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  Vol. 120 No. 6, June 2002 TABLE OF CONTENTS
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The Ocular Hypertension Treatment Study

A Randomized Trial Determines That Topical Ocular Hypotensive Medication Delays or Prevents the Onset of Primary Open-Angle Glaucoma

Michael A. Kass, MD; Dale K. Heuer, MD; Eve J. Higginbotham, MD; Chris A. Johnson, PhD; John L. Keltner, MD; J. Philip Miller, AB; Richard K. Parrish II, MD; M. Roy Wilson, MD; Mae O. Gordon, PhD; for the Ocular Hypertension Treatment Study Group

Arch Ophthalmol. 2002;120:701-713.

ABSTRACT

Background  Primary open-angle glaucoma (POAG) is one of the leading causes of blindness in the United States and worldwide. Three to 6 million people in the United States are at increased risk for developing POAG because of elevated intraocular pressure (IOP), or ocular hypertension. There is no consensus on the efficacy of medical treatment in delaying or preventing the onset of POAG in individuals with elevated IOP. Therefore, we designed a randomized clinical trial, the Ocular Hypertension Treatment Study.

Objective  To determine the safety and efficacy of topical ocular hypotensive medication in delaying or preventing the onset of POAG.

Methods  A total of 1636 participants with no evidence of glaucomatous damage, aged 40 to 80 years, and with an IOP between 24 mm Hg and 32 mm Hg in one eye and between 21 mm Hg and 32 mm Hg in the other eye were randomized to either observation or treatment with commercially available topical ocular hypotensive medication. The goal in the medication group was to reduce the IOP by 20% or more and to reach an IOP of 24 mm Hg or less.

Main Outcome Measures  The primary outcome was the development of reproducible visual field abnormality or reproducible optic disc deterioration attributed to POAG. Abnormalities were determined by masked certified readers at the reading centers, and attribution to POAG was decided by the masked Endpoint Committee.

Results  During the course of the study, the mean ± SD reduction in IOP in the medication group was 22.5% ± 9.9%. The IOP declined by 4.0% ± 11.6% in the observation group. At 60 months, the cumulative probability of developing POAG was 4.4% in the medication group and 9.5% in the observation group (hazard ratio, 0.40; 95% confidence interval, 0.27-0.59; P<.0001). There was little evidence of increased systemic or ocular risk associated with ocular hypotensive medication.

Conclusions  Topical ocular hypotensive medication was effective in delaying or preventing the onset of POAG in individuals with elevated IOP. Although this does not imply that all patients with borderline or elevated IOP should receive medication, clinicians should consider initiating treatment for individuals with ocular hypertension who are at moderate or high risk for developing POAG.



INTRODUCTION
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 •Introduction
 •Participants and methods
 •Results
 •Comment
 •Author information
 •References

SURVEYS SHOW that glaucoma is among the leading causes of blindness in the United States and worldwide.1-5 It is estimated that more than 2.5 million people in the United States have glaucoma and that more than 130 000 people are legally blind from the disease.4 Population surveys indicate that less than 50% of those with glaucomatous visual field loss have received an appropriate diagnosis or treatment.6-8

Glaucoma is the leading cause of blindness in individuals of West African origin.2, 9-12 In the Baltimore Eye Survey,2 the age-adjusted prevalence rates of primary open-angle glaucoma (POAG) were 4 to 5 times higher in African Americans than in white individuals. The prevalence ranged from 1.2% in African Americans between the ages of 40 and 49 years to 11.3% in those 80 years and older.11 Furthermore, the Barbados Eye Study7, 12 found a high prevalence and incidence of glaucoma among black individuals in an Afro-Caribbean population.

It is estimated that 3 to 6 million people in the United States, including 4% to 7% of those older than 40 years, have elevated intraocular pressure (IOP) without detectable glaucomatous damage on standard clinical tests.13 These individuals are at increased risk for developing POAG and are sometimes referred to as ocular hypertensives or glaucoma suspects.13-15 Kerrigan-Baumrind et al16 reported that a substantial percentage of the optic nerve fibers are lost before glaucomatous visual field defects can be detected with routine perimetry.

The study of Kerrigan-Baumrind and colleagues, together with the high prevalence of glaucoma and the potentially serious consequences of this disease, could suggest the need for early detection and treatment. However, there is no consensus on the efficacy of medical treatment in delaying or preventing the onset of POAG among individuals with elevated IOP.17-31 Furthermore, it is unclear whether the benefits of treatment outweigh the potential risks of long-term ocular hypotensive medication use. Therefore, the Ocular Hypertension Treatment Study (OHTS) was designed to evaluate the safety and efficacy of topical ocular hypotensive medication in delaying or preventing the onset of POAG in individuals with elevated IOP.


PARTICIPANTS AND METHODS
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The design and methods of the OHTS were described previously,32-35 can be found on the World Wide Web at http://www.vrcc.wustl.edu, and are briefly summarized as follows.

PARTICIPANTS

Eligibility criteria included age between 40 and 80 years, a qualifying IOP between 24 mm Hg and 32 mm Hg in one eye and between 21 mm Hg and 32 mm Hg in the other eye, gonioscopically open angles, 2 normal and reliable visual field tests per eye as determined by the Visual Field Reading Center, and normal optic discs seen at clinical examination and on stereoscopic photographs as determined by the Optic Disc Reading Center. Exclusion criteria included a visual acuity worse than 20/40 in either eye, previous intraocular surgery (other than uncomplicated cataract extraction with posterior chamber lens implantation), and diabetic retinopathy or other diseases capable of causing visual field loss or optic disc deterioration. Both eyes of each participant had to meet eye-specific eligibility criteria. Participants signed a statement of informed consent approved by the institutional review board of each participating clinic.

STUDY DESIGN

This study was conducted at 22 clinical centers; eligible individuals were randomized in equal proportion to either the medication group or observation group. Randomization assignments were released by the Coordinating Center during the participant's baseline visit. The randomization unit was the individual, and randomization was performed using a permuted block design stratified by clinic and race. Neither the participant nor the clinician was masked to the randomization assignment during follow-up.

Participants randomized to medication began treatment to achieve a target IOP of 24 mm Hg or less and a minimum 20% reduction in IOP from the average of the qualifying IOP and IOP at the baseline randomization visit, except that an IOP of less than 18 mm Hg was not required. Topical medication was changed and/or added until both of these goals were met or the participant was receiving maximum-tolerated topical medical therapy. Medications were added and changed in one-eyed therapeutic trials. Drugs were distributed to clinics from the study's central pharmacy, which included all topical ocular hypotensive medications commercially available in the United States. As new medications became commercially available, they were added to the study formulary.

Follow-up visits were scheduled every 6 months from the date of randomization. Each semiannual examination included an ocular and medical history, refraction, best-corrected visual acuity, full-threshold Humphrey white-on-white 30-2 visual field tests, slitlamp examination, IOP measurement, and direct ophthalmoscopy. Additional evaluations at annual visits included a dilated fundus examination and stereoscopic optic disc photographs.

Information on adverse effects was collected using diverse sources of information. Prior to each examination, the participants completed the Glaucoma Symptom Scale,36 a checklist of 13 ocular symptoms and 15 systemic symptoms. They rated the "bothersomeness" of symptoms on a scale of 1 to 4: from 1, "not at all," to 4, "a lot." At annual visits, participants completed the Medical Outcomes Study Short Form (SF-36),37 a survey of 36 questions designed to measure health-related quality of life. At each visit, clinic staff recorded medical and ocular history and completed an adverse-event form when a new health problem was diagnosed, an existing medical condition worsened, an inpatient hospitalization had occurred, or surgery had been required. Clinic staff recorded the organ system affected and determined the severity of the condition. Clinicians judged whether the event was related to the study medication. Serious adverse events were defined as death, cancer or other life-threatening conditions, inpatient hospitalization, prolongation of hospitalization, or outpatient hospitalization for an incapacitating condition. Clinic personnel obtained hospital discharge summaries and death certificates. In January 1997, the OHTS protocol for reporting adverse events was made more rigorous because of large clinic-to-clinic variation in the completion of the adverse-event forms. Therefore, data from the adverse-event forms are reported from January 1997 to the present.

PRIMARY OUTCOME AND MONITORING

The primary outcome was the development of POAG in one or both eyes. This was defined as reproducible visual field abnormality or reproducible clinically significant optic disc deterioration attributed to POAG by the masked Endpoint Committee.

