Abstract
purpose. To create a quantitative basis for diagnostic criteria for
open-angle glaucoma (OAG), to propose an epidemiologic definition for
OAG based on these, and to determine the prevalence of OAG in a general
white population.
methods. Of the 7983 subjects 55 years of age or older participating in
the population-based Rotterdam Study, 6756 subjects participated in the
ophthalmic part of this study (6281 subjects living independently and
475 in nursing homes). The criteria for the diagnosis of OAG were based
on ophthalmoscopic and semiautomated Imagenet estimations of the optic
disc such as vertical cup-to-disc ratio (VCDR), minimal width of neural
rim, or asymmetry in VCDR between both eyes, and visual field testing
with kinetic Goldmann perimetry. All criteria for the diagnosis of OAG
were assessed in a masked way independently of each other.
results. Mean VCDR on ophthalmoscopy was 0.3 and with Imagenet
0.49, and the 97.5th percentile for both was 0.7. The prevalence of
glaucomatous visual field defects was 1.5%. Overall prevalence of
definite OAG in the independently living subjects was 0.8% (95%
confidence interval [CI] 0.6, 1.0; 50 cases). Prevalence of OAG in
men was double that in women (odds ratio 2.1; 95% CI 1.2, 3.6).
Different commonly used criteria for diagnosis of OAG resulted in
prevalence figures ranging from 0.1% to 1.2%.
conclusions. The overall prevalence of OAG in the present study was
comparable to most population-based studies. However, prevalence
figures differed by a factor of 12 when their criteria for OAG were
applied to this population. A definition for definite OAG is
proposed: a glaucomatous optic neuropathy in eyes with open angles in
the absence of history or signs of secondary glaucoma characterized by
glaucomatous changes based on the 97.5 percentile for this population
together with glaucomatous visual field loss. In the absence of the
latter or of a visual field test, it is proposed to speak of probable
OAG based on the 99.5th or possible OAG based on the 97.5th percentiles
of glaucomatous disc changes for a population under
study.
Primary open-angle glaucoma (POAG) ranks third among causes of
incurable visual impairment in the Western world.
1 2 3 Despite prevalence figures in white subjects ranging from 0.8% to
3.0%,
1 4 5 6 7 8 9 10 11 12 13 14 little is known about its etiology. This may
be partly due to the lack of a worldwide epidemiologic definition of,
or standard for diagnosis of, POAG
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 (Table 1) . As a result many (epidemiologic) studies are difficult to compare,
because of the different criteria and methods used for diagnosis,
hampering meta-analyses and the search for risk factors.
It is nowadays generally accepted that POAG is an optic neuropathy
characterized by cupping of the optic nerve head, with corresponding
nerve fiber loss and visual field defects but that there is no
consensus about cutoff points for normal disc measurements. An elevated
intraocular pressure (IOP) is considered to be a risk factor for POAG,
as well as the presence of a first-degree relative with
glaucoma.
16 For the diagnosis POAG congenital forms of
glaucoma have to be excluded, as well as secondary causes of glaucoma
such as pseudoexfoliation.
The aim of the present study was to quantify in a masked way the
prevalence of determinants of open-angle glaucoma (OAG) in a white
population, to propose diagnostic criteria for OAG, and to study the
influence of various diagnostic criteria for OAG on the prevalence of
OAG. Because we did not specifically exclude pseudoexfoliation at
baseline, we will further write about OAG instead of POAG.
Methods
Population
The present study was performed as the ophthalmic part of The
Rotterdam Study, a prospective cohort study of all residents, 55 years
of age and older.
17 Results of a prevalence study in a
subset of the examined population using different criteria for OAG have
been published previously.
10 The study was performed
according to the Declaration of Helsinki and was approved by the
Medical Ethics Committee of the Erasmus University. Written informed
consent was obtained from all participants. All residents were asked to
participate in an extensive home interview, after which an appointment
was made for a medical examination, including a complete ophthalmologic
one.
Ophthalmologic Examination
The ophthalmologic examination (
Table 2 18 19 ) was performed by three ophthalmologic
residents and two technicians. After perimetry, mydriatic drops were
administered in both eyes, irrespective of the anterior chamber angle
depth or history of glaucoma,
20 for lens and fundus
examination, and photography. At the end of the first phase a miotic
(Table 2) was administered in both eyes to counteract the mydriasis.
Optic Disc Measurements
Stereo transparencies from both eyes of all individuals were
digitized and analyzed by two technicians with the semiautomated Topcon
Image Analyzer (Imagenet), using the module for the retinal nerve fiber
layer height. The system’s hardware, its software modules, and
reproducibility of measurements have been described
previously.
21 22 For both ophthalmoscopy and Imagenet, the
distribution of the measurements of the vertical cup-disc ratio (VCDR)
and the asymmetry of the VCDR between both eyes together with their
97.5th and 99.5th percentiles were determined. The neural rim width was
only determined with Imagenet and was defined as the proportion of the
diameter of the rim section, measured at each of 36 equally spaced
points on the optic disc border, in relation to the total optic disc
diameter.
Proposed Definitions for Probable and Possible Glaucomatous Optic
Neuropathies
Because cupping of the optic nerve head is the hallmark for
glaucomatous optic neuropathy (GON), we chose to use this term.
However, it does not imply that a person with GON definitely has
glaucoma.
Probable GON was defined as the presence of at least one of the
following characteristics: a VCDR, or asymmetry in VCDR between both
eyes, or minimum width of the neural rim equal to or surpassing the
99.5th percentile of the population concerned. Possible GON was defined
as the above and greater than or equal to the 97.5th but
less than the 99.5th percentile of the population.
Visual Field Screening and Determination
The visual field (VF) screening during the first phase
(Table 2) reduced examination time and the chance of rim artifacts. Three or more
contiguously missed points on the screening test (≥4 when blind spot
was included) were taken as evidence for a VF defect. In the case of a
defective or unreliable VF test, VFs were retested with the same
screening test in the second phase, about 2 weeks later. Subjects with
a VF defect or unreliable test in the second phase of the study
underwent kinetic Goldmann perimetry on both eyes, performed by a
skilled perimetrist in the third phase, some weeks later. Also, in
cases with a Goldmann VF defect gonioscopy was performed to exclude
cases with narrow angles. All subjects with glaucomatous VF defects had
normal open anterior chamber angles. VF testing was unreliable or
impossible in the institutionalized subjects, mainly due to physical
and mental disabilities.
All Goldmann VF charts were independently graded by six different
graders (three senior ophthalmologists, two residents, one perimetrist)
according to a special grading protocol. Graders were at first masked
to all clinical data and optic disc appearances. Classification of the
defects was solely based on the shape and localization of the defect.
