 |
|
Incidence of Open-Angle Glaucoma
The Barbados Eye Studies
Arch Ophthalmol. 2001;119:89-95.
ABSTRACT
| |
Objective To measure the 4-year risk of open-angle glaucoma (OAG) in a black population.
Design Population-based cohort study with 4 years of follow-up.
Setting Simple random sample of residents of Barbados, West Indies, aged 40
years or older.
Participants A total of 3427 members of the cohort (85% of those eligible).
Main Outcome Measure Development of glaucoma visual field defects and optic disc damage,
confirmed by automated perimetry, independent fundus photographic gradings,
and standardized ophthalmologic examinations.
Results The 4-year risk of OAG in black participants was 2.2% (95% confidence
interval, 1.7%-2.8%), based on 67 newly developed cases of OAG. Incidence
rates increased from 1.2% at ages 40 to 49 years to 4.2% at ages of 70 years
or more, tending to be higher in men than women (2.7% vs 1.9%). About half
of the incident cases were undiagnosed previously, and the rest were receiving
OAG treatment. Of the 67 new cases of OAG, 32 had intraocular pressure of
21 mm Hg or less at baseline (1.2% incidence) and 35 had higher pressures
(9% incidence). Risk was highest among persons classified as having suspect
OAG at baseline (26.1%), followed by those with ocular hypertension (4.9%)
and lowest in the remaining population (0.8%).
Conclusions This longitudinal study provides new information on OAG risk, as well
as the first incidence measurement in a black population. Although intraocular
pressure increased risk, about half of the new cases had baseline pressures
of 21 mm Hg or less. Results substantiate the high OAG risk in the population
of African origin, especially in older adults; the relative role of intraocular
pressure; and the considerable underdetection of new disease after 4 years
of follow-up.
INTRODUCTION
OPEN-ANGLE glaucoma (OAG), which is especially frequent in black populations,
is a leading cause of blindness worldwide. This optic neuropathy of unknown
cause mainly affects older adults, requires lifelong treatment, and causes
irreversible visual loss. Based on the results of several large prevalence
studies,1-8
approximately 3% of white Americans, 10% of African Americans, and 15% of
African Caribbeans older than 65 years have OAG. Although prevalence data
are available, few population-based studies have continued follow-up to determine
incidence.9 As such, information on the risk
of OAG is very limited, being nonexistent for populations of African descent.
Knowledge of incidence is important, as it measures the absolute risk of developing
OAG over a time period and allows meaningful evaluation of risk factors. Incidence
data are thus valuable for appraising OAG risk, understanding its etiology,
and informing public health planning, with the eventual goal of preventing
visual loss from the disease.
Because of the scarcity of population-based longitudinal studies on
OAG, most estimates of glaucoma incidence have been derived indirectly from
available prevalence data, being mainly based on white populations.10-12 This report presents
the first direct (observed) estimates of the incidence of primary OAG, which
are based on a sizable number of new cases. Furthermore, it is the first report,
to our knowledge, of OAG incidence in a predominantly black population.
PATIENTS AND METHODS
OVERVIEW
The Barbados Eye Studies cohort was identified from a prevalence study
(1988-1992), based on 84% of a simple random sample of the Barbados population
40 to 84 years old.7 Four years after this
baseline, the Barbados Incidence Study of Eye Diseases (BISED; 1992-1997)
reexamined the surviving members of the cohort to determine incidence, progression,
and risk factors for OAG, age-related cataract, age-related maculopathy, and
diabetic retinopathy. These studies were funded by the National Eye Institute,
Bethesda, Md, and included a coordinating center (University Medical Center
at Stony Brook, Stony Book, NY); a data collection center (Ministry of Health,
Bridgetown, Barbados, West Indies); and a fundus photography reading center
(The Johns Hopkins University, Baltimore, Md). Informed consent was obtained
from all study participants.
The BISED methods and protocol followed those used at baseline, which
were described in detail elsewhere.7 In brief,
the examinations included refraction and visual acuity, automated perimetry,
applanation tonometry, blood pressure with a random-zero sphygmomanometer,
anthropometric measurements, lens gradings, venipuncture for glycated hemoglobin,
color stereo fundus photography of the disc and macula, and a standardized
interview on demographic, ocular, medical, and other risk factor data. The
visual field testing protocol7 involved suprathreshold
screening of all participants with the full-field 120 program of the Humphrey
Visual Field Analyzer (Allergan-Humphrey, San Leandro, Calif) (3-zone strategy;
central 64 points only); those with 1 or more absolute defects then underwent
a full threshold test with the C24-2 program. With the use of a computer next
to the perimeter, these results were immediately analyzed by the hemimeridional
comparisons method.13 If the analysis showed
low sum or defects in the comparisons of field sectors 5 vs 6 and 7 vs 8,
individuals were referred for a full threshold test with the C30-2 program.