Development of visual field abnormality was determined by masked certified readers at the Visual Field Reading Center. A technically acceptable visual field was considered abnormal if P<.05 for the corrected pattern standard deviation or if the glaucoma hemifield test result was outside normal limits according to StatPac 2 statistical software (StatPac Inc, Minneapolis, Minn). Because most abnormal visual fields were found to be normal when retested,38 the protocol was changed (effective June 1, 1997) so that an endpoint required 3 consecutive abnormal results on visual field tests with the same type, location, and index of abnormality. If a visual field test was judged to be abnormal, the test was repeated at the next visit approximately 6 months later. If the second visual field test was judged to be abnormal, a third visual field test was performed 1 day to 8 weeks later. If 3 consecutive visual field tests met the criteria for abnormality, the Visual Field Reading Center initiated the endpoint review process. Additional details about the process of reviewing visual fields were provided in a previously published article.34

Optic disc deterioration was determined by masked certified readers at the Optic Disc Reading Center. Optic disc deterioration was defined as a generalized or localized thinning of the neuroretinal rim compared with baseline stereoscopic optic disc photographs in side-by-side comparisons. The readers were masked as to which set of photographs was taken at baseline and which set was taken at a follow-up visit. If 1 or both readers in the Optic Disc Reading Center detected a difference between the baseline and follow-up photographs, the photographs were reviewed in a masked fashion by a senior reader. If the senior reader agreed that deterioration had occurred, the Optic Disc Reading Center requested that the affected eye be rephotographed to confirm the change. If readers masked to the result of the first comparison confirmed the deterioration in the second set of photographs, the Optic Disc Reading Center initiated the endpoint review process. The classification of progression in a quality control sample of 86 eyes (50 normal eyes and 36 with progression) showed test-retest agreement at {kappa} = 0.70 (95% confidence interval [CI], 0.55-0.85). Additional details about the process of reviewing optic disc photographs were provided in a previously published article.35

The purpose of the endpoint review process was to distinguish glaucomatous optic nerve and visual field changes from changes due to other causes. The members of the Endpoint Committee were masked to the randomization assignments of the study participants. Each member of the Committee independently reviewed the participant's ocular and medical history, visual fields, and stereoscopic optic disc photographs of both eyes from baseline to the date of review. The Endpoint Committee determined whether visual field changes were due to POAG and whether optic disc deterioration was clinically significant and resulted from POAG. (Examples of clinically significant optic disc deterioration appear on the World Wide Web at http://www.vrcc.wustl.edu.) Barely detectable changes in optic discs were not considered POAG endpoints in the OHTS. Participants classified as developing POAG continued to receive follow-up with regularly scheduled visits and tests. Observation participants who reached a POAG endpoint were prescribed medication. Medication participants who reached a POAG endpoint received increased glaucoma therapy, including argon laser trabeculoplasty and trabeculectomy, at the discretion of the treating clinician.

The Data and Safety Monitoring Committee met twice yearly to review the conduct of the trial, including the safety and efficacy of medication. The Committee approved all protocol changes.

STATISTICAL ANALYSIS

The target sample size of 1500 participants (750 participants per group) was selected to provide 90% power to detect a 40% reduction in the 5-year incidence of POAG (15% incidence in the observation group and 9% incidence in the medication group) with a 2-sided error at {alpha} = .05. The sample size allowed for a 15% loss to follow-up and a 10% crossover between randomization groups. Because of the importance of glaucoma in the African American community, we set a goal of enrolling 400 African Americans among the 1500 participants. Recruitment was expected to take 24 months.

All comparisons of randomization groups were made on an intention-to-treat basis. For the purposes of the primary analysis, the number of days to the onset of POAG was determined by the date of the first abnormal finding that was subsequently confirmed and attributed to POAG. The primary hypothesis was tested using the Mantel-Haenszel log-rank test to compare the cumulative probability of developing POAG in each randomization group. Cox proportional hazards models were used to estimate hazard ratios for POAG, adjusting for the influence of baseline factors. Analyses were performed with SAS statistical software, version 8.1 (SAS Institute Inc, Cary, NC). P values were 2-tailed. To adjust for multiple interim tests of the primary hypothesis, we calculated symmetric O'Brien-Fleming sequential log-rank boundaries using the {alpha}-spending function of Lan and DeMets.39-40

The Data and Safety Monitoring Committee approved the termination of the trial when the last randomized participant reached 5 years of follow-up, as specified in the original protocol. This article includes data through November 8, 2001.


RESULTS
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RECRUITMENT AND BASELINE CHARACTERISTICS OF PARTICIPANTS

Recruitment was extended from 24 months to 30 months to achieve an enrollment of 400 African American participants. Between February 28, 1994, and October 31, 1996, 3328 individuals were considered for study enrollment, and 1636 individuals with documented informed consent were randomized as follows: 817 were assigned to receive topical ocular hypotensive medication, and 819 were assigned to observation. A total of 1692 people were not eligible for randomization for a variety of reasons including an IOP outside the specified range, abnormal or unreliable visual field test results, poor visual acuity, optic disc abnormalities, the inability to obtain clear photographs, and refusal to participate. A flowchart shows the progress of participants during the study (Figure 1).



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Figure 1. Flowchart of participant progress in the Ocular Hypertension Treatment Study (OHTS). The "not randomized" group includes individuals who were ineligible, refused, or were eligible but not randomized.


No statistically significant differences in demographic or clinical factors were found between the 2 randomized groups at baseline (for all comparisons, P>.05) (Table 1). Additional details on the randomized participants were provided in a previously published article.33


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Table 1. Baseline Characteristics by Randomization Group


FOLLOW-UP

The median duration of follow-up was 72 months for African American participants and 78 months for other participants. Of the expected follow-up visits, 90% were completed during the study, and the visit completion rate did not differ by randomization group. The visit completion rate was 86.6% for African Americans and 91.4% for other participants (P<.001). Technically acceptable visual field test results and stereoscopic optic disc photographs were obtained at 99% and 96%, respectively, of the specified completed follow-up visits and did not differ by randomization group. The numbers of participants completing each follow-up visit are shown at the bottom of Figure 2.



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Figure 2. Distribution of intraocular pressure (IOP) at baseline and follow-up for the medication (MED) and observation (OBS) groups. The median IOP in each randomization group is joined by a line. The top and bottom of the boxes include the 75th and 25th percentiles, respectively, and the marks above and below include the 90th and 10th percentiles. Each participant's right and left eye was averaged to calculate a mean. The numbers of participants completing each follow-up visit are shown at the bottom.


ADHERENCE TO RANDOMIZATION

Forty participants in the medication group (4.9%) were withdrawn from medication or chose to stop medication for 6 months or more during the study. Fifteen of these individuals eventually resumed treatment. Forty-two participants in the observation group (5.1%) received topical ocular hypotensive medication for 6 months or more during the study. In most cases, treatment was initiated by the OHTS clinician because of concern about the participant's high IOP. Three of these individuals eventually stopped treatment.

IOP REDUCTION AND MEDICATION

The baseline and follow-up IOP for the medication group and observation group are reported by race in Table 2. The distribution of IOP at baseline and follow-up for the medication and observation groups is shown in Figure 2. The IOP goal was met in both eyes at 87% (7515 of 8621) and in one eye at 7% (613 of 8621) of the scheduled follow-up visits completed by medication participants. Figure 3 shows the percentage of participants who were prescribed each class of topical ocular hypotensive medication at each follow-up visit. At 60 months, 2 or more topical medications were prescribed for 39.7% (259 of 653) of the medication participants, and 3 or more medications were prescribed for 9.3% (61 of 653) of participants in this group. At 60 months, 44.5% (65 of 146) of African American participants in the medication group were prescribed multiple medications, compared with 38.3% (194 of 507) of the other medication participants.


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Table 2. Intraocular Pressure at Baseline and Follow-up in the Medication Group and Observation Group Reported by Race*




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Figure 3. Percentage of medication participants prescribed each class of medication at each follow-up visit. Percentages sum to greater than 100% because more than 1 class of medication may be prescribed. Combination drugs are counted twice.


PRIMARY OPEN-ANGLE GLAUCOMA

Table 3 reports the progress and outcome of randomized participants, unadjusted for follow-up time. In the medication group, 36 of the 817 randomized participants developed POAG compared with 89 of 819 randomized participants in the observation group. The first POAG endpoint for each participant is reported in Table 4. At 60 months, the cumulative probability of developing POAG was 4.4% in the medication group and 9.5% in the observation group. During the course of the entire study, the cumulative probability of developing POAG was significantly lower in the medication group compared with the observation group (hazard ratio, 0.40; 95% CI, 0.27-0.59; Mantel-Haenszel log-rank test; P<.0001) (Figure 4). The estimate of the effect of treatment was not substantially altered after adjusting for baseline age, visual field pattern standard deviation, vertical cup-disc ratio, IOP, and corneal thickness, which was measured after randomization (hazard ratio, 0.34; 95% CI, 0.23-0.51). A treatment benefit was observed for reproducible visual field abnormality attributed to POAG (hazard ratio, 0.45; 95% CI, 0.27-0.76; P = .002) and for reproducible optic disc deterioration attributed to POAG (hazard ratio, 0.36; 95% CI, 0.23-0.56; P<.0001).


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Table 3. Progress and Outcome of Study Participants*



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Table 4. First POAG Endpoint for Each Participant*




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Figure 4. Kaplan-Meier plot of the cumulative probability of developing primary open-angle glaucoma (POAG) by randomization group. The number of participants at risk are those who had not developed POAG at the beginning of each 6-month period. The number of participants classified as developing POAG is given for each interval. Participants who did not develop POAG and withdrew before the end of the study or who died are censored from the interval of their last completed visit.


