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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
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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
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
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  = 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  = .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 -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
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.
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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
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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.
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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.
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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.
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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.
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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
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
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
| |
1. Quigley HA. Number of people with glaucoma worldwide. Br J Ophthalmol. 1996;80:389-393.
FREE FULL TEXT
2. Sommer A, Tielsch JM, Katz J, et al. Racial differences in the cause-specific prevalence of blindness in
East Baltimore. N Engl J Med. 1991;325:1412-1417.
ABSTRACT
3. US Department of Health, Education, and Welfare. Statistics on Blindness in the Model Reporting Area
1969-70. Washington, DC: US Government Printing Office; 1973. DHEW publication
NIH 73-427.
4. Quigley HA, Vitale S. Models of open-angle glaucoma prevalence and incidence in the United
States. Invest Ophthalmol Vis Sci. 1997;38:83-91.
FREE FULL TEXT
5. Hyman L, Wu SY, Connell AM, et al. Prevalence and causes of visual impairment in the Barbados Eye Study. Ophthalmology. 2001;108:1751-1756.
FULL TEXT
|
ISI
| PUBMED
6. Dielemans I, Vingerling JR, Wolfs RC, Hofman A, Grobbee DE, deJong PT. The prevalence of primary open-angle glaucoma in a population-based
study in the Netherlands: the Rotterdam Study. Ophthalmology. 1994;101:1851-1855.
ISI
| PUBMED
7. Leske MC, Connell AM, Schachat AP, Hyman L for the Barbados Eye Study Group. Prevalence of open-angle glaucoma. Arch Ophthalmol. 1994;112:821-829.
FREE FULL TEXT
8. Mitchell P, Smith W, Attebo K, Healey PR. Prevalence of open-angle glaucoma in Australia: the Blue Mountains
Eye Study. Ophthalmology. 1996;103:1661-1669.
ISI
| PUBMED
9. Mason RP, Kosoko O, Wilson MR, Cowan CL Jr, Gear JC, Ross-Degnan D. National survey of the prevalence and risk factors of glaucoma in St
Lucia, West Indies, I: prevalence findings. Ophthalmology. 1989;96:1363-1368.
ISI
| PUBMED
10. Wallace J, Lovell HG. Glaucoma and intraocular pressure in Jamaica. Am J Ophthalmol. 1969;67:93-100.
ISI
| PUBMED
11. Tielsch JM, Sommer A, Katz J, Royall RM, Quigley HA, Javitt J. Racial variations in the prevalence of primary open-angle glaucoma:
the Baltimore Eye Survey. JAMA. 1991;266:369-374.
FREE FULL TEXT
12. Leske MC, Connell AM, Wu SY, et al for the Barbados Eye Studies Group. Incidence of open-angle glaucoma: the Barbados Eye Studies. Arch Ophthalmol. 2001;119:89-95.
FREE FULL TEXT
13. Leibowitz HM, Krueger DE, Maunder LR, et al. The Framingham Eye Study monograph: an ophthalmological and epidemiological
study of cataract, glaucoma, diabetic retinopathy, macular degeneration, and
visual acuity in a general population of 2631 adults, 1973-1975. Surv Ophthalmol. 1980;24(suppl):335-610.
14. Armaly MF, Krueger DE, Maunder L, et al. Biostatistical analysis of the collaborative glaucoma study, I: summary
report of the risk factors for glaucomatous visual-field defects. Arch Ophthalmol. 1980;98:2163-2171.
FREE FULL TEXT
15. Quigley HA, Enger C, Katz J, Sommer A, Scott R, Gilbert D. Risk factors for the development of glaucomatous visual field loss
in ocular hypertension. Arch Ophthalmol. 1994;112:644-649.
FREE FULL TEXT
16. Kerrigan-Baumrind LA, Quigley HA, Pease ME, Kerrigan DF, Mitchell RS. Number of ganglion cells in glaucoma eyes compared with threshold visual
field tests in the same persons. Invest Ophthalmol Vis Sci. 2000;41:741-748.
FREE FULL TEXT
17. Eddy DM, Billings J. The Quality of Medical Evidence and Medical Practice. Washington, DC: National Leadership Commission on Health Care; 1987.
18. Boivin JF, McGregor M, Archer C. Cost effectiveness of screening for primary open angle glaucoma. J Med Screen. 1996;3:154-164.
PUBMED
19. Graham PA. The definition of pre-glaucoma: a prospective study. Trans Ophthalmol Soc U K. 1969;88:153-165.
PUBMED
20. Norskov K. Routine tonometry in ophthalmic practice, II: five-year follow-up. Acta Ophthalmol (Copenh). 1970;48:873-895.
21. Levene RZ. Uniocular miotic therapy. Trans Am Acad Ophthalmol Otolaryngol. 1975;79:OP376-OPH380.
22. David R, Livingston DG, Luntz MH. Ocular hypertension: a long-term follow-up of treated and untreated
patients. Br J Ophthalmol. 1977;61:668-674.