The C30-2 results were similarly analyzed by the hemimeridional method. All
participants with positive examination findings (best-corrected visual acuity
<20/30, visual field defects by hemimeridional analyses of threshold tests,
intraocular pressure [IOP] >21 mm Hg, history of major eye diseases, family
history of glaucoma, diabetes history, or inability to undergo perimetry,
fundus photographs, or lens gradings) and a 10% sample were referred for a
comprehensive ophthalmologic evaluation, repeated tonometry, and any additional
visits needed to complete the visual field testing protocol.7
The study ophthalmologist reviewed all visual fields to provide a clinical
interpretation of the results.
The baseline and follow-up photographs of the disc and macula were independently
classified at the reading center by 2 masked graders. Discrepancies were resolved
by consensus or adjudication by a third grader. Optic disc features evaluated
to assess OAG status were horizontal and vertical cup-disc ratio with the
use of a template, narrowest remaining neuroretinal rim, notching, asymmetry
in cup-disc ratios between eyes, and disc hemorrhages. For comparability,
these same features were also graded at the ophthalmologic examination. The
quality assurance system for photographic gradings used in the prevalence
study7 continued throughout BISED. The system
involved evaluation of reproducibility within and between individual graders,
as well as assessment of drift in photographic gradings over time.
OAG CLASSIFICATION
Definite OAG was defined by the presence of both visual field defects
and optic disc damage in at least 1 eye, after the exclusion of other possible
causes. Intraocular pressure was not considered in this definition. All participants
were classified independently at the coordinating center according to an algorithm
based on specific, predefined criteria. If all criteria were not fully met,
individuals were classified as having suspect OAG and were not included in
the incidence estimates. Because some participants were unable to undergo
the full perimetry protocol or to have fundus photographs taken (eg, because
of advanced visual loss or media opacities), the classification criteria accounted
for data completeness. As in the prevalence study,7
double plus signs (++) denoted the most complete data for OAG classification,
and a single plus sign (+) denoted less complete data, but sufficient for
definite classification. A description of the specific criteria for classification
follows.
VISUAL FIELD CRITERIA
++: At least 2 abnormal visual field tests by Humphrey automated perimetry,
as defined by computer-based objective criteria, ie, positive results of hemimeridional
analyses13 of threshold tests (C24-2 or C30-2
program) and/or the presence of 1 or more absolute defects in the central
30° as tested with the full-field 120 suprathreshold program (central
64 points; 3-zone strategy), with ophthalmologic interpretation as definite
or suspect glaucomatous field loss.
+: Fewer than 2 abnormal visual field
tests or an inability to perform automated perimetry (eg, because of blindness
or severe visual impairment), with ophthalmologic interpretation as definite
glaucomatous field loss.
OPTIC DISC CRITERIA
++: At least 2 signs of optic disc damage present in fundus photographs
and/or the ophthalmologic evaluation, including either a horizontal or vertical
cup-disc ratio of 0.7 or more, narrowest remaining neuroretinal rim 0.1 disc
diameter or less, notching, asymmetry in cup-disc ratios between eyes greater
than 0.2, or disc hemorrhages.
+: Fewer than 2 signs of optic disc damage
as described above (or unavailable photographs), with an ophthalmologic assessment
or clinical record documenting definite glaucomatous optic nerve damage.
OPHTHALMOLOGIC EXAMINATION
++: Clinical diagnosis of definite OAG after examination by the BISED
ophthalmologist to exclude other possible causes for disc and field changes.
+: Previous OAG history and treatment and/or visual field and disc damage,
yet the definite OAG diagnosis was not made at the time of the BISED visit
(eg, because of inconclusive or incomplete data); the study ophthalmologist
confirmed the diagnosis through record review or reexamination.
INCIDENCE CALCULATIONS
The direct 4-year incidence rate was calculated as m/n, where m denotes
the participants newly diagnosed with primary OAG at the BISED follow-up examination,
and n is the number of participants at risk of developing
OAG (that is, without OAG at baseline). Percentage incidence is reported as
the observed incidence rate among BISED participants. An age- and sex-adjusted
rate was also calculated to account for the age and sex distribution of nonparticipants;
these calculations assumed equal incidence rates in participants and nonparticipants
in each age-sex stratum.
RESULTS
Of the 4631 original participants with baseline examinations at the
study site, 4040 (87%) were eligible for the follow-up visit, as 329 were
deceased, 34 were too ill or disabled to complete the full study examination,
and 228 had moved away. Among those eligible, 3427 (85%) participated in BISED. Table 1 shows that BISED participants had
a median age of 57 years at baseline and 58.1% were female, with 93.2% self-reporting
their race as black, 4.1% as mixed (black and white), and 2.7% as white or
other. This demographic distribution was similar to that obtained at baseline
and closely represents the racial composition of the Barbados population.7 As compared with the 3427 participants, the nonparticipants
were older, as expected (median age at baseline was 61 years). Although they
had fewer years of education (P = .01), no significant
differences were found in other demographic variables (eg, sex, race, or residence)
or in major diagnoses (eg, OAG or cataract) in logistic regression analyses.