There was a trend for treatment to be less protective among self-identified African American participants (hazard ratio, 0.54; 95% CI, 0.28-1.03) compared with the other participants in the trial (hazard ratio, 0.34; 95% CI, 0.21-0.56), although this difference was not statistically significant (P = .26). Primary open-angle glaucoma developed in 14 (6.9%) of 203 African American participants in the medication group and 26 (12.7%) of 205 African Americans in the observation group, compared with 22 (3.6%) of 614 other medication participants and 63 (10.2%) of 614 other observation participants.

A total of 218 participants (137 participants in the observation group and 81 participants in the medication group) developed reproducible visual field abnormality or reproducible optic disc deterioration due to POAG or a variety of other causes including trauma, stroke, branch retinal vein occlusion, macular degeneration, and testing artifact. The cumulative probability of developing a reproducible abnormality from any cause was statistically significantly lower in the medication group than in the observation group (hazard ratio, 0.58; 95% CI, 0.44-0.76; P = .00008).

SAFETY

To ascertain the safety of treatment, the medication and observation groups were compared for participant self-report of symptoms (Glaucoma Symptom Scale and SF-36) and for medical and ocular history (new conditions, worsening of existing conditions, hospitalization, prolongation of hospitalization, or death) as collected by clinic staff during the course of the study. The following P values are unadjusted for multiple comparisons between groups. In the self-administered surveys, there was no evidence that the medication group had increased ocular or systemic symptoms compared with the observation group (Figure 5). In the medical and ocular histories collected by clinic staff, a higher percentage of participants in the medication group, compared with the observation group, reported ocular symptoms (57% vs 47%; P<.001) or symptoms affecting the skin, hair, or nails (23% vs 18%; P<.001). The most common symptoms affecting the eyes were dryness, tearing, and itching. Changes in iris color, darkening of the eyelids, and growth of eyelashes occurred in 17% (65 of 380) of the medication participants who were prescribed a prostaglandin analogue for 6 months or longer, compared with 7.6% (48 of 631) of the participants in the observation group (P<.001). There was no difference between randomization groups in total hospitalizations (P = .56), worsening of preexisting conditions (P = .28), or mortality rates (P = .70). There was no difference between groups in visual acuity throughout the study (P>.05 at all follow-up periods). There was a slight excess of cataract surgery in the medication group: 6.4% (52 of 806) of participants compared with 4.3% (35 of 813) of participants in the observation group (P = .06).



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Figure 5. Percentage of participants in the medication group and observation group who rated that they were bothered "a lot" by ocular or systemic symptoms at 1 or more follow-up visits.


Clinic staff recorded serious psychiatric adverse events in 1.5% (12 of 800) of the medication participants compared with 0.5% (4 of 802) of the observation participants (P = .05). Clinicians judged none of the 12 serious psychiatric adverse events in the medication group to be "probably" or "definitely" related to the study medication. Clinic staff recorded serious genitourinary adverse events in 5.5% (44 of 800) of the medication participants compared with 3.4% (27 of 802) of the observation participants (P = .04). Clinicians judged none of the 44 serious genitourinary adverse events in the medication group to be "probably" or "definitely" related to the study medication. These differences were not statistically significant when corrected for multiple comparisons. No differences between randomization groups were found in the rates of serious adverse events for the 11 other organ systems inventoried, including ocular events or those related to the skin, hair, or nails (P>.05).


COMMENT
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 •Participants and methods
 •Results
 •Comment
 •Author information
 •References

The OHTS has shown that topical ocular hypotensive medication is effective in reducing the incidence of glaucomatous visual field loss and/or optic nerve deterioration in individuals with elevated IOP between 24 mm Hg and 32 mm Hg. The mean ± SD baseline IOP of all participants was 24.9 ± 2.7 mm Hg with no difference between randomization groups. Individuals were randomized either to observation or to receive topical ocular hypotensive medication. The goal of treatment was to reduce the IOP by 20% or more and to reach an IOP of 24 mm Hg or less. In the medication group, the mean ± SD reduction in IOP during the follow-up period was 22.5% ± 9.9%. The IOP declined by 4.0% ± 11.6% in the observation group. Randomization groups had similar baseline demographic and clinical characteristics as well as similar rates of visit completion and outcome ascertainment throughout follow-up. The rate of adherence to randomization assignment was high and did not differ by group.

To our knowledge, the OHTS is the largest randomized trial to date of the safety and efficacy of ocular hypotensive medication in delaying or preventing the onset of POAG in individuals with ocular hypertension. At 60 months, the cumulative probability of developing POAG was 4.4% in the medication group and 9.5% in the observation group. It is difficult to compare the incidence of POAG in this study with that in many previous publications because the incidence rate reflects both study-specific eligibility criteria and endpoint criteria. The OHTS used strict entry criteria and included generally healthy volunteers. In addition, stringent endpoint criteria included only reproducible visual field abnormality and optic disc deterioration attributable to POAG. The OHTS used quality control criteria for certifying and monitoring visual field technicians and photographers.

Criteria for POAG were made more stringent during the course of the study. The number of consecutive abnormal visual field test results required to confirm an abnormality was increased from 2 to 3. In addition, the criterion for optic disc deterioration was increased from a "barely detectable difference" to a "clinically significant change" in the optic disc neuroretinal rim.

Because glaucoma is the leading cause of blindness in African Americans, recruitment was extended to ensure that 25% of the sample was of African American origin. Although there was a trend for the treatment benefit to be lower in African Americans than for other participants, the median follow-up time for African American participants was 6 months shorter. It is therefore possible that the treatment response would be more similar with additional follow-up, particularly because the baseline and follow-up IOP in the observation and medication groups did not differ by race.

Topical ocular hypotensive medication reduced the incidence of both glaucomatous visual field abnormality and optic disc deterioration. Approximately 55% (69 of 125) of the initial POAG endpoints involved optic disc deterioration in the absence of visual field abnormalities meeting study criteria for a visual field endpoint. With longer follow-up, we will be able to report how many of the individuals with optic disc deterioration eventually develop visual field loss.

Previous randomized trials on the efficacy of ocular hypotensive medication in delaying or preventing the onset of POAG were divided between those that demonstrated a treatment benefit25-29 and those that did not.19-24,30 However, many of these trials had relatively small sample sizes, short follow-up, and a less sensitive assessment of visual fields. Most previous trials did not evaluate structural changes in the optic disc as a glaucoma outcome. In addition, most trials used only 1 drug, so treatment efficacy was reduced by drug specific nonresponsiveness and medication intolerance.

The OHTS demonstrated that moderate IOP reductions could be attained and maintained during a median follow-up period of 72 months. The treatment target was an IOP of 24 mm Hg or less and a 20% reduction from the average of the qualifying and baseline IOP, but not necessarily a reduction to less than 18 mm Hg. These treatment objectives reflect common clinical practice, but no assumption was made that these IOP levels were ideal for each participant. During the course of the trial, 87% of the medication participants achieved this IOP target reduction in both eyes, and an additional 7% did so in one eye. The use of all commercially available topical ocular hypotensive medications prescribed singly or in combination allowed a high proportion of participants to reach their IOP target.

We monitored the safety of treatment through diverse sources of information. Throughout the study, there was no evidence of excess risk in the medication group for participant-reported symptoms according to the Glaucoma Symptom Scale or SF-36. The medication group had a similar mean visual acuity to the observation group throughout the study. There was no evidence of excess risk in the medication group for the overall number of new medical conditions, worsening of preexisting conditions, hospitalizations, or mortality. We noted a possible excess of serious psychiatric and genitourinary adverse events and cataract surgery in the medication participants. It is unclear whether these few differences are real or a chance occurrence resulting from the large number of comparisons made between the randomization groups. Although the differences between randomization groups were not statistically significant after correcting for multiple comparisons, these findings warrant further study. The use of ocular hypotensive medication may cause more adverse effects in routine practice than reported in this article because the OHTS sample consists of relatively healthy volunteers, with a mean age younger than 60 years, who may be less susceptible to the adverse effects of topical hypotensive medication. The safety experience reported in the OHTS implies the safety of the treatment protocol, not of particular medications. The recent availability of many different types of ocular hypotensive medications should allow clinicians to choose a safe regimen for most patients.

The results of the OHTS do not imply that all individuals with elevated IOP should be treated with ocular hypotensive medication. The decision to recommend treatment should involve many factors, such as (1) the low overall incidence of POAG among individuals with ocular hypertension in population-based studies and this study; (2) the burden of long-term treatment, including possible adverse effects, cost, and inconvenience; (3) the individual's risk of developing POAG; (4) the individual's likelihood of being helped by treatment; and (5) the individual's health status and life expectancy. In our companion article,41 we report baseline factors that predict which participants in the OHTS developed POAG. These factors may be useful to a clinician caring for a patient with ocular hypertension.