With regard to glaucomatous VF defects (GVFDs) special attention was
put on a nasal step, paracentral defects, arcuate scotomas, central
rests, remaining peripheral islands, and temporal nerve fiber bundle
defects. For fields with inconsistent classifications (30%) a
consensus was reached among the graders. The fundus and optic disc
transparencies were examined in a masked way for clues for retinal
causes of VF defects and, if present, for the expected location of the
VF defect. For exclusion of other nonglaucomatous causes of VF defects
all other data available in The Rotterdam Study was used, including
questionnaire data on and neurologic examination of all subjects, and
(history) data from general practitioners including reports from all
medical specialists who had treated the subject in the past.
Definition of Glaucomatous VF Defect
Glaucomatous VF defect (GVFD) was as defined as any Goldmann VF
defect for which no other (neur)ophthalmologic cause could be found
(see previous paragraph), thus excluding, for example, hemianopias and
quadrantanopias.
Definitions for Definite, Probable, and Possible OAGs, Ocular
Hypertension, and Elevated IOP
The following OAG definitions hold for a subject in whom in one or
both eyes an open angle was present in the absence of a history or
signs of angle closure or secondary glaucoma.
Definite OAG is the presence of a GVFD in combination with at least
possible GON.
Probable OAG is either the presence of a GVFD in the absence of a GON
or the absence of a GVFD with a probable GON.
Possible OAG is the presence of possible GON in the absence of either a
GVFD or a VF test.
For logistic reasons subjects underwent a glucose tolerance test (GTT;
by the cardiovascular research group) approximately 20 minutes before
IOP measurement in the first testing phase. This GTT was carried out by
giving an oral glucose load of 75 g in 200 ml of water and was
performed on all nondiabetic subjects who had not had a gastrectomy.
The IOP was not used in the definition of OAG, neither was the use of
IOP-lowering medication or the performance of an IOP-lowering (laser)
operation in the absence of our criteria for OAG. Elevated IOP was
defined as an IOP > 21 mm Hg or an IOP ≤ 21 mm Hg with any
form of IOP-lowering treatment. Ocular hypertension was defined as an
IOP > 21 mm Hg (or ≤21 mm Hg with any IOP-lowering treatment) in
the absence of a GVFD or a GON. IOP values were adjusted for the
IOP-lowering effect of the GTT.
Data Analysis
Although the distribution of IOP and VCDR was not completely
gaussian we thought it sound to assume a normal distribution because of
the large numbers in our study. Their 97.5th and 99.5th percentiles,
also corrected for disc area quartiles and age strata, were
parametrically calculated for each eye separately for the whole cohort,
including the OAG cases. These percentiles were rounded up or down to
the closest one decimal but for the minimum neural rim width (to two
decimals), in an attempt to include all OAG cases. In analyses in which
Imagenet data were combined with ophthalmoscopic data, the latter was
only used when the Imagenet data were missing or unreliable
(n = 84).
Prevalence figures of GVFDs; definite, probable, and possible OAGs;
elevated IOP; and ocular hypertension were calculated by 5-year age
categories and by gender. Prevalence figures of definite, probable, and
possible OAGs were calculated using disc data obtained by
ophthalmoscopy, by Imagenet and both. To estimate the influence of age
and gender on these prevalence figures, logistic regression analysis
was used. The odds ratio (OR) was used in these analyses as an
approximation of the relative risk. Sensitivity, specificity, and
predictive values of different cutoff points for VCDR for the presence
of a GVFD and, thus, OAG were calculated.
All analyses were adjusted for age and gender when appropriate and were
performed separately for the independently living subjects and for
those living in nursing homes.
Finally, definitions of definite OAG used in other population-based
studies
(Table 1) were, as far as available and common to those in our
study, applied to our data.
Results
Population
Interview data were collected for 78% (
n = 7983)
of the eligible persons (
n = 10,275; independently
living subjects plus nursing home subjects). The overall response rate
for the center visit was 69% (
n = 7129). A total of
6756 subjects participated in the ophthalmic part of the study.
Table 3 shows the response figures, focused on the ophthalmologic examinations.
The availability of ophthalmologic data in nursing homes was limited.
Distribution of Optic Disc Dimensions
The distribution of the optic disc dimensions in the independently
living subjects, determined by Imagenet and ophthalmoscopy, is shown in
Table 4 . The mean VCDR for ophthalmoscopy was 0.3, for Imagenet 0.49. Mean VCDR
was significantly higher with Imagenet compared with ophthalmoscopy.
Mean VCDR, its asymmetry between both eyes, and mean minimal rim width
were not significantly different in independently living subjects and
those in nursing homes (data not shown). The influences of disc area
and age on those disc measures are given in
Tables 5 and 6 , respectively. The 97.5th percentile of the VCDR was similar for right
and left eyes and differed 0.05 between the lowest and highest
quartiles of disc area. Subjects 75 years of age or older had on
ophthalmoscopy on average a 0.1 higher VCDR than those between 55 and
75 years of age.
Table 7 shows the 97.5th and 99.5th percentiles for VCDR, asymmetry in VCDR,
and minimal neural rim width together with the chosen cutoff points for
criteria for GON, based on the findings in
Tables 4 5 and 6 .
The 97.5th percentile of the VCDR for both ophthalmoscopy and Imagenet
was ≥ 0.7 (as it was in a different substudy on this population
for the Heidelberg Retina Tomograph). The cutoff point for
asymmetry in VCDR between both eyes was ≥ 0.2 for both
ophthalmoscopy and Imagenet. The chosen cutoff points for
definitions of GON derived from
Table 7 , thus were used for definitions
of OAG in the Rotterdam Study
(Table 1) .
Prevalence of Glaucomatous VF Defects
The number of subjects with a GVFD is shown in
Table 8 . The odds for men to have a GVFD were twice higher than for women (OR
2.0; 95% CI 1.3, 3.1). GVFDs were present in 8.6% of all subjects
with a VCDR ≥ 0.7. This prevalence increased to 38% in subjects
with a VCDR ≥ 0.8 and to 60% in subjects with a VCDR ≥
0.9.
Prevalence of Definite, Probable, and Possible OAGs
Table 9 shows the overall prevalence of definite, probable, and possible OAGs
for the various age groups derived from combined Imagenet and
ophthalmoscopic data. When Imagenet was not available or unreliable,
ophthalmoscopic data were used.
Tables 10 and 11 show the data derived when these techniques were separated. Between the
cases in
Tables 10 and 11 there was overlap but not complete
concordance. Of the independently living subjects, 50 had definite OAG
(0.8%; 95% CI 0.6, 1.0) with an OR of 2.1 (95% CI 1.2, 3.6) for men
versus women. The risk estimates between OAG, age, and gender remained
the same when the OAG cases defined with Imagenet or with
ophthalmoscopy were analyzed separately or by pooling (see
Tables 9 10 11 ).
In nursing homes no VFs were tested. In these subjects only probable or
possible OAG could be diagnosed based on optic disc appearance. The
prevalence of possible OAG was comparable with prevalence figures of
possible OAG in the independently living subjects in the same age
categories.
IOP Distribution in this Population
Although IOP was not used for the diagnosis of OAG in this study,
we will present our data on IOP here for comparison with other studies.