|
|
|
|
Table 1. Demographic Characteristics of BISED Participants and Nonparticipants*
|
|
|
Table 2 indicates that BISED
achieved a high degree of data completeness for the OAG classification, with
3321 (97%) of participants completing at least 1 visual field test. Fundus
photography was completed by 3335 participants, and 3140 (94%) had disc photographs
of gradable quality. Good reproducibility between 2 independent graders was
achieved, with weighted  ranging from 0.69 to 0.74 for horizontal and
0.73 to 0.78 for vertical cup-disc ratios, as well as from 0.71 to 0.75 for
neuroretinal rim sizes. A total of 3298 participants (96%) had photographic
and/or clinical gradings of the optic disc. Among those referred for an ophthalmologic
evaluation, 96% completed the examination. A high correlation was found between
photographic and clinical cup-disc ratio gradings (r
= 0.79 and 0.81 for horizontal and vertical, respectively). The main reasons
for incomplete visual field or photographic data were advanced cataract and
severe visual loss; an additional reason was that 44 ophthalmologic examinations
were performed at the participants' homes.
|
|
|
|
Table 2. Data on Open-Angle Glaucoma Classification (n = 3427)
|
|
|
At baseline, 207 persons in the BISED cohort were classified as having
OAG and 3 had bilateral secondary or other types of glaucoma, thus leaving
3217 individuals as the population at risk for OAG. Of these, 71 met the criteria
for incident OAG at follow-up: 67 were black, 2 were mixed, and 2 were white
participants. Most cases were unilateral, with 25 newly affecting the right
eye; 28, the left eye; and 18, both eyes. Because of the small number of white
and mixed participants, these are excluded from the remaining analyses.
Table 3 presents OAG incidence
estimates in black participants, by age at baseline and sex. The 4-year incidence
of OAG was 2.2% (95% confidence interval, 1.7%-2.8%), based on 67 incident
cases of glaucoma. An additional 81 black participants were classified as
having suspect OAG and thus were not included in the incidence estimates.
Age-specific incidence increased from 1.2% (95% confidence interval, 0.6%-2.1%)
in persons 40 to 49 years of age to 4.2% (95% confidence interval, 2.6%-6.3%)
in those aged 70 years and older. Incidence was consistently higher among
men than women in each age group. The age- and sex-adjusted incidence, accounting
for nonparticipation, remained the same.
|
|
|
|
Table 3. Age- and Sex-Specific Incidence of Open-Angle Glaucoma in
Black Participants
|
|
|
Table 4 shows that, of the
67 black participants with incident OAG, four fifths met the most stringent
criteria for visual field loss (groups 1, 3, and 5) and 88% for optic disc
damage (groups 1, 2, 5, and 6) in at least 1 eye. A similarly high percentage
had a definite clinical diagnosis of OAG at the BISED visit (groups 1, 2,
3, and 4); of those confirmed at a later time by the study ophthalmologist,
9 had the most complete (++) visual field and optic disc data (group 5). In
addition, 59.7% had the most complete data for all the criteria (group 1).
|
|
|
|
Table 4. Distribution of Criteria for Open-Angle Glaucoma (n = 67)*
|
|
|
Table 5 compares examination
findings between baseline and follow-up for incident cases and the rest of
the study population. At baseline, about one tenth of the incident cases were
receiving IOP-lowering treatment but did not meet the study criteria for OAG
at that time. By the 4-year follow-up, only about half of the incident cases
were aware of their OAG diagnosis and receiving treatment; the rest were previously
undiagnosed and newly discovered by the study. Lower frequencies of treatment
were reported in the larger, nonincident group.
|
|
|
|
Table 5. Comparisons Between Baseline and Follow-up for Incident and
Nonincident Cases*
|
|
|
The median level of IOP in the affected eye (or the highest value in
both affected eyes) increased from 21.3 mm Hg at baseline to 23.7 mm Hg at
the 4-year follow-up, for a difference of 2.4 mm Hg. Likewise, 52.2% of the
cases had IOP greater than 21 mm Hg during their initial visit, whereas 68.7%
had reached such level 4 years later. When the remaining study participants
were considered, their median IOP at follow-up (highest value in either eye)
was 1.6 mm Hg higher than at baseline; the frequency of IOP greater than 21
mm Hg increased from 12.1% at baseline to 21% at follow-up. The interpretation
of the IOP levels must consider the IOP-lowering treatment received by some
participants.
Increases in vertical and horizontal cup-disc ratios were also apparent
among the incident group, with the median ratios increasing from 0.5 to 0.7
at follow-up. The frequency of cup-disc ratios of 0.7 or more markedly increased
during follow-up, especially for vertical cup-disc ratios. For the remaining
study population, smaller changes in cup-disc ratios were observed. In addition,
differences in visual acuity were noted, with 10.4% of incident cases of OAG
having an acuity worse than 20/40 at baseline, as opposed to 17.9%, 4 years
later. Although these frequencies were somewhat higher than in the nonincident
group, they could be influenced by age differences between groups, as visual
acuity losses were mainly caused by cataract. None of the new cases had visual
acuity impairment (acuity of 20/200 or worse) caused by glaucoma.