For years, ophthalmologists and health policy experts have discussed the lack of data on whether lowering the IOP is useful in POAG.17, 31 The OHTS provides clear proof of the benefit of lowering the IOP. Taken with results from the Normal-Tension Glaucoma Study42 and the Advanced Glaucoma Intervention Study,43 there is now strong evidence that lowering the IOP preserves vision in POAG.


AUTHOR INFORMATION
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Submitted for publication March 6, 2002; final revision received, not applicable; accepted April 10, 2002.

This study was supported by grants EY09341 and EY09307 from the National Eye Institute and the National Center on Minority Health and Health Disparities, National Institutes of Health, Bethesda, Md; Merck Research Laboratories, White House Station, NJ; and by an unrestricted grant from Research to Prevent Blindness, New York, NY.

Drugs were donated by the following pharmaceutical companies: Alcon Laboratories Inc, Fort Worth, Tex; Allergan Therapeutics Group, Irvine, Calif; Bausch & Lomb Pharmaceutical Division, Tampa, Fla; CIBA Vision Corporation, Duluth, Ga; Merck Research Laboratories; Novartis Ophthalmics Inc, Duluth; Otsuka America Pharmaceutical Inc, Rockville, Md; and Pharmacia & Upjohn, Peapack, NJ. Pachymeters were loaned to the clinical centers by DGH Technology, Exton, Pa.

Drs Kass and Gordon take responsibility for authorship, financial disclosure, and copyright transfer for the group.

Financial Disclosures

The following investigators have disclosed a proprietary or financial interest in companies providing medications and/or equipment to the Ocular Hypertension Treatment Study. This information is for 2000-2001, the most current reporting period.

Ingrid Adamsons, MD: Merck, full-time employee. Frank Ashburn, MD: Merck, stock. Roy Beck, MD: Allergan, consultant. Terry Bergstrom, MD: Merck, stock. James D. Brandt, MD: Merck, study principal investigator, honoraria; Allergan, study principal investigator, honoraria. G. A. Cioffi, MD: Alcon, grant support, honoraria; Merck, honoraria; Bausch and Lomb, honoraria; CIBA Vision, honoraria, consultant; Allergan, consultant, grant support, honoraria; Otsuka American Pharmaceutical, grant support; Pharmacia/Upjohn, consultant, grant support, honoraria. Anne Coleman, MD: Merck, stock, honoraria. Anastasios Costarides, MD: Merck, stock; Medi-Pro, consultant. Barry Davis, MD, PhD: Merck, consultant; Pharmacia/Upjohn, consultant. Ronald Gross, MD: Alcon, consultant, grant support, speakers bureau; Allergan, consultant, grant support, speakers bureau; Novartis, grant support, speakers bureau. Dale Heuer, MD: Merck, honoraria, consultant; Pharmacia, honoraria, consultant; Allergan, grant support. Eve Higginbotham, MD: Pharmacia/Upjohn, honoraria; CIBA Vision, consultant; Merck, grant support, honoraria. Nauman Imami, MD: Merck, honoraria; Pharmacia, speakers bureau. Chris Johnson, MD: Humphrey Systems, consultant, grant support; Allergan, consultant; Merck, honoraria; Pharmacia, honoraria. Douglas Johnson, MD: Allergan, grant support. Paul Kalina, MD: Merck, stock. Michael Kass, MD: Merck, consultant; Pharmacia, consultant; Allergan, grant support. John Keltner, MD: Merck, stock. Jody Piltz-Seymour, MD: Merck, consultant; Allergan, grant support. Alan Robin, MD: Alcon, consultant; Pharmacia/Upjohn, honoraria; Humphrey Zeiss, consultant. Arthur Schwartz, MD: Merck, stock; Allergan, consultant; Alcon, consultant; Pharmacia, consultant. Mark Sherwood, MD: Allergan, consultant; CIBA Vision, consultant; Merck, consultant; Pharmacia/Upjohn, consultant. Gregory Skuta, MD: Pharmacia/Upjohn, consultant; Allergan, honoraria; Pharmacia/Upjohn, honoraria. Robert L. Stamper, MD: Allergan, consultant, speakers bureau; Pharmacia, speakers bureau; Alcon, speakers bureau; Merck, speakers bureau. Martin Wax, MD: Pharmacia, consultant. Paul Weber, MD: Merck, stock. Robert N. Weinreb, MD: Allergan, consultant, grant support; Merck, stock, consultant, grant support; Humphrey, grant support; Heidelberg, grant support; Pharmacia/Upjohn, consultant, grant support.

Participating Clinics, Committees, and Resource Centers in the Ocular Hypertension Treatment Study

The following participants were certified on or before November 11, 2001. Principal investigators are listed in italics. Names marked with an asterisk are no longer part of the study.

Clinical Centers

Bascom Palmer Eye Institute, University of Miami, Miami, Fla

Investigators: Donald L. Budenz, MD; Francisco E. Fantes, MD; Steven J. Gedde, MD; Richard K. Parrish II, MD. Coordinators and Staff: Madeline L. Del Calvo, BS; James R. Davis*; Elena Ferrer.*

Eye Consultants of Atlanta (formerly M. Angela Vela, MD, PC), Atlanta, Ga

Investigators: Thomas S. Harbin, Jr, MD; Paul McManus, MD; Charles J. Patorgis, OD; Ron Tilford, MD*; M. Angela Vela, MD*; Randall R. Ozment, MD.* Coordinators and Staff: Laura Brannon, COMT; Montana L. Hooper, COT; Stacey S. Goldstein, COMT; June M. LaSalle Gartlir, COA; Debbie L. Lee, COT; Michelle D. Mondshein; Marianne L. Perry, COT; Julie M. Wright, COT; Linda Butler, COT*; Carla F. Crissey*; Mary Pat Hubert*; Marsha B. Liner*; Teresa Long, COT*; Alma Newkirk*; Emily J. Reese, COA*; Shelly R. Smith, COA*; Ramona Weeden.*

Cullen Eye Institute, Baylor College of Medicine, Houston, Tex

Investigators: Ronald L. Gross, MD; Silvia Orengo-Nania, MD. Coordinators and Staff: Pamela M. Frady, COMT, CCRC; Benita D. Slight, COT, EMT-P, CCRP; Sandy A. Ellis, COA.*

Devers Eye Institute, Portland, Ore

Investigators: George A. (Jack) Cioffi, MD; Elizabeth Donohue, MD; Steven Mansberger, MD; E. Michael Van Buskirk, MD; Julia Whiteside-Michel, MD.* Coordinators and Staff: Kathryn Sherman; JoAnne M. Fraser, COT; Linda Diehl Boly, RN*; Vanora Volk.*

Emory University Eye Center, Atlanta, Ga

Investigators: Allen D. Beck, MD; Anastasias Costarides, MD, PhD; Reay H. Brown, MD*; Mary Lynch, MD*; John Rieser, MD.* Coordinators and Staff: Donna Leef, MMSc, COMT; Jatinder Bansal, COT*; David Jones, COT*; Lillie Reyes, COT.*

Henry Ford Medical Center, Detroit, Mich

Investigators: G. Robert Lesser, MD; Deborah Darnley-Fisch, MD; Nauman R. Imami, MD; James Klein, MD*; Talya Kupin, MD*; Rhett Schiffman, MD.* Coordinators and Staff: Melanie Gutkowski, COMT, CO; Jim Bryant, COT; Ingrid Crystal Fugmann, COMT; Monica R. Gibson, COT; Wendy Gilroy, COMT; Monica Lacoursiere; Sue Loomis, COT; Lauren S. Turner; Amanda Cole-Brown*; Amy Draghiceanu, COMT*; Jeannine M. Gartner*; Norma Hollins, COT, RN*; Melina Mazurk, COT*; Colleen Wojtala.*

Johns Hopkins University School of Medicine, Baltimore, Md

Investigators: Donald J. Zack, MD, PhD; Donald A. Abrams, MD; Nathan G. Congdon, MD, MPH; Robert A. Copeland, MD; David S. Friedman, MD, MPH; Ramzi Hemady, MD; Eve J. Higginbotham, MD; Henry D. Jampel, MD, MHS; Irvin P. Pollack, MD; Harry A. Quigley, MD; Alan L. Robin, MD; Agnes S. Huang, MD*; Omofolasade B. Kosoko, MD, MSPH*; Scott LaBorwit, MD*; Stuart J. McKinnon, MD, PhD*; Sreedhar V. Potarazu, MD*; Scott Drew Smith, MD*; Nancy E. Williams, MD. Coordinators and Staff: Rachel Scott, BS, COA; Rani Kalsi; Felicia Keel, COT; Lisa Levin; Robyn Priest-Reed, MMSc; Mary Ellen Flaks*; Kathy A. Hoffman*; Claudia Johns*; Nicole K. Laviniere*; Patricia Zwaska.*

Charles R. Drew University, Jules Stein Eye Institute, University of California, Los Angeles