Our IOP data were influenced by the GTT. The IOP-lowering effect of the
GTT was studied by comparing the IOPs of subjects who had undergone a
GTT with those of subjects who had not (those who refused and diabetic
subjects). Subjects with a GTT had a significantly lower mean IOP
(−1.13 mm Hg; 95% CI −1.41, −0.84) than subjects without GTT
(similar in diabetic subgroup and refuser subgroup). Unadjusted for the
effect of the GTT the mean IOP (subjects with IOP-lowering treatment
were excluded) was 14.5 mm Hg (95% CI 14.46, 14.61). After correction
for the IOP-lowering effect of the glucose solution, the mean IOP was
15.6 mm Hg (95% CI 15.48, 15.64). The cumulative distribution of IOP
(adjusted for the GTT) is shown in
Figure 1 . There were no significant IOP differences between independently living
subjects and subjects in nursing homes (
P = 0.185,
adjusted for age and gender), or between men and women, and there was
no clinically significant change in IOP with increasing age.
The prevalence figures of elevated IOP (>21 mm Hg) are shown in
Table 12 for the independently living subjects. The OR for men to have an
IOP > 21 mm Hg compared with women was 1.35 (95% CI 1.10, 1.66).
Ocular hypertension was present in 5.6% of participants and also was
more prevalent in men than in women (OR 1.26; 95% CI 1.02, 1.56).
Again, the prevalence of ocular hypertension in subjects in nursing
homes was not significantly different from the prevalence in
independently living subjects (
P = 0.48, adjusted for
age and gender).
Of the 50 diagnosed OAG cases (using the combined Imagenet and
ophthalmoscopy data), 23 subjects (OR 46.0%; 95% CI 45.9, 46.1) were
previously known to have OAG and received IOP-lowering treatment. Of
the remaining 27 OAG cases, only three had an IOP > 21 mm Hg.
On the other hand, of the 242 independently living subjects with
IOP-lowering treatment, only 13 (OR 8.7%; 95% CI 5.1, 12.2) had
definite OAG when using only ophthalmoscopic data, and 23 (9.5%, 95%
CI 5.8, 13.2) subjects had definite OAG using the combined Imagenet and
ophthalmoscopy data. The sensitivity of elevated IOP for detection of
OAG was calculated only in the newly diagnosed OAG cases (because
the IOPs at the time of diagnosis of the known OAG cases were not
available). The sensitivity was 11.1% (3 of 27 cases had an elevated
IOP) and the specificity 98.0% (5827 of 5943 subjects had no definite
OAG). The predictive value of an IOP > 21 mm Hg for the detection
of OAG was only 2.5%; the predictive value of an IOP ≤ 21 mm Hg
for its absence was 99.6%.
Figure 2 shows the variation in prevalence of OAG by age in our study, when OAG
definitions from other large population-based studies were applied to
our data. This resulted in prevalence figures varying between 0.1% and
1.4% in the youngest age-categories to prevalence figures between
0.9% and 5.9% in the oldest ones.
Discussion
In this article we have given the rationale for the
following proposal for an international definition of (primary) OAG in
epidemiologic research: POAG is a disorder characterized by a GVFD, in
combination with probable or possible GON based on cutoff points
approximating the 99.5th and 97.5th percentiles, respectively, in that
population in at least one eye of a subject with open chamber angle,
and no history or sign of angle closure or secondary glaucoma. Thus, an
algorithm may be created leading to the diagnosis of definite,
probable, or possible POAG (see addendum). If other research groups use
a similar approach, one is free to pool definite and probable OAG or
not.
When looking at
Table 1 and reference 15, it seems that we have
not made much progress in defining glaucoma since Donders coined the
term glaucoma simplex in 1861.
23 It, thus, seems like a
risky enterprise to start defining criteria for POAG nearly 150 years
later. On the other hand, it is clear also from
Figure 2 that there is
a need for valid comparisons between studies. Current variations
in definition allow wide variations in prevalence data, as well as
justification for treatment. In this study we define cutoff values for
OAG determinants based on statistical grounds. This means that on
arbitrary statistical grounds a division is made between normal and
abnormal discs. We realize that this might be artificial and that some
subjects may falsely be defined as healthy or abnormal. However,
because of the large variation in OAG definitions in epidemiologic
and/or clinical research, we think it is for the time being a good
starting point to use such a definition for better comparison and
pooling of study results. In due time further refinement of the
definition may become possible when more incidence data become
available. Using 97.5th or 99.5th percentiles to define abnormality
does not mean that we used these criteria to define someone as being
diseased. Only in combination with other signs we propose the term
definite OAG. We felt that our database allowed for the definition of
OAG on statistical grounds and that such an approach may become a
starting point for future diagnostic fine-tuning. This may not be too
far away because some large population-based studies are working on
incidence data on POAG.
We did not fully exclude pseudoexfoliation as a cause of OAG during
baseline examination and, thus, refer in this article to OAG instead of
POAG. As no case of OAG in this cohort had pseudoexfoliation on
follow-up clinical examination we feel that in practice we may assume
that our data are valid as POAG data as did two studies that included
pseudoexfoliation in the diagnosis of POAG.
11 13
In this study we present prevalence figures for OAG combining GON
data obtained by Imagenet and ophthalmoscopy. We think the Imagenet
data are the more reliable data, especially for follow-up and
risk-factor analyses. However, because the Imagenet module for the
optic disc is not available any more, and neither is the simultaneous
stereoscopic Topcon TRC-SS2 camera, also essential for this module, we
also present prevalence figures based on only ophthalmoscopic optic
disc data for comparison with other studies. We found in a substudy
that Imagenet and the Heidelberg Retina Tomograph had much higher
correlations for the estimation of the VCDR than ophthalmoscopy,
showing that ophthalmoscopy is less reliable than these semiautomated
apparatuses, even carried out by trained examiners. Still we felt that
in daily practice ophthalmoscopy will be the method of choice during
the coming years. Therefore, in choosing cutoff points for the VCDR and
other disc measures we looked primarily at feasibility and tried to
choose cutoff points that were also ophthalmoscopically assessable.
Thus, to create as simple as possible a definition for OAG, based on
glaucomatous VF loss and GON, we propose as a cutoff point for a
statistically abnormal, and thus arbitrarily pathologic, possible GON a
VCDR ≥ 0.7, asymmetry in VCDR between both eyes ≥ 0.2 or
neuroretinal rim width < 0.1 for data obtained by ophthalmoscopy.
The latter was not assessed in this study by ophthalmoscopy but would
probably be necessary in other studies to detect discs with local
notching of the rim. From
Tables 5 and 6 one may see that for the
largest discs the cutoff for pathologic VCDR might have been chosen
as ≥ 0.8, and the same holds for those 75 years of age and older.
All these subdivisions make the definition more and more complicated
and that is why we propose to keep as the cutoff point for a possible
GON a VCDR ≥ 0.7. It should be borne in mind that this definition
exists for the cohort studied and that for other cohorts and especially
different races this type of definition might have different values.