Table 6 shows that OAG risk
varied with the baseline glaucoma classification and the baseline IOP. When
the baseline classification was considered, the highest risk (26.1%) was found
among participants previously classified as having suspect OAG because they
met some, but not all, of the study criteria for definite OAG. Among the rest
of the population, those with the next highest risk (4.9%) were participants
classified as having ocular hypertension, that is, with IOP greater than 21
mm Hg and no glaucoma findings at the initial examination. The lowest risk
(0.8%) was observed in participants without glaucoma or ocular hypertension
at baseline. If one only considers IOP at baseline, regardless of glaucoma
classification, 35 of the 389 participants with IOP greater than 21 mm Hg
at baseline developed OAG, for an incidence of 9.0%. In contrast, 32 of the
remaining 2600 participants with IOP of 21 mm Hg or less at baseline developed
OAG, for an incidence of 1.2%.
|
|
|
|
Table 6. Incidence of Open-Angle Glaucoma by Baseline Classification
and Intraocular Pressure (IOP)
|
|
|
Figure 1 presents the
baseline IOP distribution of the incident and nonincident cases. Although
the incident cases tended to have higher IOP at baseline, there was considerable
overlap between both distributions. Almost as many cases developed in participants
with IOP of 21 mm Hg or less at baseline than in those with higher values.
|
|
|
|
Baseline intraocular pressure (IOP) in incident cases and the remaining
black participants.
|
|
|
COMMENT
The study provides new information on the risk of developing OAG in
a population after a 4-year interval. This report is based on the largest
number, to our knowledge, of incident cases of OAG in any population-based
study, thus allowing reasonably precise estimates. Furthermore, this investigation
presents the first observed incidence estimates for OAG in a population of
African origin. The results indicate a large risk of OAG in the cohort, which
increased with age and tended to be higher in men than women (Table 3). In persons 40 years of age or older, the 4-year incidence
of OAG was 2.2% (95% confidence interval, 1.7%-2.8%), based on 67 incident
cases, or 0.6% per year (Table 3). This risk was especially high for older adults, exceeding 1% per year in the
oldest age group. In fact, almost two thirds of the new cases developed in
participants who were at least 60 years of age at baseline. Incidence was
consistently higher in men than women for every age group, following the age-
and sex-specific pattern observed at baseline.7, 14
Despite this trend, the sex difference in risk was not statistically significant,
which could be a result of insufficient sample size. Whereas prevalence studies
have varied concerning sex differences in OAG,3, 5, 15-17
our results suggest a higher OAG risk in men than women in our study population.
About half of the new cases were undiagnosed before the follow-up examination
and the rest were receiving treatment (Table 5). No significant differences in age, sex, or IOP were found
between newly diagnosed and previously diagnosed cases. This result parallels
our findings at the baseline examination, where only half of the participants
with OAG reported previous diagnosis and treatment.7
Similar results were reported by other studies of OAG prevalence15, 18-20
with different populations and varying access to eye care, indicating that
about half of cases of established OAG may be undetected. Our comparable observation
for the detection of newly developed OAG is of interest, especially considering
the relatively short interval between the baseline and follow-up examinations.
These results suggest that early detection of all new OAG in a population
may require examination intervals of 4 years or less.
Participants with higher IOP at baseline were at increased risk of OAG,
as expected, with higher incidences observed for those with IOP greater than
21 mm Hg (9% vs 1.2%; Table 6).
These findings were similar to those seen at baseline, where IOP was a major
risk factor and was strongly associated with OAG.7, 14, 21
Although the role of IOP as a risk factor for OAG is well known, it is important
to consider its role from a population perspective, where most individuals
do not have high IOP levels. In our population, almost as many new cases arose
in persons with IOP of 21 mm Hg or less at baseline as in those with higher
pressures (32 vs 35; Table 6).
Given the variability of IOP, the baseline measurements may have misclassified
the IOP status of some individuals. Even with this possibility accounted for,
our results indicate that a considerable percentage of OAG risk can be attributed
to factors other than IOP.22 In fact, when
the traditional, arbitrary criterion of greater than 21 mm Hg is used to define
"high IOP" (which encompassed 13% of the population at risk), the risk attributable
to high IOP was 46%. Using a criterion based on the highest 10% of the IOP
distribution (>25.3 mm Hg in our population at risk) yielded an attributable
risk of 37%. The inconstant relationship between IOP and OAG risk is further
documented by the overlap of the IOP distribution of the incident and nonincident
cases at baseline (Figure 1). Still,
higher-than-average IOP was an important finding among incident cases. Persons
with newly diagnosed OAG showed significant increases in IOP at follow-up
(Table 5), with the median IOP
being 2.4 mm Hg higher than at baseline. Similarly, although about half of
the incident cases had IOP greater than 21 mm Hg at baseline, more than two
thirds had reached these levels at follow-up.
In addition to changes in IOP, increases were seen in horizontal and
vertical cup-disc ratios, especially for the latter, as four fifths of the
incident cases had reached vertical cup-disc ratio of 0.7 or higher (Table 5). Although deterioration in visual
acuity was noted during the 4-year period, most acuity losses were attributed
to cataract and none of the new cases had visual acuity impairment (as previously
defined) caused by OAG.