Investigators: Anne L. Coleman, MD, PhD; Richard S. Baker, MD; Michelle C. Banks, MD; Y. P. Dang, MD; Simon K. Law, MD; Dana P. Tannenbaum, MD; Baber H. Ali, MD*; Luca O. Brigatti, MD*; Mary R. Chang, MD*; Hyong S. Choe, MD*; Nichola X. Hamush, MD*; Ricky S. Huo, MD*; Leonidas A. Johnson, OD*; Michael S. Kook, MD*; Francis A. La Rosa, MD*; Hung H. Le, MD*; David A. Lee, MD*; John C. Marsh, MD*; Mamdouh L. Nakla, MD*; Irene Fong Sasaki, MD*; Robert K. Stevens, MD*; M. Roy Wilson, MD.* Coordinators and Staff: Jackie R. Sanguinet, BS, COT; Bobbie Ballenberg, COMT; Salvador Murillo; Manju Sharma; Rodolfo X. Garcia*; Rebecca A. Rudenko.*

W. K. Kellogg Eye Center, Ann Arbor, Mich

Investigators: Terry J. Bergstrom, MD; Sayoko E. Moroi, MD, PhD; Andrew N. Bainnson, MD*; Bruce D. Cameron, MD*; Maria S. Gottfreds, MD*; Pam R. Henderson, MD*; Eve J. Higginbotham, MD*; A. Tim Johnson, MD*; Kurt K. Lark, MD*; Mariannette Miller-Meeks, MD*; Robert M. Schertzer, MD.* Coordinators and Staff: Carol J. Pollack-Rundle, BS, COMT; Michelle A. Tehranisa, COT.

Kresge Eye Institute, Wayne State University, Detroit

Investigators: Bret A. Hughes, MD; Monica Y. Allen, MD; Mark S. Juzych, MD; Mark L. McDermott, MD; John M. O'Grady, MD; John M. Ramocki, MD; Dian Shi, MD; Dong H. Shin, MD, PhD; Robert V. Finlay, OD*; Stephen Y. Reed, MD.* Coordinators and Staff: Juan Allen; Laura L. Schulz, CNA; Linda A. Van Conett, COT; Mary B. Hall; Beverly McCarty, LPN;* Chris R. Foster.*

University of Louisville, Louisville, Ky

Investigators: Joern B. Soltau, MD; Gustavo E. Gamero, MD; Judit Mohay, MD; Gökhan Özdemir, MD; Robb R. Shrader, MD; Richard M. Fenton, MD*; Robert D. Fechtner, MD*; Nicholas Karunaratne, MD*; Albert S. Khoury, MD*; Mahnud A. Naser, MD*; Tony Realini, MD*; Jianming Ren, MD*; Michelle Robison, MD*; George V. Shafranov, MD*; Gilbert Sussman, MD*; Mike Roy Willman, MD*; Thomas W. Uihlein, MD*; Thom J. Zimmerman, MD, PhD.* Coordinators and Staff: Sandy Lear, RN; Kathleen Coons, COT; Jane H. Fenton, COT*; Nancy Mahoney*; Linda Upton, COA.*

Mayo Clinic/Foundation, Rochester, Minn

Investigators: David C. Herman, MD; Douglas H. Johnson, MD; Paul H. Kalina, MD; Matthew Hattenhauer, MD*; Erik O. Schoff, MD.* Coordinators and Staff: Becky A. Nielsen, LPN; Nancy J. Tvedt.

New York Eye & Ear Infirmary, New York

Investigators: Jeffrey M. Liebmann, MD; Robert Ritch, MD; Celso A. Tello, MD; Ronald M.Caronia, MD*; David S. Greenfield, MD*; Alyson L. Hall, MD*; Elisa N. Morinelli, MD*; Robert F. Rothman, MD.* Coordinators and Staff: Jean L. Walker, BS, COA; Deborah L. Simon, COA; Kim A. Barget*; Debra Beck, BA, COA*; Jean E. Denaro, MA*; E. Eugenie Hartmann, PhD*; Anna A. Norris*; Melissa X. Perez*; David A. Steinberger.*

Ohio State University, Columbus

Investigators: Paul Weber, MD; N. Douglas Baker, MD; Robert J. Derick, MD; David Lehmann, MD; Omar Mobin-Uddin, MD. Coordinators and Staff: Kathryne McKinney, COMT; Cynthia Hutchinson; Diane Moore, COA; Cynthia A. Williams; Lori Black, COA*; Becky Gloeckner, COT*; Crystal Y. Hendrix Coleman, COT*; Tammy Lauderbaugh*; Billie J. Romans.*

Pennsylvania College of Optometry/MCP Hahnemann University School of Medicine, Philadelphia

Investigators: G. Richard Bennett, MS, OD; Elliot Werner, MD; Myron Yanoff, MD; Sara Foster, OD.* Coordinators and Staff:Lindsay C. Bennett, BA; Mary Jameson, Opt, TR; Maria Massini*; Kim M. Yoakum, BS.*

Scheie Eye Institute, University of Pennsylvania, Philadelphia

Investigators: Jody R. Piltz-Seymour, MD; Teresa L. Brevetti, MD; Donald L. Budenz, MD*; Jeff A. Gordon, MD*; Madhu S. Gorla, MD*; Oneca Heath-Phillip, MD*; Lydia Matkovich, MD*; Frank S. Parisi, MD*; Michelle R. Piccone, MD*; Anna Purna Singh, MD*; Rebecca S. Walker, MD.* Coordinators and Staff: Jane L. Anderson, MS, CCRC; Cheryl McGill, COA; Janice T. Petner, COA; Debbie D. Curry*; Diane L. McDonald, COT*; Bonnie L. Stintsman.*

University of California–Davis, Sacramento

Investigators: James D. Brandt, MD; Jeffrey J. Casper, MD; John T. Dragicevich, MD; Thomas R. Johansen, MD; Esther S. Kim, MD; Michele C. Lim, MD; Michael B. Mizoguchi, MD; Alan M. Roth, MD; Ivan R. Schwab, MD; Richard Bernheimer, MD*; Marcia V. Beveridge, MD*; Craig Bindi, MD*; Marina Chechelnitsky, MD*; Janet K. Han, MD*; Edward V. Hernandez, MD*; Andrea V. Gray, MD*; Denise Kayser, MD*; Soohyung Kim, MD*; Richard L. Nguyen*; Loan Tran, MD.* Coordinators and Staff: Ingrid J. Clark, COA; Vachiraporn X. Jaicheun, COA*; Denise M. Owensby, BS, COA; Marilyn A. Sponzo, COA.

University of California–San Diego, La Jolla

Investigators: Robert N. Weinreb, MD; J. Rigby Slight, MD. Coordinators and Staff: Eva Kroneker, COA; Barbara Brunet*; Maritza K. Antunez*; Dawn Frasier, COT*; Rivak Hoffman, COT*; Kimberly Kebabjian*; Jennifer Kraker*; Marina Madrid*; Julia M. Williams.*

University of California–San Francisco

Investigators: Michael V. Drake, MD; Allan J. Flach, MD; Robert Stamper, MD. Coordinators and Staff: Fermin P. Ballesteros, Jr; Marjan Karimabadi; Valerie Margol; Peggy Yamada, COT; Lou Anne Aber, COA*; Ilya Saltykov.*

University Suburban Health Center, South Euclid, Ohio

Investigators: Kathleen A. Lamping, MD; Gregory A. Eippert, MD; Beverly C. Forcier, MD*; Laurence D. Kaye, MD.* Coordinators and Staff: Angela K. McKean; Bettina J. Modica; Tonya Sims; Susan Van Huss*; Cheryl L. Vitelli; Laura Brevard*; Sheri Burkett Porter, COA*; Elizabeth Laux*; Carla R. DeLaRosa Valenti*; Dina DeLisio*; Kimberly Purkey.*

Washington OHTS Center, Washington DC

Investigators: Douglas E. Gaasterland, MD; Frank S. Ashburn, MD; Arthur L. Schwartz, MD; Howard S. Weiss, MD; Sherri L. Berman, MD*; Alice T. Gasch, MD*; Jane Hughes, MD*; John D. Mitchell, MD*; Guy S. Mullin, MD*; Pedro M. Rivera, MD*; Soo Y. Shin, MD*; Thomas H. Yau, MD*. Coordinators and Staff: Robin L. Montgomery, COA; Donna M. Claggert; Karen D. Schacht, COT; Anne M. Bocckl, MS; Ellen T. Coyle, COMT*; Christopher T. Garvin, COA*; Jennifer A. Gloor*; Melissa M. Kellogg, COA*; Jocelyn Kotey*; Diane Latham*; Vikki L. Monks*; Suzanne M. Flavnieks, COT*; Dina E. Rothlin*; Lynne S. Vayer, BS, COT*; Cindy V. Witol,CO*; Jing Cheng Zhao.*

Washington University School of Medicine, St Louis, Mo

Investigators: Martin B. Wax, MD; Edward M. Barnett, MD; Bernard Becker, MD; Michael A. Kass, MD; Allan E. Kolker, MD; Carla J. Siegfried, MD; Regina M. Smolyak, MD; Dipali V. Apte, MD*; David C. Ball, MD*; John C. Burchfield, MD*; Deepak P. Edward, MD*; Rebecca S. Heaps, MD*; Pierre G. Mardelli, MD*; J. Eric Pepperl, MD*; Jonathan Silbert, MD*; Marshall W. Stafford, MD*; Paul M. Tesser, MD*; James W. Umlas, MD.* Coordinators and Staff: Arnold D. Jones, COA; Lori A. Clark, COT*; Fortunata Darmody, COT*; Diana L. Moellering, COT.