Hitherto, some studies did not specify whether one used information on
IOP or disc measures to grade VF defects as
glaucomatous.
2 8 13 Two were masked in this
respect
9 11 and one was not.
14 Similarly,
before deciding whether a subject had OAG, all studies mentioned in
Table 1 looked at the combined data of a case while we tried to do so
by combining strictly defined determinants without subjective overall
evaluation at the end. We believed that this would lead to less
assessment bias. On the other hand, this resulted in small differences
in prevalence of OAG when the Imagenet or ophthalmoscopy data were
used.
Our overall prevalence of definite OAG of 0.8% (with combined
use of Imagenet and ophthalmoscopic data; 0.7% when only using
ophthalmoscopic data) and its rise with age are comparable with
prevalence figures of the Framingham Study
24 (1.2%), of
The Baltimore Eye Survey
7 (1.1%), and among the white
subjects of the Barbados Eye Study
9 (0.8%). The Beaver
Dam Eye Study and the Blue Mountains Eye Study, on the other hand,
found a higher overall prevalence, 2.1%
8 and
3.0%,
11 respectively. The prevalence of definite plus
probable OAG in the Rotterdam Study was 3.2% and this may explain the
gap. Several more reasons for these differences exist. All studies
mentioned in
Table 1 but the Egna-Neumarkt and the Rotterdam Study
used for final assignment to glaucoma diagnosis a review of
all data by one or more principal investigators, glaucoma specialists,
or ophthalmologists. In this study we combined the VF and optic disc
data, and this led straightforward to one of three diagnostic
categories (apart from normals) without additional influence on the
final results. The discrepancy with the Beaver Dam Study could be
explained by their wider criteria for POAG. Other sources for
differences between studies include sampling and perimetry techniques,
screening methods for glaucoma, subjective interpretation of
examination data, diagnostic criteria, age distributions, and real
geographic contrasts in prevalence due to differences in lifestyle or
genetic drift.
The VF screening and grading procedure in our study resulted in a
prevalence of 1.5% of GVFDs compatible with OAG. This is comparable
with the findings of the Framingham Study (1.4%, screening in a subset
only, enlargement of blind spot excluded)
25 but lower than
that found in Australia (3.1%).
11 The Blue Mountains Eye
Study used, after screening, Humphrey full threshold perimetry (C30-2),
which is more sensitive than kinetic Goldmann perimetry,
26 especially in glaucoma where it might detect up to 21% more
defects.
27 Full threshold automated perimetry is nowadays
considered to be the gold standard for VF examination, but at baseline
in 1990 we felt that especially in older subjects it may create more
false-positive errors compared with Goldmann perimetry. This might be
because of poor fixation that accounted for 9% of inadequate Humphrey
fields versus 2% at the Goldmann perimeter.
27 Between
threshold Humphrey perimetry and kinetic Goldmann perimetry there is
88% concordance when both tests appeared reliable.
27 Because the Humphrey algorithms also have changed in the meantime and
because we now perform both Humphrey 30-2 and Goldmann perimetry in the
follow-up study, a more valid comparison between both methods will be
possible within a year from now. It also has been shown that supra
threshold perimetry identifies about two thirds of all cases identified
by full-threshold perimetry.
28 Using this latter test our
prevalence of definite OAG might have risen to approximately 1.4%.
Even then there still would have been a twofold difference in
prevalence by comparison with the Blue Mountains Eye Study. Given the
variation in techniques and differences between various studies we
believe that conclusions on geographic differences are for the time
being not justifiable.
Our study differed from other large population-based studies with
regard to the use of Imagenet to assess the optic nerve. Imagenet used
strict criteria for defining the cup margins, based only on topographic
data, thus reducing variation due to different observers. This makes it
also particularly interesting for follow-up studies.
21 We
found a higher mean VCDR on Imagenet measurements (0.49) compared with
studies using other methods for examining the optic disc (mean VCDR
0.28,
5 0.3
10 using ophthalmoscopy by several
examiners, 0.36
8 and 0.43
11 by grading of
photographs). As a result, the prevalence of an enlarged VCDR was also
higher in our study than in other studies (VCDR ≥ 0.4: 76.7%
compared with 27.1%
5 or 37.0%
8 ). However,
our prevalence of a VCDR ≥ 0.7 (5.1%) was only slightly
different from the findings of the Blue Mountains Eye Study
(5.0%), which examined stereo transparencies with a
viewer.
11 Also, asymmetry in VCDR between both eyes
was more prevalent in our study, compared with findings of other studies (4.6% asymmetry ≥ 0.2,
25 0.7%
asymmetry ≥ 0.3
11 ).
The relation between OAG and gender is still controversial. In
Framingham
5 and Barbados
9 a higher prevalence
of POAG was found in men, which matched our finding. However, in the
Blue Mountains Eye Study a (borderline significantly) higher OR of 1.55
for POAG was found for women,
11 and in
Baltimore
7 and Beaver Dam
8 no difference was
found. It might be that in younger subjects the association between OAG
and gender is not yet present. It would seem possible that if the study
cohort had a greater proportion of younger subjects the gender risk
would disappear.
Our study did not show any correlation between age, gender, or
IOP. This is in contrast to previously published
results,
1 4 29 but is in agreement with
others.
1 5 8 Our findings do agree with prevalence data on
IOP and VCDR in nursing home inhabitants.
30 However, the
response in the nursing homes was low, especially in the older
subjects, increasing the risk of selection bias. This could explain our
lower OAG prevalences compared with that study.
30 One
could adjust the prevalence rates for probable and possible OAGs in the
nursing homes by raising them by 25% similar to the lower
response rates in these homes than in the independently living
subjects.
In conclusion, the overall prevalence of definite OAG in the
Rotterdam Study was 0.8%, which is comparable to findings of other
population-based studies on whites. The OR for men to
have OAG was higher than for women. There was a significant increase in
prevalence of OAG with increasing age. The overall prevalence of OAG
varied 12-fold with different criteria and screening algorithms. We
hope that standardizing diagnostic procedures and our proposed
definitions will improve future (epidemiologic) glaucoma research.
Appendix AA
Supported by grants from the Nestor Stimulation Program for Geriatric Research in the Netherlands (Ministry of Health and Ministry of Education), Rijswijk; Topcon Europe BV for optical equipment, Cappele a/d IJssel; the Netherlands Society for Prevention of Blindness, Amsterdam; Landelijke Stichting voor Blinden en Slechtzienden, Utrecht; Health Research and Development Council, The Hague; Haagsch Oogheelkundig Fonds, The Hague; Stichting Blindenpenning, Amsterdam; Optimix Foundation, Amsterdam; Rotterdamse Vereniging voor Blindenbelangen, Rotterdam; Stichting Fondsenwervingsacties Volksgezondheid, The Hague; G.Ph. Verhagen Stichting, Rotterdam; Stichting voor Ooglijders, Rotterdam; Stichting Blindenhulp, The Hague; Stichting ROOS, Rotterdam; and Merck Sharp & Dohme, Haarlem; the Edmond & Marianne Blaauw Foundation, Amsterdam; all in The Netherlands.