What is the validity of these results? The study has several methodologic
strengths, which add support to its conclusions. A participation rate of 85%
was achieved in those eligible for follow-up, which is high for a population-based
study of an aged cohort. Furthermore, the analyses comparing participants
and nonparticipants suggest a good overall representation of the original
cohort. Although nonparticipants were older and of lower educational status,
both groups were similar in other demographic factors and major ocular diagnoses
(Table 1). A creditable participation
rate was achieved even when all losses to follow-up were considered, which
were mainly the result of death, since 74% of the entire cohort had a follow-up
examination.
A well-defined categorization system was used to classify incident cases
of OAG, which required 3 sets of criteria: visual field defects (determined
by computer-based perimetric criteria with clinical interpretation by an ophthalmologist),
optic disc abnormality (determined by independent gradings of fundus photographs
and ophthalmologic evaluation), and an ophthalmologic assessment to exclude
other possible causes. This classification system aimed to achieve high specificity
of the OAG diagnosis, thus reducing misclassification of cases of suspect
glaucoma as early OAG. A high degree of data completeness was achieved for
the OAG classification, with most individuals completing automated perimetry,
optic disc gradings, and an ophthalmologic examination in the study (Table 2 and Table 4). The completeness of the information available enhanced
the study's ability to classify OAG status, which is an especially difficult
process in a population study. This process was further complicated by the
advanced age of incident cases at the BISED examination, which led to the
single-plus (+) and double-plus (++) system to classify data completeness
(Table 4). However, most of the
incident cases were classified as ++ for completeness of visual fields (81%),
optic disc (88%), and clinical (85%) criteria, with correspondingly small
frequencies classified as + for these criteria. If we were to exclude the
participants with less complete data, the incidence estimates would be reduced
accordingly. Such selective estimates, however, would not provide a representative
measurement of the underlying risk in the general population. Similarly, the
use of different definitions, eg, those based only on optic disc or visual
field damage (rather than on both), would lead to different estimates. To
place our results in context with our earlier prevalence data, we reported
incidence based on a glaucoma definition that parallels that used at baseline.
The exploration of alternative diagnostic criteria, which would be of methodologic
interest, is a complex issue that merits a separate article.
Because of the high specificity of the criteria to define OAG, the incidence
rates reported herein represent conservative estimates. Nonetheless, even
when participants with less complete data are excluded, the estimates are
still considerably higher than those previously available. To date, only 1
known study by Bengtsson,9 in Dalby, Sweden,
has the distinction of reporting direct OAG incidence estimates, which were
based on population-based longitudinal data. Persons were classified as having
manifest glaucoma if repeatable visual field defects, not explained by other
causes, coexisted with a loss of neural tissue in the optic nerve head of
the same eye. The incidence rate of manifest glaucoma was 0.24% per year for
persons 55 to 85 years of age and was based on 26 incident cases, which developed
during about 10 years of follow-up. In addition to finding a much lower overall
risk of OAG than in Barbados, the Swedish study reported that manifest glaucoma
was independent of age and that OAG incidence was higher in women than in
men. Given the differences between studies, these inconsistent findings may
result from underlying differences in populations, study criteria, or other
reasons.
Leske et al10 developed a method to estimate
incidence from age-specific prevalence data and used it to estimate OAG incidence,
based on the white adult populations from the Ferndale and Framingham studies.10-11,23 Open-angle glaucoma
was defined as the presence of at least 1 glaucomatous visual field defect,
after other possible causes were excluded. The 5-year incidence rates with
this method translate to 1-year rates of 0.04% and 0.22% for ages 55 and 75
years, respectively. Similar yearly estimates (0.06% and 0.20% at ages 55
and 75 years, respectively) were derived with the same method12
by pooling age-specific prevalences from several studies of whites. When OAG
prevalence from African Americans and African Caribbeans was pooled,3, 7, 24 the resulting incidence
estimates were 4 times higher at age 55 years (0.26%) and 2 to 3 times higher
at age 75 years (0.54%) than those in whites.12
The precision of these estimates is difficult to interpret because of the
diversity of OAG definitions and accuracy of the prevalence data from the
different studies. Nevertheless, all of these estimates are lower than the
current results, a discrepancy explained by the lower pooled prevalence used
to derive the incidence estimates. For example, although the prevalence of
OAG in black participants from the Barbados Eye Study was 7%,7
the prevalence in African American participants in the Baltimore Eye Study
was 4%.3 The pooling of data from both studies
results in lower estimates than those based on the Barbados data alone. In
fact, indirect estimates based on our prevalence data, using the same statistical
methods, closely approximate our observed incidence rates.25
What is the applicability of the current findings to other populations?
The incidence rates reported document the high risk of OAG in populations
of African descent, especially at older ages, which is not explained by IOP
alone. Although incidence rates for African American populations are not available,
indirect estimates also suggest an increased risk, which may be somewhat higher
in African Caribbeans. Although both groups originated from the same area
in Africa, varying degrees of admixture occurred in both populations26 and may account, to some degree, for the observed
differences in frequency of OAG. For example, the 4% prevalence in the black
participants of the Baltimore Eye Survey was similar to the 4% prevalence
found among the mixed (black and white) participants of the Barbados Eye Study.7 In the latter study, the racial categories were well
supported by results of skin pigmentation gradings and blood group distribution.27 Gene-environment interactions, yet to be determined,
may also play a major role. However, although the frequency of OAG may vary
across populations, there is no reason to believe that the intrinsic mechanisms
of the disease will differ. As such, whereas the magnitude of the OAG risk
may be higher in the BISED population than in others, the underlying risk
factors identified by the study should be generally applicable to other populations.