Committees

Executive/Steering Committee: Ingrid Adamsons, MD (nonvoting); Douglas R. Anderson, MD; James D. Brandt, MD; Anne L. Coleman, MD, PhD; Michael Drake, MD; Donald F. Everett, MA; Robert Fechtner, MD*; Douglas Gaasterland, MD; Mae D. Gordon, PhD; Dale K. Heuer, MD; Eve J. Higginbotham, MD; Chris A. Johnson, PhD; Michael A. Kass, MD (chair); John L. Keltner, MD; Richard K. Parrish II, MD; Jody R. Piltz-Seymour, MD; M. Roy Wilson, MD; Arthur Shedden, MD* (nonvoting); Roger Vogel, MD* (nonvoting); Jane L. Anderson, MS, CCRC; Debra Beck, BA, COA*; Ingrid Clark, COA*; Donna Leef, MMSc, COMT*; Patricia A. Morris (nonvoting); Carol J. Pollack-Rundle, COMT; Ann K. Wilder, RN, BSN (nonvoting).

Data and Safety Monitoring Committee: Ingrid Adamsons, MD (nonvoting; open session); Roy Beck, MD, PhD; John Connett, PhD; Claude Cowan, MD; Barry Davis, MD, PhD (chair); Donald F. Everett, MA (nonvoting); Mae O. Gordon, PhD (nonvoting); Michael A. Kass, MD (nonvoting; open session, 11/4/93 to 4/30/98; closed session, 5/1/98 to present); Ronald Munson, PhD; Mark Sherwood, MD; Gregory L. Skuta, MD; Keven O'Rourke, OP, JCL, STEM.*

Endpoint Committee: Dale K. Heuer, MD; Eve J. Higginbotham, MD; Richard K. Parrish II, MD; Mae O. Gordon, PhD.

Resource Centers

Coordinating Center: Washington University School of Medicine, St Louis

Investigators: Mae O. Gordon, PhD; J. Philip Miller, AB; Kenneth Schechtman, PhD.* Coordinators and Staff: Joel Achtenberg, MSW; Mary Bednarski, MAS; Julia Beiser, MS; Karen Clark, BS; Christopher Ewing, BA; Elizabeth Hornbeck, BS; Ellen Long, CCRA; Carolyn R. Miles, MA; Patricia Morris; Denise Morrison; Ann K. Wilder, RN, BSN, CCRP.

Chairman's Office: Washington University School of Medicine, St Louis

Investigator: Michael A. Kass, MD. Coordinators and Staff: Deborah Dunn; Debra Browning*; Dawn Tourville.*

Project Office: National Eye Institute, Rockville, Md

Donald F. Everett, MA; Richard Mowery, PhD.*

Optic Disc Reading Center: Bascom Palmer Eye Institute, University of Miami, Miami, Fla

Investigators: Richard K. Parrish II, MD; Douglas R. Anderson, MD; Donald L. Budenz, MD. Coordinators and Staff: Maria-Cristina Wells-Albornoz, MPH; William Feuer, MS; Ditte Hess, CRA; Heather Johnson; Joyce Schiffman, MS; Ruth Vandenbroucke.

Visual Field Reading Centers: University of California–Davis, Sacramento; Discoveries in Sight, Devers Eye Institute, Portland, Ore

Investigators: John L. Keltner, MD (Sacramento); Chris A. Johnson, PhD (Portland). Coordinators and Staff: Kimberly E. Cello, BS; Shannan E. Bandermann, MA; Bhupinder S. Dhillon, BS; Daniel Redline, BS; David Claunch*; Mary A. Edwards, BS*; Peter Gunther*; Jacqueline Quigg*; John Spurr.*

Ancillary Study Reading Centers

Confocal Scanning Laser Ophthalmoscopy Reading Center: University of California–San Diego, La Jolla

Investigators: Robert N. Weinreb, MD; Linda Zangwill, PhD. Coordinators and Staff: Keri Dirkes, MPH; Amanda R. Smith, BS.

Short Wavelength Automated Perimetry Reading Center: Devers Eye Institute, Legacy Portland Hospitals, Portland, Ore

Investigator: Chris A. Johnson, PhD. Coordinator: Erna Hibbitts.

Corneal Endothelial Cell Density Reading Center: Mayo Clinic/Foundation, Rochester, Minn

Investigator: William M. Bourne, MD.

Coordinators and Staff: Becky A. Nielsen, LPN; Thomas P. Link, CRA, BA; Jay A. Rostvold.

Corresponding author and reprints: Mae O. Gordon, PhD, OHTS Coordinating Center, Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, Box 8203, 660 South Euclid, St Louis, MO 63110 (e-mail: mae{at}vrcc.wustl.edu).

From the Department of Ophthalmology and Visual Sciences (Drs Kass and Gordon) and the Division of Biostatistics (Mr Miller), Washington University School of Medicine, St Louis, Mo; Department of Ophthalmology, Medical College of Wisconsin, Milwaukee (Dr Heuer); Maryland Center for Eye Care Associates and the Department of Ophthalmology, University of Maryland, Baltimore (Dr Higginbotham); Devers Eye Institute, Portland Ore (Dr Johnson); Department of Ophthalmology, University of California, Davis (Dr Keltner); Bascom Palmer Eye Institute, University of Miami School of Medicine, Miami, Fla (Dr Parrish); and Creighton University School of Medicine, Omaha, Neb (Dr Wilson).


REFERENCES
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Morrison et al.
IOVS 2009;50:2802-2808.
ABSTRACT | FULL TEXT  

An Objective Evaluation of Eyedrop Instillation in Patients With Glaucoma
Stone et al.
Arch Ophthalmol 2009;127:732-736.
ABSTRACT | FULL TEXT  

Interpretation of the glaucoma "landmark studies"
Wishart
Br. J. Ophthalmol. 2009;93:561-562.
FULL TEXT  

Genetic Risk for Primary Open-Angle Glaucoma Determined by LMX1B Haplotypes
Park et al.
IOVS 2009;50:1522-1530.
ABSTRACT | FULL TEXT  

Detection of Progressive Retinal Nerve Fiber Layer Loss in Glaucoma Using Scanning Laser Polarimetry with Variable Corneal Compensation
Medeiros et al.
IOVS 2009;50:1675-1681.
ABSTRACT | FULL TEXT  

Primary Open-Angle Glaucoma
Kwon et al.
NEJM 2009;360:1113-1124.
FULL TEXT  

Conjunctival hyperaemia with the use of latanoprost versus other prostaglandin analogues in patients with ocular hypertension or glaucoma: a meta-analysis of randomised clinical trials
Honrubia et al.
Br. J. Ophthalmol. 2009;93:316-321.
ABSTRACT | FULL TEXT  

Ocular Hypertension Treatment Study
Higginbotham
Arch Ophthalmol 2009;127:213-215.
FULL TEXT  

Preventing Glaucoma in a High-Risk Population: Impact and Observations of the Ocular Hypertension Treatment Study
Rhee
Arch Ophthalmol 2009;127:216-218.
FULL TEXT  

Intracranial Pressure in Primary Open Angle Glaucoma, Normal Tension Glaucoma, and Ocular Hypertension: A Case-Control Study
Berdahl et al.
IOVS 2008;49:5412-5418.
ABSTRACT | FULL TEXT  

Effects of the Timolol-Dorzolamide Fixed Combination and Latanoprost on Circadian Diastolic Ocular Perfusion Pressure in Glaucoma
Quaranta et al.
IOVS 2008;49:4226-4231.
ABSTRACT | FULL TEXT  

Predictors of and Barriers Associated With Poor Follow-up in Patients With Glaucoma in South India
Lee et al.
Arch Ophthalmol 2008;126:1448-1454.
ABSTRACT | FULL TEXT  

Long-term efficacy and safety of bimatoprost for intraocular pressure lowering in glaucoma and ocular hypertension: year 4
Williams et al.
Br. J. Ophthalmol. 2008;92:1387-1392.
ABSTRACT | FULL TEXT  

A Viscoelastic Biomechanical Model of the Cornea Describing the Effect of Viscosity and Elasticity on Hysteresis
Glass et al.
IOVS 2008;49:3919-3926.
ABSTRACT | FULL TEXT  

Canadian Glaucoma Study: 2. Risk Factors for the Progression of Open-angle Glaucoma
Chauhan et al.
Arch Ophthalmol 2008;126:1030-1036.
ABSTRACT | FULL TEXT  