Submitted for publication February 11, 2000; revised April 27, 2000; accepted May 24, 2000.
Commercial relationships policy: N.
Presented at the annual meeting of the Association for Research in Vision and Ophthalmology, Fort Lauderdale, Florida, May, 1999.
Corresponding author: Paulus T. V. M. de Jong, The Netherlands Ophthalmic Research Institute, Meibergdreef 47, 1105 BA Amsterdam, The Netherlands.
p.dejong@ioi.knaw.nl
Table 1. Different Criteria for OAG
Table 1. Different Criteria for OAG
| Baltimore Eye Survey 7 |
| Definite, probable, and uncertain classification. Best available from eight, sometimes not quantified, different disc criteria (CDR ≥ 0.8, or difference between OU ≥ 0.3 or 0.4). VF defect not explainable by other causes. No IOP criterion. |
| Barbados Eye Study 9 |
| VF, optic disc, and ophthalmic examination criteria. Seven combinations possible. Definite: At least on succession 2 abnormal VF together with 2 of 3 of following criteria: CDR ≥ 0.7, asymmetry ≥ 0.2, rim width ≤ 0.1, notching, disc hemorrhage. If not: suspect. IOP no criterion. |
| Beaver Dam Eye Study 8 |
| At least two of the following criteria: VF defect not explainable by other causes, CDR ≥ 0.8 or an asymmetry in CDR ≥ 0.2, IOP ≥ 22 mm Hg, or IOP-lowering treatment. |
| Blue Mountains Eye Study 11 |
| Glaucomatous VF defect not explainable by other causes, combined with VCDR ≥ 0.7, or asymmetry in VCDR between both eyes ≥ 0.3. |
| Egna-Neumarkt Study 13 |
| At least 2 of the following criteria with open angle: Glaucomatous VF defect, IOP ≥ 22 mm Hg and 1 of the following disc criteria: CDR ≥ 0.7, or asymmetry > 0.2, or difference in VCDR and HCDR > 0.2, or notching, or disc hemorrhage, or excavation reaching disc margin. |
| Framingham Study 25 |
| VF defect not explainable by other cases (only in selected part of the population), combined with VCDR ≥ 0.6, or asymmetry in VCDR between both eyes ≥ 0.2. |
| Melbourne Visual Impairment Project 14 |
| No strict criteria due to uncertainty of diagnostic criteria. Panel discussion with 6 ophthalmologists grading in none, possible, probable, or definite POAG. Criteria: past POAG history, IOP > 21 mm Hg, VF defect including enlarged blind spot, CDR ≥ 0.7, or asymmetry ≥ 0.3. |
| Ponza Glaucoma Study 12 |
| Glaucomatous VF defects and 1 of the following criteria: IOP > 20 mm Hg, CDR ≥ 0.5, or asymmetry ≥ 0.2. Suspect if questionable VF loss. |
| Rotterdam Study (2000 criteria) |
| If present in at least 1 eye with open angle and no history or sign of secondary glaucoma. No IOP criteria. |
| Definite OAG: GVFD combined with at least possible GON: VCDR ≥ 0.7, or asymmetry between both eyes ≥ 0.2, or a minimal rim width < 0.1. |
| Probable OAG: (1) GVFD without possible GON or (2) absence of GVFD or of any VF test with probable GON: VCDR ≥ 0.9, or asymmetry ≥ 0.3, or minimal rim width < 0.05. |
| Possible OAG: possible GON and no GVFD. |
Table 2. Ophthalmologic Examination and OAG Screening: The Rotterdam Study,
1990–1993
Table 2. Ophthalmologic Examination and OAG Screening: The Rotterdam Study,
1990–1993
| Examination Type/Method/Tool | Manufacturer/Method Reference/Specifications |
| Phase I | |
| Autorefraction | Topcon RMA 2000* |
| Best corrected visual acuity | Lighthouse Visual Acuity Chart (2nd edition) |
| Keratometry | Topcon OM-4 Ophthalmometer* |
| Slit-lamp examination | Topcon SL-3E slit-lamp* |
| Chamber angle slit-lamp estimation | Van Herick 18 |
| IOP measurement | Goldmann applanation tonometer 19 , † |
| VF screening of both eyes separately | Modified 52-point supra threshold screening test central 24° radius (Humphrey VFA), ‡ |
| Mydriatic drops | Tropicamide 0.5% and phenylephrine 5% |
| Color transparencies macular area | 35° field; TRC-50VT camera* in mydriasis |
| Stereo simultaneous color transparencies optic disc | 20° field; TRC-SS2 camera* in mydriasis |
| Ophthalmoscopy | Direct and indirect (AusJena ophthalmoscope, Zeiss bonoscope) in mydriasis |
| Miotic drop | One drop of thymoxamine-hydrochloride 0.5% |
| |
| Phase II | |
| Visual field screening | As in phase I in case of unreliable or defective VF |
| |
| Phase III | |
| Visual field determination | In case of unreliable or defective VF in phase II: kinetic Goldmann perimetry, † , experienced perimetrist |
| IOP measurement | Goldmann applanation tonometer 19 , † |
| Gonioscopy (Shaffer) | Goldmann 3-mirror contact lens, † |