FREE FULL TEXT
23. Chisholm IA, Stead S, Tan L, Melenchuk JW. Prognostic indicators in ocular hypertension. Can J Ophthalmol. 1980;15:4-8.
ISI
| PUBMED
24. Schulzer M, Drance SM, Douglas GR. A comparison of treated and untreated glaucoma suspects. Ophthalmology. 1991;98:301-307.
ISI
| PUBMED
25. Becker B, Morton WR. Topical epinephrine in glaucoma suspects. Am J Ophthalmol. 1966;62:272-277.
ISI
| PUBMED
26. Shin DH, Kolker AE, Kass MA, Kaback MB, Becker B. Long-term epinephrine therapy of ocular hypertension. Arch Ophthalmol. 1976;94:2059-2060.
FREE FULL TEXT
27. Kitazawa Y. Prophylactic therapy of ocular hypertension: a prospective study. Trans Ophthalmol Soc N Z. 1981;33:30-32.
PUBMED
28. Epstein DL, Krug JH Jr, Hertzmark E, Remis LL, Edelstein DJ. A long-term clinical trial of timolol therapy versus no treatment in
the management of glaucoma suspects. Ophthalmology. 1989;96:1460-1467.
ISI
| PUBMED
29. Kass MA, Gordon MO, Hoff MR, et al. Topical timolol administration reduces the incidence of glaucomatous
damage in ocular hypertensive individuals: a randomized, double-masked, long-term
clinical trial. Arch Ophthalmol. 1989;107:1590-1598.
FREE FULL TEXT
30. Heijl A, Bengstsson B. Long-term effects of timolol therapy in ocular hypertension: a double-masked,
randomized trial. Graefes Arch Clin Exp Ophthalmol. 2000;238:877-883.
FULL TEXT
|
ISI
| PUBMED
31. Rossetti L, Marchetti I, Orzalesi N, Scorpiglione N, Torri V, Liberati A. Randomized clinical trials on medical treatment of glaucoma: are they
appropriate to guide clinical practice? Arch Ophthalmol. 1993;111:96-103.
FREE FULL TEXT
32. Gordon MO, Kass MA and the Ocular Hypertension Study Group (OHTS). Manual of Procedures. Springfield, Va: National Technical Information Service; 1997. Publication
PB97-148308NZ.
33. Gordon MO, Kass MA for the Ocular HypertensionTreatment Study Group. The Ocular Hypertension Treatment Study: design and baseline description
of the participants. Arch Ophthalmol. 1999;117:573-583.
FREE FULL TEXT
34. Johnson CA, Keltner JL, Cello KE, et al. Baseline visual field characteristics in the ocular hypertension treatment
study. Ophthalmology. 2002;109:432-437.
FULL TEXT
|
ISI
| PUBMED
35. Feuer WJ, Parrish II RK, Schiffman JC, et al. The Ocular Hypertension Treatment Study: reproducibility of cup/disk
ratio measurements over time at an optic disc reading center. Am J Ophthalmol. 2002;133:19-28.
FULL TEXT
|
ISI
| PUBMED
36. Lee BL, Gutierrez P, Gordon M, et al. The Glaucoma Symptom Scale: a brief index of glaucoma-specific symptoms. Arch Ophthalmol. 1998;116:861-866.
FREE FULL TEXT
37. Ware JE, Snow KK, Kosinski M, Gandek B. SF-36 Health Survey: Manual and Interpretation Guide. Boston, Mass: The Health Institute, New England Medical Center; 1993.
38. Keltner JL, Johnson CA, Quigg JM, Cello KE, Kass MA, Gordon MO for the Ocular Hypertension Study Group. Confirmation of visual field abnormalities in the Ocular Hypertension
Treatment Study. Arch Ophthalmol. 2000;118:1187-1194.
FREE FULL TEXT
39. Lan KK, DeMets DL. Changing frequency of interim analysis in sequential monitoring. Biometrics. 1989;45:1017-1020.
FULL TEXT
|
ISI
| PUBMED
40. Reboussin DM, DeMets DL, Kim KM, Lan KK. Computations for group sequential boundaries using the Lan-DeMets spending
function method. Control Clin Trials. 2000;21:190-207.
FULL TEXT
|
ISI
| PUBMED
41. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict
the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120:714-720.
FREE FULL TEXT
42. Collaborative Normal-Tension Glaucoma Study Group. Comparison of glaucomatous progression between untreated patients with
normal-tension glaucoma and patients with therapeutically reduced intraocular
pressures. Am J Ophthalmol. 1998;126:487-497.
FULL TEXT
|
ISI
| PUBMED
43. The AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS), 7: the relationship
between control of intraocular pressure and visual field deterioration. Am J Ophthalmol. 2000;130:429-440.
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