CONCLUSIONS
This is the first study, to our knowledge, to measure the risk of OAG
in a black population. Given its sample size, it is also the first study to
provide sufficiently precise incidence estimates for any population. The magnitude
of the risk increased with age, reaching 1% per year at older ages. In addition
to quantifying risk over a relatively short interval, the data substantiate
the underdetection of new disease. After 4 years of follow-up, about half
of the incident cases were undiagnosed, suggesting the need for frequent examinations
to detect early OAG, especially at older ages.
Although participants with higher IOP were at higher risk, about half
of the new cases developed in persons with IOP of 21 mm Hg or less at baseline.
These results highlight the importance of prognostic factors, other than IOP,
in determining the development of OAG. The high risk of OAG in populations
of African descent, where the disease is a primary cause of blindness, emphasizes
the public health implications of our findings. Additional information will
be gleaned from the continuing follow-up of the cohort.
AUTHOR INFORMATION
Accepted for publication March 21, 2000.
This study was supported by grants EYO7625 and EYO7617 from the National
Eye Institute, Bethesda, Md.
We thank the Barbados Eye Studies participants and the Ministry of Health,
Barbados, for their role in the study.
| The Barbados Eye Studies Group
Principal Investigator: M. Cristina Leske,
MD, MPH. Coordinating Center: State University of
New York at Stony Brook, Stony Brook, NY: M. Cristina Leske, MD, MPH; Barbara
Nemesure, PhD; Suh-Yuh Wu, MA; Leslie Hyman, PhD; Xiaowei Li, PhD; Shu-Hong
Xie, MS; Lixin Jiang, MS; Kasthuri Sarma; Barbara Springhorn; Koumudi Manthani. Data Collection Center: Ministry of Health, Bridgetown,
Barbados, West Indies: Anthea M. S. Connell, FRCS, FRCOphth; Anselm Hennis,
MRCP(UK), PhD; Ann Bannister, MB, BS, DO; Muthu A. Thangaraj, MB, BS, DO;
Rajiv Luthra, MD, MPH; Coreen Barrow; Patricia Basdeo; Kim Bayley; Anthanette
Holder. Fundus Photography Reading Center: The Johns
Hopkins University, Baltimore, Md: Andrew P. Schachat, MD; Judith A. Alexander;
Noreen B. Javornik, MS; Cheryl J. Hiner; Deborah A. Phillips; Reva Ward; Terry
W. George.
|
|
Reprints: M. Cristina Leske, MD, MPH, Department of Preventive Medicine,
State University of New York at Stony Brook, HSC L3 086, Stony Brook,
NY 11794-8036 (e-mail: cleske{at}uhmc.sunysb.edu).
M. Cristina Leske, MD, MPH;
Anthea M. S. Connell, FRCS, FRCOphth;
Suh-Yuh Wu, MA;
Barbara Nemesure, PhD;
Xiaowei Li, PhD;
Andrew Schachat, MD;
Anselm Hennis, MRCP(UK), PhD;
for the Barbados Eye Studies Group
From the Department of Preventive Medicine, State University of New
York at Stony Brook, Stony Brook, NY (Drs Leske, Nemesure, Li, and Hennis;
Ms Wu; and Barbados Eye Studies Group); Ministry of Health, Barbados, West
Indies (Drs Connell and Hennis and Barbados Eye Studies Group); The Johns
Hopkins University, School of Medicine, Baltimore, Md (Dr Schachat and Barbados
Eye Studies Group); and School of Clinical Medicine and Research, University
of the West Indies, Bridgetown, Barbados (Dr Hennis and Barbados Eye Studies
Group).
REFERENCES
1. Kahn HA, Milton RC. Alternative definitions of open-angle glaucoma: effect on prevalence
and associations in the Framingham Eye Study. Arch Ophthalmol. 1980;98:2172-2177.
FREE FULL TEXT
2. Bengtsson B. The prevalence of glaucoma. Br J Ophthalmol. 1981;65:46-49.
FREE FULL TEXT
3. 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
4. Ringvold A, Blika S, Elsas T, et al. The Middle-Norway eye-screening study, II: prevalence of simple and
capsular glaucoma. Acta Ophthalmol (Copenh). 1991;69:273-280.
PUBMED
5. Klein B, Klein R, Sponsel WE, et al. Prevalence of glaucoma: the Beaver Dam Eye Study. Ophthalmology. 1992;99:1499-1504.
WEB OF SCIENCE
| PUBMED
6. Dielemans I, Vingerling JR, Wolfs RCW, Hofman A, Grobbee DE, de Jong PT. The prevalence of primary open-angle glaucoma in a population-based
study in the Netherlands. Ophthalmology. 1994;101:1851-1855.
WEB OF SCIENCE
| PUBMED
7. Leske MC, Connell AMS, Schachat AP, Hyman L for the Barbados Eye Study Group. The Barbados Eye Study: 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.