Table 3. Response Figures of the Rotterdam Study, 1990–1993
Table 3. Response Figures of the Rotterdam Study, 1990–1993
| Age Category, y | 55–59 | 60–64 | 65–69 | 70–74 | 75–79 | 80+ | Total |
| Independently living subjects | | | | | | | |
| Total eligibles | 1480 | 1761 | 1737 | 1606 | 1286 | 1291 | 9161 |
| Total examined | 1172 (79.2) | 1421 (80.7) | 1327 (76.4) | 1157 (72.0) | 834 (64.9) | 583 (45.2) | 6494 (70.9) |
| Ophthalmologically examined | 1162 (78.5) | 1399 (79.4) | 1278 (73.0) | 1108 (69.0) | 795 (61.8) | 594 (41.8) | 6281 (68.6) |
| Men | 483 (75.1) | 616 (79.1) | 594 (75.7) | 452 (69.5) | 315 (63.0) | 166 (44.0) | 2626 (70.5) |
| Women | 679 (81.0) | 783 (79.5) | 684 (70.8) | 656 (68.6) | 480 (61.1) | 373 (40.8) | 3655 (67.2) |
| Nursing homes | | | | | | | |
| Total eligibles | 1 | 4 | 14 | 29 | 125 | 941 | 1114 |
| Total examined | 1 (100) | 3 (75.0) | 12 (85.7) | 20 (69.0) | 72 (57.6) | 527 (56.0) | 635 (57.0) |
| Ophthalmologically examined | 0 (0.0) | 1 (25.0) | 8 (57.1) | 12 (41.4) | 60 (48.0) | 394 (41.9) | 475 (42.6) |
| Men | 0 (0.0) | 0 (0.0) | 4 (50.0) | 4 (50.0) | 18 (48.6) | 93 (54.7) | 119 (53.1) |
| Women | 0 (0.0) | 1 (33.3) | 4 (66.7) | 8 (38.1) | 42 (47.7) | 301 (39.0) | 356 (40.0) |
Table 4. Distribution of Optic Disc Dimensions in Independently Living Subjects
Determined by Imagenet and Ophthalmoscopy
Table 4. Distribution of Optic Disc Dimensions in Independently Living Subjects
Determined by Imagenet and Ophthalmoscopy
| Imagenet (SE) n = 5619 | Ophthalmoscopy (SE) n = 6199 |
| Mean VCDR | 0.49 (0.0018) | 0.30 (0.0024) |
| Median asymmetry in VCDR | 0.06 | 0.00 |
| Mean minimal neural rim width | 0.17 (0.001) | not assessed |
| Percentage of Subjects | Percentage of Subjects |
| Disc dimension VCDR ≥ | | |
| 0.4 | 76.7 | 43.2 |
| 0.5 | 55.0 | 19.6 |
| 0.6 | 26.5 | 9.0 |
| 0.7 | 5.1 | 4.0 |
| 0.8 | 0.4 | 1.6 |
| 0.9 | 0.0 | 0.7 |
| Asymmetry in VCDR ≥ | | |
| 0.2 | 7.5 | 5.8 |
| 0.3 | 1.3 | 1.6 |
| 0.4 | 0.1 | 0.6 |
| Minimal neural rim width < | | |
| 0.25 | 80.5 | Not assessed |
| 0.20 | 58.2 | |
| 0.15 | 26.2 | |
| 0.10 | 4.1 | |
| 0.05 | 0.1 | |
Table 5. Influence of Disc Area on 97.5th Percentile of VCDR Both Determined by
Imagenet (n = 5619 Subjects)
Table 5. Influence of Disc Area on 97.5th Percentile of VCDR Both Determined by
Imagenet (n = 5619 Subjects)
| Right Eyes | | Left Eyes | |
| Disc Area (quartiles) | VCDR | Disc Area (quartiles) | VCDR |
| ;l;col><2.11 mm2 | ≥0.68 | ;l;col><2.07 mm2 | ≥0.68 |
| 2.11–2.39 mm2 | ≥0.71 | 2.07–2.36 mm2 | ≥0.71 |
| 2.39–2.71 mm2 | ≥0.73 | 2.36–2.68 mm2 | ≥0.73 |
| ≥2.71 mm2 | ≥0.76 | ≥2.68 mm2 | ≥0.75 |
| Overall | ≥0.73 | Overall | ≥0.73 |
Table 6. Influence of Age on 97.5th Percentile of VCDR and VCDR Asymmetry
between Both Eyes for Ophthalmoscopy and Imagenet Data
Table 6. Influence of Age on 97.5th Percentile of VCDR and VCDR Asymmetry
between Both Eyes for Ophthalmoscopy and Imagenet Data
| Age, y | VCDR OD Imagenet | VCDR OD Ophthalmoscopy | VCDR OS Imagenet | VCDR OS Ophthalmoscopy | Asymmetry Imagenet | Asymmetry Ophthalmoscopy |
| 55–64 | 0.72 | 0.7 | 0.72 | 0.7 | 0.26 | 0.2 |
| 65–74 | 0.73 | 0.7 | 0.72 | 0.7 | 0.26 | 0.2 |
| 75–84 | 0.74 | 0.8 | 0.74 | 0.8 | 0.3 | 0.2 |
| 85+ | 0.77 | 0.8 | 0.74 | 0.8 | 0.31 | 0.2 |
Table 7. Percentiles of Optic Disc Dimensions in Independently Living Subjects
and Derived Cutoff Points Leading to Criteria for Probable and Possible
Glaucomatous Optic Disc Neuropathy (GON)
Table 7. Percentiles of Optic Disc Dimensions in Independently Living Subjects
and Derived Cutoff Points Leading to Criteria for Probable and Possible
Glaucomatous Optic Disc Neuropathy (GON)
| Percentiles | Imagenet n = 5619 | | Ophthalmoscopy n = 6199 | |
| 97.5 | 99.5 | 97.5 | 99.5 |
| VCDR ≥ | 0.73 | 0.78 | 0.7 | 0.9 |
| Chosen cutoff point ≥ | 0.7 | 0.8 | 0.7 | 0.9 |
| Asymmetry in VCDR ≥ | 0.26 | 0.34 | 0.2 | 0.3 |
| Chosen cutoff point ≥ | 0.2 | 0.3 | 0.2 | 0.3 |
| Minimal neural rim width < | 0.08 | 0.05 | Not assessed | |
| Chosen cutoff point < | 0.1 | 0.05 | | |
| Age, y | Men (%) | Women (%) | Total (%) |
| ;l;row>55–59 | 2/479 (0.4) | 0/672 (0.0) | 2/1151 (0.2) |
| 60–64 | 5/609 (0.8) | 4/773 (0.5) | 9/1382 (0.7) |
| 65–69 | 11/588 (1.9) | 7/670 (1.0) | 18/1258 (1.4) |
| 70–74 | 13/442 (2.9) | 11/643 (1.7) | 24/1085 (2.2) |
| 75–79 | 8/295 (2.7) | 7/461 (1.5) | 15/756 (2.0) |
| 80+ | 10/152 (6.6) | 9/338 (2.7) | 19/490 (3.9) |