Finding Risks for Glaucoma
Brandt
Arch Ophthalmol 2008;126:1138-1139.
FULL TEXT  

Heritability of intraocular pressure: a classical twin study
Carbonaro et al.
Br. J. Ophthalmol. 2008;92:1125-1128.
ABSTRACT | FULL TEXT  

Mapping Standard Automated Perimetry to the Peripapillary Retinal Nerve Fiber Layer in Glaucoma
Ferreras et al.
IOVS 2008;49:3018-3025.
ABSTRACT | FULL TEXT  

Glaucoma and Fitness to Drive: Using Binocular Visual Fields to Predict a Milestone to Blindness
Owen et al.
IOVS 2008;49:2449-2455.
ABSTRACT | FULL TEXT  

An unexpectedly low Stratus optical coherence tomography false-positive rate in the non-nasal quadrants of Asian eyes: indirect evidence of differing retinal nerve fibre layer thickness profiles according to ethnicity
Kim et al.
Br. J. Ophthalmol. 2008;92:735-739.
ABSTRACT | FULL TEXT  

Health literacy and vision-related quality of life
Muir et al.
Br. J. Ophthalmol. 2008;92:779-782.
ABSTRACT | FULL TEXT  

Transgenic Mice Expressing the Tyr437His Mutant of Human Myocilin Protein Develop Glaucoma
Zhou et al.
IOVS 2008;49:1932-1939.
ABSTRACT | FULL TEXT  

Bayesian Machine Learning Classifiers for Combining Structural and Functional Measurements to Classify Healthy and Glaucomatous Eyes
Bowd et al.
IOVS 2008;49:945-953.
ABSTRACT | FULL TEXT  

Open-angle Glaucoma and Mortality: The Barbados Eye Studies
Wu et al.
Arch Ophthalmol 2008;126:365-370.
ABSTRACT | FULL TEXT  

Tissue Transglutaminase Expression and Activity in Normal and Glaucomatous Human Trabecular Meshwork Cells and Tissues
Tovar-Vidales et al.
IOVS 2008;49:622-628.
ABSTRACT | FULL TEXT  

Misclassification: Who Really Lives in This Neighborhood?
Sommer
Arch Ophthalmol 2008;126:265-266.
FULL TEXT  

Is a History of Diabetes Mellitus Protective Against Developing Primary Open-angle Glaucoma?
Gordon et al.
Arch Ophthalmol 2008;126:280-281.
FULL TEXT  

Estimating the Rate of Progressive Visual Field Damage in Those with Open-Angle Glaucoma, from Cross-Sectional Data
Broman et al.
IOVS 2008;49:66-76.
ABSTRACT | FULL TEXT  

Optimizing Therapy for Newly Diagnosed Open-angle Glaucoma: Lessons Learned From the Collaborative Initial Glaucoma Treatment Study
Pasquale
Arch Ophthalmol 2008;126:125-127.
FULL TEXT  

Using Pharmacy Claims Data to Study Adherence to Glaucoma Medications: Methodology and Findings of the Glaucoma Adherence and Persistency Study (GAPS)
Friedman et al.
IOVS 2007;48:5052-5057.
ABSTRACT | FULL TEXT  

What's in a name? Medication terms: what they mean and when to use them
Wride et al.
Br. J. Ophthalmol. 2007;91:1422-1424.
FULL TEXT  

Novel pressure-to-cornea index in glaucoma
Iliev et al.
Br. J. Ophthalmol. 2007;91:1364-1368.
ABSTRACT | FULL TEXT  

Expression of ephrinB1 and its receptor in glaucomatous optic neuropathy
Schmidt et al.
Br. J. Ophthalmol. 2007;91:1219-1224.
ABSTRACT | FULL TEXT  

Intraocular Pressure Fluctuation: An Independent Risk Factor for Glaucoma?
Caprioli
Arch Ophthalmol 2007;125:1124-1125.
FULL TEXT  

Presence of an Established Calcification Marker in Trabecular Meshwork Tissue of Glaucoma Donors
Xue et al.
IOVS 2007;48:3184-3194.
ABSTRACT | FULL TEXT  

The 100 Most Frequently Cited Articles in Ophthalmology Journals
Ohba et al.
Arch Ophthalmol 2007;125:952-960.
ABSTRACT | FULL TEXT  

Comparison of Initial Intraocular Pressure Response With Topical beta-Adrenergic Antagonists and Prostaglandin Analogues in African American and White Individuals in the Ocular Hypertension Treatment Study
Mansberger et al.
Arch Ophthalmol 2007;125:454-459.
ABSTRACT | FULL TEXT  

Effects of TGF-{beta}2, BMP-4, and Gremlin in the Trabecular Meshwork: Implications for Glaucoma
Wordinger et al.
IOVS 2007;48:1191-1200.
ABSTRACT | FULL TEXT  

Genes Involved in the Pathogenesis of Primary Open-Angle Glaucoma: In Search of the Holy Grail
Pasquale
JAMA 2007;297:306-307.
FULL TEXT  

Blood flow in glaucoma
Orgul
Br. J. Ophthalmol. 2007;91:3-5.
FULL TEXT  

Comparison of the Stability, Efficacy, and Adverse Effect Profile of the Innovator 0.005% Latanoprost Ophthalmic Solution and a Novel Cyclodextrin-containing Formulation
Gonzalez et al.
J Clin Pharmacol 2007;47:121-126.
ABSTRACT | FULL TEXT  

Expression of Mutated Mouse Myocilin Induces Open-Angle Glaucoma in Transgenic Mice.
Senatorov et al.
J. Neurosci. 2006;26:11903-11914.
ABSTRACT | FULL TEXT  

Effect of beta radiation on success of glaucoma drainage surgery in South Africa: randomised controlled trial
Kirwan et al.
BMJ 2006;333:942.
ABSTRACT | FULL TEXT  

Concordance of Aqueous Humor Flow in the Morning and at Night in Normal Humans
Radenbaugh et al.
IOVS 2006;47:4860-4864.
ABSTRACT | FULL TEXT  

The Rate of Functional Recovery from Acute IOP Elevation
He et al.
IOVS 2006;47:4872-4880.
ABSTRACT | FULL TEXT  

Pattern ERG as an Early Glaucoma Indicator in Ocular Hypertension: A Long-Term, Prospective Study
Bach et al.
IOVS 2006;47:4881-4887.
ABSTRACT | FULL TEXT  

Ocular Response Analyzer versus Goldmann Applanation Tonometry for Intraocular Pressure Measurements.
Martinez-de-la-Casa et al.
IOVS 2006;47:4410-4414.
ABSTRACT | FULL TEXT  

Asymmetries and visual field summaries as predictors of glaucoma in the ocular hypertension treatment study.
Levine et al.
IOVS 2006;47:3896-3903.
ABSTRACT | FULL TEXT  

Twice-Daily 0.2% Brimonidine-0.5% Timolol Fixed-Combination Therapy vs Monotherapy With Timolol or Brimonidine in Patients With Glaucoma or Ocular Hypertension: A 12-Month Randomized Trial.
Sherwood et al.
Arch Ophthalmol 2006;124:1230-1238.
ABSTRACT | FULL TEXT  

Genomewide scan and fine mapping of quantitative trait Loci for intraocular pressure on 5q and 14q in west africans.
Rotimi et al.
IOVS 2006;47:3262-3267.
ABSTRACT | FULL TEXT  

Structure-function relationships using confocal scanning laser ophthalmoscopy, optical coherence tomography, and scanning laser polarimetry.
Bowd et al.
IOVS 2006;47:2889-2895.
ABSTRACT | FULL TEXT  

Effects of Topical Hypotensive Drugs on Circadian IOP, Blood Pressure, and Calculated Diastolic Ocular Perfusion Pressure in Patients with Glaucoma.
Quaranta et al.
IOVS 2006;47:2917-2923.
ABSTRACT | FULL TEXT  

Visual field defects and retinal ganglion cell losses in patients with glaucoma.
Harwerth and Quigley
Arch Ophthalmol 2006;124:853-859.
ABSTRACT | FULL TEXT  

Comparison of a non-preserved 0.1% T-Gel eye gel (single dose unit) with a preserved 0.1% T-Gel eye gel (multidose) in ocular hypertension and glaucomatous patients
Easty et al.
Br. J. Ophthalmol. 2006;90:574-578.
ABSTRACT | FULL TEXT  

Matrix GLA Protein Function in Human Trabecular Meshwork Cells: Inhibition of BMP2-Induced Calcification Process.
Xue et al.
IOVS 2006;47:997-1007.
ABSTRACT | FULL TEXT  

Detection of psychophysical and structural injury in eyes with glaucomatous optic neuropathy and normal standard automated perimetry.
Bagga et al.
Arch Ophthalmol 2006;124:169-176.
ABSTRACT | FULL TEXT  

The rising cost of glaucoma drugs
Azuara-Blanco and Burr
Br. J. Ophthalmol. 2006;90:130-131.
FULL TEXT  