WEB OF SCIENCE
| PUBMED
9. Bengtsson B. Incidence of manifest glaucoma. Br J Ophthalmol. 1989;73:483-487.
FREE FULL TEXT
10. Leske MC, Ederer F, Podgor M. Estimating incidence from age-specific prevalence in glaucoma. Am J Epidemiol. 1981;113:606-613.
FREE FULL TEXT
11. Podgor MJ, Leske MC, Ederer F. Incidence estimates for lens changes, macular changes, open-angle glaucoma,
and diabetic retinopathy. Am J Epidemiol. 1983;118:206-212.
FREE FULL TEXT
12. 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
13. Sommer A, Enger C, Witt K. Screening for glaucomatous visual field depth with automated threshold
perimetry. Am J Ophthalmol. 1987;103:681-684.
WEB OF SCIENCE
| PUBMED
14. Leske MC, Connell AM, Wu SY, Hyman L, Schachat AP for the Barbados Eye Study Group. Risk factors for open-angle glaucoma: the Barbados Eye Study. Arch Ophthalmol. 1995;113:918-924.
FREE FULL TEXT
15. Leske MC. The epidemiology of open-angle glaucoma: a review. Am J Epidemiol. 1983;118:166-191.
FREE FULL TEXT
16. Kahn HA, Leibowitz HM, Ganley JP, et al. The Framingham Eye Study, I: outline and major prevalence findings. Am J Epidemiol. 1977;106:17-32.
FREE FULL TEXT
17. Viggosson G, Bjornsson G, Ingvason JG. The prevalence of open-angle glaucoma in Iceland. Acta Ophthalmol (Copenh). 1986;64:138-141.
18. Hollows FC, Graham PA. Intraocular pressure, glaucoma, and glaucoma suspects in a defined
population. Br J Ophthalmol. 1966;50:570-586.
FREE FULL TEXT
19. Leske MC, Hawkins B. Screening: relationship to diagnosis and therapy. In: Duane TD, ed. Clinical Ophthalmology.
Vol 5. Philadelphia, Pa: Harper & Row; 1994:chap 54.
20. Sommer A, Tielsch JM, Katz J, et al. Relationship between intraocular pressure and primary open-angle glaucoma
among white and black Americans: the Baltimore Eye Survey. Arch Ophthalmol. 1991;109:1090-1095.
FREE FULL TEXT
21. Leske MC, Wu S-Y for the Barbados Eye Study Group. Distribution of intraocular pressure: the Barbados Eye Study. Arch Ophthalmol. 1997;115:1051-1057.
FREE FULL TEXT
22. Wu S-Y, Leske MC for the Barbados Eye Study Group. Associations with intraocular pressure in the Barbados Eye Study. Arch Ophthalmol. 1997;115:1572-1576.
FREE FULL TEXT
23. Podgor MJ, Leske MC. Estimating incidence from age-specific prevalence for irreversible
diseases with differential mortality. Stat Med. 1986;5:573-578.
WEB OF SCIENCE
| PUBMED
24. Mason RP, Omofolasade K, Wilson MR, et al. National prevalence and risk factors of glaucoma in St. Lucia, West
Indies. Ophthalmology. 1989;96:1363-1368.
WEB OF SCIENCE
| PUBMED
25. Wu S-Y, Nemesure B, Leske MC for the Barbados Eye Study Group. Observed vs. indirect estimates of incidence of open-angle glaucoma. Am J Epidemiol. In press.
26. Chakraboty R, Kamboh MI, Ferrel RE. "Unique" alleles in admixed populations: a strategy for determining
"hereditary" population differences of allele frequencies. Ethn Dis. 1991;1:245-256.
PUBMED
27. Leske MC, Nemesure B, He Q, et al. Open-angle glaucoma and blood groups: the Barbados Eye Study. Arch Ophthalmol. 1996;114:205-210.
FREE FULL TEXT
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati  Twitter
What's this?
RELATED ARTICLE
Insights From Incidence: The Barbados Eye Studies
David C. Musch
Arch Ophthalmol. 2001;119(1):117-118.
EXTRACT
| FULL TEXT
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
|
Comparison of Risk Factors for Bilateral and Unilateral Eye Involvement in Normal-Tension Glaucoma
Kim and Kim
IOVS 2009;50:1215-1220.
ABSTRACT
| FULL TEXT
Visual acuity impairment and vision-related quality of life: the Barbados Eye Studies
Wu et al.
British Journal of Visual Impairment 2009;27:9-24.
ABSTRACT
Evidence of Retinal Vascular Narrowing in Glaucomatous Eyes in an Asian Population
Amerasinghe et al.
IOVS 2008;49:5397-5402.
ABSTRACT
| FULL TEXT
Effects of optic nerve injury, glaucoma, and neuroprotection on the survival, structure, and function of ganglion cells in the mammalian retina
Weber et al.
J. Physiol. 2008;586:4393-4400.
ABSTRACT
| FULL TEXT
Caffeine Consumption and the Risk of Primary Open-Angle Glaucoma: A Prospective Cohort Study
Kang et al.
IOVS 2008;49:1924-1931.