| Total | 49/2565 (1.9) | 38/3557 (1.1) | 87/6122 (1.4) |
| [SE = 0.27] | [SE = 0.17] | [SE = 0.15] |
Table 9. Prevalence of OAG: The Rotterdam Study, 1990–1993—Imagenet Data
Combined with Ophthalmoscopic Data
Table 9. Prevalence of OAG: The Rotterdam Study, 1990–1993—Imagenet Data
Combined with Ophthalmoscopic Data
| Age, y | Men (n) | Definite OAG | Probable OAG GVFD | Probable OAG GON | Possible OAG | Women (n) | Definite OAG | Probable OAG GVFD | Probable OAG GON | Possible OAG | Total (n) | Definite OAG | Probable OAG GVFD | Probable OAG GON | Possible OAG |
| Independently living subjects | | | | | | | | | | | | | | | |
| 55–59 | 483 | 1 (0.2) | 1 (0.2) | 7 (1.4) | 72 (14.9) | 679 | 0 (0) | 0 (0) | 10 (1.5) | 94 (13.8) | 1162 | 1 (0.1) | 1 (0.1) | 17 (1.4) | 166 (14.2) |
| 60–64 | 616 | 4 (0.6) | 1 (0.2) | 10 (1.6) | 83 (13.5) | 783 | 1 (0.1) | 3 (0.4) | 10 (1.3) | 114 (14.6) | 1399 | 5 (0.4) | 4 (0.3) | 20 (1.4) | 197 (14.1) |
| 65–69 | 594 | 5 (0.8) | 6 (1.0) | 6 (1.0) | 98 (16.5) | 684 | 6 (0.9) | 1 (0.1) | 17 (2.5) | 105 (15.4) | 1278 | 11 (0.9) | 7 (0.5) | 23 (1.8) | 203 (15.9) |
| 70–74 | 452 | 6 (1.3) | 7 (1.5) | 5 (1.1) | 57 (12.6) | 656 | 7 (1.1) | 4 (0.6) | 8 (1.2) | 97 (14.8) | 1108 | 13 (1.2) | 11 (1.1) | 13 (1.2) | 154 (13.9) |
| 75–79 | 315 | 6 (1.9) | 2 (0.6) | 11 (11.1) | 51 (16.2) | 480 | 3 (0.6) | 4 (0.8) | 16 (3.3) | 70 (14.6) | 795 | 9 (1.1) | 6 (0.8) | 27 (3.4) | 121 (15.2) |
| 80+ | 166 | 6 (3.6) | 4 (2.4) | 5 (3.0) | 39 (23.5) | 373 | 5 (1.3) | 4 (1.1) | 10 (2.7) | 60 (16.1) | 539 | 11 (2.0) | 8 (1.5) | 15 (2.8) | 99 (18.4) |
| Total | 2626 | 28 (1.1) | 21 (0.8) | 44 (1.7) | 400 (15.2) | 3655 | 22 (0.6) | 16 (0.4) | 71 (1.9) | 540 (14.8) | 6281 | 50 (0.8) | 37 (0.6) | 115 (1.8) | 940 (15.0) |
| SEM | | 0.0020 | 0.0018 | 0.0025 | 0.0069 | | 0.0013 | 0.0011 | 0.0022 | 0.0058 | | 0.0011 | 0.0010 | 0.0017 | 0.0044 |
| Dependently living subjects* | | | | | | | | | | | | | | | |
| 55–59 | 0 | | | | | 0 | | | | | 0 | | | | |
| 60–64 | 0 | | | | | 1 | | | | | 1 | | | | |
| 65–69 | 4 | | | | | 4 | | | | | 8 | | | | |
| 70–74 | 4 | | | | 1 (25.0) | 8 | | | | 1 (12.5) | 12 | | | | 2 (16.7) |
| 75–79 | 18 | | | | 3 (16.7) | 42 | | | 2 (4.8) | 6 (14.3) | 60 | | | 2 (3.3) | 9 (15.0) |
| 80+ | 93 | | | 4 (4.3) | 21 (22.6) | 301 | | | 18 (6.0) | 42 (14.0) | 394 | | | 22 (5.6) | 63 (16.0) |
| Total | 119 | | | 4 (3.4) | 25 (21.0) | 356 | | | 20 (5.6) | 49 (13.8) | 475 | | | 24 (5.1) | 74 (15.6) |
| SEM | | — | — | 0.0165 | 0.0375 | — | — | — | 0.0122 | 0.0183 | | — | — | 0.0100 | 0.0166 |
Table 10. Prevalence of OAG: The Rotterdam Study, 1990–1993—Ophthalmoscopic
Disc Data Only
Table 10. Prevalence of OAG: The Rotterdam Study, 1990–1993—Ophthalmoscopic
Disc Data Only
| Age, y | Men (n) | Definite OAG | Probable OAG GVFD | Probable OAG GON | Possible OAG | Women (n) | Definite OAG | Probable OAG GVFD | Probable OAG GON | Possible OAG | Total (n) | Definite OAG | Probable OAG GVFD | Probable OAG GON | Possible OAG |
| Independently living subjects | | | | | | | | | | | | | | | |
| 55–59 | 483 | 0 (0) | 2 (0.4) | 4 (0.8) | 31 (6.4) | 679 | 0 (0) | 0 (0) | 10 (1.5) | 40 (5.9) | 1162 | 0 (0) | 2 (0.1) | 14 (1.2) | 71 (6.1) |
| 60–64 | 616 | 3 (0.5) | 2 (0.3) | 10 (1.6) | 41 (6.7) | 783 | 1 (0.1) | 3 (0.4) | 7 (0.9) | 58 (7.4) | 1399 | 4 (0.3) | 5 (0.4) | 17 (1.2) | 99 (7.1) |
| 65–69 | 594 | 5 (0.8) | 6 (1.0) | 6 (1.0) | 45 (7.6) | 684 | 6 (0.9) | 1 (0.1) | 10 (1.5) | 55 (8.0) | 1278 | 11 (0.9) | 7 (0.5) | 16 (1.3) | 100 (7.8) |
| 70–74 | 452 | 9 (2.0) | 4 (0.9) | 10 (2.2) | 19 (4.2) | 656 | 8 (1.2) | 3 (0.5) | 10 (1.5) | 53 (8.1) | 1108 | 17 (1.5) | 7 (0.6) | 20 (1.8) | 72 (6.5) |
| 75–79 | 315 | 3 (1.0) | 5 (1.6) | 10 (3.2) | 26 (8.3) | 480 | 2 (0.4) | 5 (1.0) | 10 (2.1) | 39 (8.1) | 795 | 5 (0.6) | 10 (1.3) | 20 (2.5) | 65 (8.2) |
| 80+ | 166 | 6 (3.6) | 4 (2.4) | 2 (1.2) | 22 (13.3) | 373 | 4 (1.1) | 5 (1.3) | 7 (1.9) | 33 (8.8) | 539 | 10 (1.9) | 9 (1.7) | 9 (1.7) | 55 (10.2) |
| Total | 2626 | 26 (1.0) | 23 (0.9) | 42 (1.6) | 184 (7.0) | 3655 | 21 (0.6) | 17 (0.5) | 54 (1.5) | 278 (7.6) | 6281 | 47 (0.7) | 40 (0.6) | 96 (1.6) | 462 (7.4) |
| SEM | | 0.0019 | 0.0018 | 0.0024 | 0.0050 | | 0.0013 | 0.0011 | 0.0020 | 0.0044 | | 0.0011 | 0.0010 | 0.0015 | 0.0033 |
| Dependently living subjects* | | | | | | | | | | | | | | | |
| 55–59 | 0 | | | | | 0 | | | | | 0 | | | | |
| 60–64 | 0 | | | | | 1 | | | | | 1 | | | | |
| 65–69 | 4 | | | | | 4 | | | | | 8 | | | | |