The rising cost of glaucoma drugs in Ireland 1996-2003
Knox et al.
Br. J. Ophthalmol. 2006;90:162-165.
ABSTRACT | FULL TEXT  

A Multicenter, Retrospective Pilot Study of Resource Use and Costs Associated With Severity of Disease in Glaucoma
Lee et al.
Arch Ophthalmol 2006;124:12-19.
ABSTRACT | FULL TEXT  

Factors affecting the test-retest variability of Heidelberg retina tomograph and Heidelberg retina tomograph II measurements
Strouthidis et al.
Br. J. Ophthalmol. 2005;89:1427-1432.
ABSTRACT | FULL TEXT  

Unsupervised Machine Learning with Independent Component Analysis to Identify Areas of Progression in Glaucomatous Visual Fields
Sample et al.
IOVS 2005;46:3684-3692.
ABSTRACT | FULL TEXT  

Validation of a Predictive Model to Estimate the Risk of Conversion From Ocular Hypertension to Glaucoma
Medeiros et al.
Arch Ophthalmol 2005;123:1351-1360.
ABSTRACT | FULL TEXT  

Screening for glaucoma
Harris
BMJ 2005;331:E376-E377.
FULL TEXT  

Baseline Topographic Optic Disc Measurements Are Associated With the Development of Primary Open-Angle Glaucoma: The Confocal Scanning Laser Ophthalmoscopy Ancillary Study to the Ocular Hypertension Treatment Study
Zangwill et al.
Arch Ophthalmol 2005;123:1188-1197.
ABSTRACT | FULL TEXT  

Normal Visual Field Test Results Following Glaucomatous Visual Field End Points in the Ocular Hypertension Treatment Study
Keltner et al.
Arch Ophthalmol 2005;123:1201-1206.
ABSTRACT | FULL TEXT  

Mechanistic Insights into Glaucoma Provided by Experimental Genetics The Cogan Lecture
John
IOVS 2005;46:2650-2661.
FULL TEXT  

Hypophosphorylation of Aqueous Humor sCD44 and Primary Open-Angle Glaucoma
Knepper et al.
IOVS 2005;46:2829-2837.
ABSTRACT | FULL TEXT  

Treatment of ocular hypertension and open angle glaucoma: meta-analysis of randomised controlled trials
Maier et al.
BMJ 2005;331:134.
ABSTRACT | FULL TEXT  

Reproducibility of Retinal Nerve Fiber Thickness Measurements Using the Stratus OCT in Normal and Glaucomatous Eyes
Budenz et al.
IOVS 2005;46:2440-2443.
ABSTRACT | FULL TEXT  

Twenty-four-Hour Control With Latanoprost-Timolol-Fixed Combination Therapy vs Latanoprost Therapy
Konstas et al.
Arch Ophthalmol 2005;123:898-902.
ABSTRACT | FULL TEXT  

Incorporating the Results of the Ocular Hypertension Treatment Study Into Clinical Practice
Kass et al.
Arch Ophthalmol 2005;123:1021-1022.
FULL TEXT  

Intraocular pressure in the Middle East
Hennis
Br. J. Ophthalmol. 2005;89:647-648.
FULL TEXT  

Glaucoma and its treatment: A review
Lee and Higginbotham
Am J Health Syst Pharm 2005;62:691-699.
ABSTRACT | FULL TEXT  

Optical Coherence Tomography Longitudinal Evaluation of Retinal Nerve Fiber Layer Thickness in Glaucoma
Wollstein et al.
Arch Ophthalmol 2005;123:464-470.
ABSTRACT | FULL TEXT  

Long term effect on IOP of a stainless steel glaucoma drainage implant (Ex-PRESS) in combined surgery with phacoemulsification
Traverso et al.
Br. J. Ophthalmol. 2005;89:425-429.
ABSTRACT | FULL TEXT  

Screening for Primary Open-Angle Glaucoma in the Primary Care Setting: An Update for the US Preventive Services Task Force
Fleming et al.
Ann Fam Med 2005;3:167-170.
ABSTRACT | FULL TEXT  

Plasminogen Activator Inhibitor-1 in the Aqueous Humor of Patients With and Without Glaucoma
Dan et al.
Arch Ophthalmol 2005;123:220-224.
ABSTRACT | FULL TEXT  

Neural Losses Correlated with Visual Losses in Clinical Perimetry
Harwerth et al.
IOVS 2004;45:3152-3160.
ABSTRACT | FULL TEXT  

Ocular Hypertension Treatment Study
Yablonski
Arch Ophthalmol 2004;122:1088-1089.
FULL TEXT  

Ocular Hypertension Treatment Study--Reply
Kass and Gordon
Arch Ophthalmol 2004;122:1089-1089.
FULL TEXT  

A comparison of the fixed combination of latanoprost and timolol with the unfixed combination of brimonidine and timolol in patients with elevated intraocular pressure. A six month, evaluator masked, multicentre study in Europe
Garcia-Sanchez et al.
Br. J. Ophthalmol. 2004;88:877-883.
ABSTRACT | FULL TEXT  

The Ocular Hypertension Treatment Study: Topical Medication Delays or Prevents Primary Open-angle Glaucoma in African American Individuals
Higginbotham et al.
Arch Ophthalmol 2004;122:813-820.
ABSTRACT | FULL TEXT  

Statins and Other Cholesterol-Lowering Medications and the Presence of Glaucoma
McGwin et al.
Arch Ophthalmol 2004;122:822-826.
ABSTRACT | FULL TEXT  

Comparison of the GDx VCC Scanning Laser Polarimeter, HRT II Confocal Scanning Laser Ophthalmoscope, and Stratus OCT Optical Coherence Tomograph for the Detection of Glaucoma
Medeiros et al.
Arch Ophthalmol 2004;122:827-837.
ABSTRACT | FULL TEXT  

Race and the Risk of Glaucoma
Miller
Arch Ophthalmol 2004;122:909-910.
FULL TEXT  

Dietary fat consumption and primary open-angle glaucoma
Kang et al.
Am. J. Clin. Nutr. 2004;79:755-764.
ABSTRACT | FULL TEXT  

DNA microarray analysis of gene expression in human optic nerve head astrocytes in response to hydrostatic pressure
Yang et al.
Physiol. Genomics 2004;17:157-169.
ABSTRACT | FULL TEXT  

Prevalence of Open-Angle Glaucoma Among Adults in the United States
The Eye Diseases Prevalence Research Group
Arch Ophthalmol 2004;122:532-538.
ABSTRACT | FULL TEXT  

The Ocular Hypertension Treatment Study: Intraocular Pressure Lowering Prevents the Development of Glaucoma, but Does That Mean We Should Treat Before the Onset of Disease?
Robin et al.
Arch Ophthalmol 2004;122:376-378.
FULL TEXT  

We Should Treat Fewer Patients With Elevated Intraocular Pressure Now That We Know the Results of the Ocular Hypertension Treatment Study
Jampel
Arch Ophthalmol 2004;122:378-379.
FULL TEXT  

Intraobserver and interobserver reproducibility in the evaluation of ultrasonic pachymetry measurements of central corneal thickness
Miglior et al.
Br. J. Ophthalmol. 2004;88:174-177.
ABSTRACT | FULL TEXT  

Do selective topical {beta} antagonists for glaucoma have respiratory side effects?
Kirwan et al.
Br. J. Ophthalmol. 2004;88:196-198.
ABSTRACT | FULL TEXT  

Heritability of Risk Factors for Primary Open-Angle Glaucoma: The Beaver Dam Eye Study
Klein et al.
IOVS 2004;45:59-62.
ABSTRACT | FULL TEXT  

Glaucomatous Optic Neuropathy: When Glia Misbehave
Neufeld and Liu
Neuroscientist 2003;9:485-495.
ABSTRACT  

Important Causes of Visual Impairment in the World Today
Congdon et al.
JAMA 2003;290:2057-2060.
FULL TEXT  

Gene Therapy with Brain-Derived Neurotrophic Factor As a Protection: Retinal Ganglion Cells in a Rat Glaucoma Model
Martin et al.
IOVS 2003;44:4357-4365.
ABSTRACT | FULL TEXT  

Primary open angle glaucoma. The need for a consensus case definition
Kroese and Burton
J. Epidemiol. Community Health 2003;57:752-754.
ABSTRACT | FULL TEXT  

Selective Laser Trabeculoplasty as Primary Treatment for Open-angle Glaucoma: A Prospective, Nonrandomized Pilot Study
Melamed et al.
Arch Ophthalmol 2003;121:957-960.
ABSTRACT | FULL TEXT  

Ocular Hypertension Treatment Study Results Could Be Misconstrued
Weene
Arch Ophthalmol 2003;121:1070-1070.
FULL TEXT  

Ocular Hypertension Treatment Study Results Could Be Misconstrued--Reply
Kass and Gordon
Arch Ophthalmol 2003;121:1070-1070.
FULL TEXT  





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