ABSTRACT
| FULL TEXT
Impact of Glaucoma, Lens Opacities, and Cataract Surgery on Visual Functioning and Related Quality of Life: The Barbados Eye Studies
Wu et al.
IOVS 2008;49:1333-1338.
ABSTRACT
| FULL TEXT
Open-angle Glaucoma and Mortality: The Barbados Eye Studies
Wu et al.
Arch Ophthalmol 2008;126:365-370.
ABSTRACT
| 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
Socioeconomic status, systolic blood pressure and intraocular pressure: the Tanjong Pagar Study
Yip et al.
Br J Ophthalmol 2007;91:56-61.
ABSTRACT
| FULL TEXT
Nine-year changes in intraocular pressure: the barbados eye studies.
Wu et al.
Arch Ophthalmol 2006;124:1631-1636.
ABSTRACT
| FULL TEXT
Nine-year incidence of diabetic retinopathy in the barbados eye studies.
Leske et al.
Arch Ophthalmol 2006;124:250-255.
ABSTRACT
| FULL TEXT
Longitudinal glaucoma screening for siblings of patients with primary open angle glaucoma: the Nottingham Family Glaucoma Screening Study
Sung et al.
Br J Ophthalmol 2006;90:59-63.
ABSTRACT
| FULL TEXT
Nine-Year Refractive Changes in the Barbados Eye Studies
Wu et al.
IOVS 2005;46:4032-4039.
ABSTRACT
| FULL TEXT
Glaucoma: Macrocosm to Microcosm The Friedenwald Lecture
Quigley
IOVS 2005;46:2663-2670.
FULL TEXT
Intraocular pressure in the Middle East
Hennis
Br J Ophthalmol 2005;89:647-648.
FULL TEXT
Distribution of intraocular pressure in healthy Iranian individuals: the Tehran Eye Study
Hashemi et al.
Br J Ophthalmol 2005;89:652-657.
ABSTRACT
| FULL TEXT
Prevalence and Risk Factors for Self-Reported Visual Impairment Among Middle-Aged and Older Adults
Horowitz et al.
Research on Aging 2005;27:307-326.
ABSTRACT
Retinal Vessel Diameters and Incident Open-Angle Glaucoma and Optic Disc Changes: The Rotterdam Study
Ikram et al.
IOVS 2005;46:1182-1187.
ABSTRACT
| FULL TEXT
Causes of Incident Visual Field Loss in a General Elderly Population: The Rotterdam Study
Skenduli-Bala et al.
Arch Ophthalmol 2005;123:233-238.
ABSTRACT
| FULL TEXT
Dietary fat consumption and primary open-angle glaucoma
Kang et al.
Am. J. Clin. Nutr. 2004;79:755-764.
ABSTRACT
| FULL TEXT
Risk Factors for Incident Cortical and Posterior Subcapsular Lens Opacities in the Barbados Eye Studies
Hennis et al.
Arch Ophthalmol 2004;122:525-530.
ABSTRACT
| 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
Estimates of Incidence Rates With Longitudinal Claims Data
Sloan et al.
Arch Ophthalmol 2003;121:1462-1468.
ABSTRACT
| FULL TEXT
Risk Factors Associated with the Incidence of Open-Angle Glaucoma: The Visual Impairment Project
Le et al.
IOVS 2003;44:3783-3789.
ABSTRACT
| FULL TEXT
Factors Related to the 4-Year Risk of High Intraocular Pressure: The Barbados Eye Studies
Nemesure et al.
Arch Ophthalmol 2003;121:856-862.
ABSTRACT
| FULL TEXT
Corneal Thickness and Intraocular Pressure in the Barbados Eye Studies
Nemesure et al.
Arch Ophthalmol 2003;121:240-244.
ABSTRACT
| FULL TEXT
Reduction of Intraocular Pressure and Glaucoma Progression: Results From the Early Manifest Glaucoma Trial
Heijl et al.
Arch Ophthalmol 2002;120:1268-1279.
ABSTRACT
| FULL TEXT
Incident Open-Angle Glaucoma and Blood Pressure
Leske et al.
Arch Ophthalmol 2002;120:954-959.
ABSTRACT
| FULL TEXT
The Ocular Hypertension Treatment Study: A Randomized Trial Determines That Topical Ocular Hypotensive Medication Delays or Prevents the Onset of Primary Open-Angle Glaucoma
Kass et al.
Arch Ophthalmol 2002;120:701-713.
ABSTRACT
| FULL TEXT
The Ocular Hypertension Treatment Study: Baseline Factors That Predict the Onset of Primary Open-Angle Glaucoma
Gordon et al.
Arch Ophthalmol 2002;120:714-720.
ABSTRACT
| FULL TEXT
Blindness and visual impairment in the Americas and the Caribbean
Munoz and West
Br J Ophthalmol 2002;86:498-504.
ABSTRACT
| FULL TEXT
Incidence Studies on Open-Angle Glaucoma
Ekstrom et al.
Arch Ophthalmol 2002;120:522-522.
FULL TEXT
Insights From Incidence: The Barbados Eye Studies
Musch
Arch Ophthalmol 2001;119:117-118.
FULL TEXT
|
