate-intensity white burns were placed approximately one-half-spot apart. Photocoagulation was not applied to the neovascular ridge. Cryotherapy was applied as previously described. All infants were subjected to external ocular examinations 24 hours after therapy. Dilated funduscopic examinations to evaluate for re¬ gression of ROP were conducted 4 to 6 days after therapy on a weekly basis until the disease had been treated, then every 2 weeks there¬ after. Treatment was readministered according to CRYO-ROP crite¬ ria. If necessary, the same treatment modality was administered. All six infants in this series developed bilateral TS III ROP. There were three male and three female infants. Estimated gestational age ranged from 24 to 27 weeks. Birth weights ranged from 597 to 936 g. Age at the time of treatment ranged from 33 to 38 weeks. All infants were followed up for at least 8 weeks after treatment. Two eyes of different infants had zone 1 neovascularization; one eye was random¬ ized to cryotherapy and the other underwent laser photocoagulation. The mean number of freezing applications was 51, ranging from 46 to 61. The mean number of photocoagulation burns was 410, ranging from 138 to 655. Regression was evident within 7 to 10 days after a single treatment with either modality in 10 of 12 eyes. Two eyes of different infants, one randomized to laser therapy and the other to cryotherapy, required repeated treatment with the same modality 2 weeks after the initial therapy. The eye undergoing photocoagula¬ tion developed vitreous hemorrhage after administration of the initial therapy. This hemorrhage cleared within 2 weeks, allowing repeated treatment with subsequent regression. The eye requiring repeated treatment with cryotherapy developed a stage 4B retinal
using
detachment.
Comment. —Photocoagulation was as effective as cryother¬ apy in producing regression of TS III ROP in this small series. Photocoagulation may be less injurious to the sclera, minimiz¬ ing treatment effect on eye growth. There were no apparent complications from treatment with the binocular indirect la¬ ser delivery system. All eyes undergoing photocoagulation appeared less inflamed and had less conjunctival chemosis in the period immediately after therapy. Although longer fol¬ low-up is required, laser therapy appears at least as effective as cryotherapy in inducing regression of TS III ROP. Deborah A. Iverson, MD Michael T. Trese, MD Ira K. Orgel, MD George A. Williams, MD Royal Oak, Mich
Reprint requests to Associated Retinal Consultants, 3535 W Thirteen Mile Rd, Suite 632, Royal Oak, MI 48073 (Dr Trese). 1.
Cryotherapy for Retinopathy of Prematurity Cooperative Group.
Multi-
center trial of cryotherapy for retinopathy of prematurity: one-year outcome\p=m-\
structure and function. Arch Ophthalmol. 1990;108:1408-1416. 2. Nagata M, Yamagishi N, Ikeda S. Summarized results of treatment of acute proliferative retinopathy of prematurity during the past 15 years in Tenri Hospital. Acta Soc Ophthalmol Jpn. 1982;86:1236-1244. 3. NcNamara JA, Tasman WS, Brown GC. Laser photocoagulation for retinopathy of prematurity. Presented at the 23rd Annual Scientific Meeting of The Retina Society; October 5,1990; Key Largo, Fla. 4. Landers M III, Semple H, Ruben J, Serdahl C. Argon laser photocoagulation for advanced retinopathy of prematurity. Am J Ophthalmol. 1990;110:429\x=req-\ 430.
Medication-induced Bilateral Anterior Uveitis
To the Editor.\p=m-\I was interested to see the recent article by Tilden et al1 reporting 13 cases of bilateral anterior uveitis caused by systemic use of sulfonamides. It was surprising to learn that, as mentioned in the article, only one case of this cause-effect relationship had been previously reported.2 It reminded me of a patient I saw in 1974 whom I believed had two episodes of medication-induced anterior uveitis; the first as a response to methenamine hippurate, and the second caused by sulfamethoxazole and trimethoprim.
Report of a Case.\p=m-\On November 26, 1974, a 28-year-old black presented with a symmetric, moderately severe, bilateral, anterior uveitis and presumed trabeculitis 2 days after beginning methenamine hippurate for a bladder infection. She had a history of congenital bladder problems that resulted in frequent bladder infections requiring antibiotic treatment. On presentation she had elevated intraocular pressure (27 mm Hg OD and 32 mm Hg OS), corneal bedewing, and decreased visual acuity (20/30 OD and 20/30 OS). All of her signs and symptoms cleared nicely as a result of topical steroids and mydriatic treatment. Ten months later, the patient presented again complaining of photophobia, redness, and aching eyes, which she noted 2 hours after beginning treatment with sulfamethoxazole and trimethoprim and phenazopyridine hydrochloride for another bladder infection. Exami¬ nation revealed bilateral, symmetric, moderate, anterior chamber cell and flare, 360° limbal corneal infiltrates, and mild episcleral hyperemia. Visual acuity and intraocular pressures were normal. Her inflammation again resolved as a result of topical steroids and mydriatic treatment. While avoiding systemic use of the above medications, she had had woman
no recurrence
of anterior uveitis when last seen in 1988.
Comment.—The authors mention that systemic use of sul¬ fonamides as a cause of anterior uveitis is a rarely diagnosed clinical event. This is probably so, but possibly this associa¬ tion has been seen more than is currently appreciated. I encourage others who may have seen such a case, and like me, did not realize that this association was not well documented in the literature, to make their cases known. Richard J. Kolker, MD Baltimore, Md 1. Tilden ME, Rosenbaum JT, Fraunfelder FT. Systemic sulfonamides as a of bilateral, anterior uveitis. Arch Ophthalmol. 1991;109:67-69. 2. Fujardo RV. Acute bilateral anterior uveitis caused by sulfa drugs. In: Saari KM, ed. Uveitis Update. Princeton, NJ: Excerpta Medica; 1984:115-118. cause
A Multilens Case
To the Editor\p=m-\Ophthalmologistscarry several lenses and a scleral depressor for use in eye examinations. Most lenses are kept in individual protective cases that add bulk to laboratory coat pockets (Fig 1). A scleral depressor can easily fall out of a pocket. A wooden case designed to contain three lenses (ie, 20 diopter (D), 28 D, and 90 D) was recently described.1 We describe an easy modification of an existing multilens case that holds a 20-D or panretinal lens, a 28-D or 30-D lens, a 90-D lens, a four-mirror gonioscopic lens, and a scleral
depressor.
Downloaded From: http://archopht.jamanetwork.com/ by a Georgetown University Medical Center User on 05/22/2015