| 70–74 | 4 | | | | | 8 | | | | | 12 | | | | |
| 75–79 | 18 | | | | 2 (11.1) | 41 | | | 2 (4.9) | 3 (7.3) | 59 | | | 2 (3.4) | 5 (8.5) |
| 80+ | 93 | | | 6 (6.5) | 7 (7.5) | 297 | | | 13 (4.4) | 22 (7.4) | 390 | | | 19 (4.9) | 29 (7.4) |
| Total | 119 | | | 6 (5.0) | 9 (7.6) | 351 | | | 15 (4.3) | 25 (7.1) | 470 | | | 21 (4.5) | 34 (7.2) |
| SEM | | — | — | 0.0201 | 0.0243 | | — | — | 0.0108 | 0.0138 | | — | — | 0.0095 | 0.0120 |
Table 11. Prevalence of OAG: The Rotterdam Study, 1990–1993—Imagenet Data Only
Table 11. Prevalence of OAG: The Rotterdam Study, 1990–1993—Imagenet Data Only
| Age, y | Men (n) | Definite OAG | Probable OAG GVFD | Probable OAG GON | Possible OAG | Women (n) | Definite OAG | Probable OAG GVFD | Probable OAG GON | Possible OAG | Total (n) | Definite OAG | Probable OAG GVFD | Probable OAG GON | Possible OAG |
| Independently living subjects | | | | | | | | | | | | | | | |
| 55–59 | 434 | 1 (0.2) | 1 (0.2) | 6 (1.4) | 67 (15.4) | 620 | 0 (0) | 0 (0) | 7 (1.1) | 85 (13.7) | 1054 | 1 (0.1) | 1 (0.1) | 13 (1.2) | 152 (14.4) |
| 60–64 | 563 | 4 (0.7) | 1 (0.2) | 8 (1.4) | 80 (14.2) | 722 | 0 (0) | 4 (0.6) | 6 (0.8) | 108 (15.0) | 1285 | 4 (0.3) | 5 (0.4) | 14 (1.1) | 188 (14.6) |
| 65–69 | 539 | 2 (0.4) | 9 (1.7) | 5 (0.9) | 90 (16.7) | 626 | 4 (0.6) | 3 (0.5) | 14 (2.2) | 100 (16.0) | 1165 | 6 (0.5) | 12 (1.0) | 19 (1.6) | 190 (16.3) |
| 70–74 | 399 | 3 (0.8) | 10 (2.5) | 0 (0) | 55 (13.8) | 592 | 4 (0.7) | 7 (1.2) | 7 (1.2) | 93 (15.7) | 991 | 7 (0.7) | 17 (1.7) | 7 (0.7) | 148 (14.9) |
| 75–79 | 252 | 4 (1.6) | 4 (1.6) | 6 (2.4) | 44 (17.5) | 399 | 3 (0.8) | 4 (1.0) | 15 (3.8) | 64 (16.0) | 651 | 7 (1.1) | 8 (1.2) | 21 (3.2) | 108 (16.6) |
| 80+ | 122 | 2 (1.6) | 8 (6.6) | 5 (4.1) | 36 (29.5) | 262 | 4 (1.5) | 5 (1.9) | 7 (2.7) | 49 (18.7) | 384 | 6 (1.6) | 13 (3.4) | 12 (3.1) | 85 (22.1) |
| Total | 2309 | 16 (0.7) | 33 (1.4) | 30 (1.3) | 372 (16.1) | 3221 | 15 (0.5) | 23 (0.7) | 56 (1.7) | 499 (15.5) | 5530 | 31 (0.6) | 56 (1.0) | 86 (1.6) | 871 (15.8) |
| SEM | | 0.0017 | 0.0025 | 0.0024 | 0.0077 | | 0.0012 | 0.0015 | 0.0023 | 0.0064 | | 0.0010 | 0.0013 | 0.0017 | 0.0049 |
| Dependently living subjects* | | | | | | | | | | | | | | | |
| 55–59 | 0 | | | | | 0 | | | | | 0 | | | | |
| 60–64 | 0 | | | | | 1 | | | | | 1 | | | | |
| 65–69 | 4 | | | | | 2 | | | | | 6 | | | | |
| 70–74 | 4 | | | | 1 (25.0) | 7 | | | | 1 (14.3) | 11 | | | | 2 (18.1) |
| 75–79 | 13 | | | | 3 (23.1) | 24 | | | | 5 (20.8) | 37 | | | | 8 (21.6) |
| 80+ | 57 | | | 1 (1.8) | 17 (29.3) | 169 | | | 8 (4.7) | 33 (19.5) | 226 | | | 9 (3.9) | 50 (22.1) |
| Total | 78 | | | 1 (1.3) | 21 (26.9) | 203 | | | 8 (3.9) | 39 (19.2) | 281 | | | 9 (3.2) | 60 (21.4) |
| SEM | | — | — | 0.0128 | 0.0506 | | — | — | 0.0137 | 0.0277 | | — | — | 0.0105 | 0.0245 |
Table 12. Prevalence of Elevated IOP* and IOP-Lowering Treatment: The Rotterdam
Study, 1990–1993
Table 12. Prevalence of Elevated IOP* and IOP-Lowering Treatment: The Rotterdam
Study, 1990–1993
| Age, y | Independently Living Subjects | | | | Nursing Home Subjects | | | |
| Elevated IOP | | Ocular Hypertension | | Elevated IOP | | Ocular Hypertension | |
| Men (%) | Women (%) | Men (%) | Women (%) | Men (%) | Women (%) | Men (%) | Women (%) |
| 55–59 | 12/478 (2.5) | 25/673 (3.7) | 10/478 (2.1) | 22/673 (3.3) | — | — | — | — |
| 60–64 | 38/609 (6.2) | 22/777 (2.8) | 28/609 (4.6) | 15/777 (1.9) | — | 0/1 (0.0) | — | 0/1 (0.0) |
| 65–69 | 44/582 (7.6) | 33/681 (4.8) | 30/582 (5.2) | 21/681 (3.1) | 0/4 (0.0) | 0/1 (0.0) | 0/4 (0.0) | 0/1 (0.0) |
| 70–74 | 34/446 (7.6) | 36/651 (5.5) | 20/446 (4.5) | 24/651 (3.7) | 0/4 (0.0) | 0/8 (0.0) | 0/4 (0.0) | 0/8 (0.0) |
| 75–79 | 25/315 (7.9) | 40/476 (8.4) | 17/315 (5.4) | 29/476 (6.1) | 0/16 (0.0) | 5/36 (13.9) | 0/16 (0.0) | 2/36 (5.6) |
| 80+ | 21/165 (12.7) | 31/366 (8.5) | 8/165 (4.8) | 24/366 (6.6) | 7/87 (8.0) | 23/289 (8.0) | 1/87 (1.1) | 13/289 (4.5) |
| Total | 174/2595 (6.7) | 187/3624 (5.2) | 113/2595 (4.4) | 135/3624 (3.7) | 7/111 (6.3) | 28/335 (8.4) | 1/111 (0.9) | 15/335 (4.5) |
The authors thank the coworkers of the Rotterdam Study (in
particular Diana Bakker, Corina Brussee, Tineke Dekker, Ada Hooghart,
Anneke Korving, Jeanette Noordzij, and Els van den Oever) for their
assistance in this study. Also, special thanks to Douwe Bakker, JB
Jonas, and S. Panda–Jonas for their help in the grading of the VF
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