Race and AMD
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more frequent in non-Hispanic whites than in blacks in the United
States. This was based on observations reported in clinical case
series. The use of new AMD classification schemes and severity scales
in large population-based studies has confirmed that non-Hispanic
whites have higher prevalences of late AMD, both neovascular AMD and
geographic atrophy, than in non-Hispanic blacks and Hispanics. For
example, in the Salisbury Eye Examination (SEE), the prevalence of
neovascular AMD (1.7% vs 1.1%) and geographic atrophy (1.8% vs 0.3%)
was higher in whites than in blacks. Age-specific prevalence of late
AMD was consistently lower in Mexican Americans in the Los Angeles
Latino Eye Study (LALES) than in whites in the Beaver Dam Eye Study
(BDES) (eg, 70-79 years, 1.5% vs 3.7%; ≥80 years, 8.5% vs 9.5%). In
the Multi-Ethnic Study of Atherosclerosis (MESA), the prevalence of
late AMD was higher in Chinese Americans than in whites. Similar risk
factors, for example older age, family history, and smoking, were
associated with AMD regardless of race/ethnicity.
There are few population-based studies describing the incidence or
progression of AMD in different racial/ethnic groups. These studies,
using newer standardized grading schemes, have shown that while
younger non-Hispanic blacks and Mexican Americans manifest early AMD
with almost the same prevalence as in whites, they are less likely to
develop late AMD than non-Hispanic whites. In the SEE, blacks were
more likely than whites to develop early AMD after 2 years of
follow-up examination but had similar risk of progression to more
severe AMD. Over a 9-year period in the population-based Barbados Eye
Study, the overall incidence rate of early AMD in blacks was 13% and
that of late AMD was 0.7%, significantly lower than found in whites in
the BDES, a white population of similar age. In the LALES, the 4-year
incidence of both early (7.5%) and late (0.2%) AMD was significantly
lower than the estimated incidence in non-Hispanic whites in the BDES.
When the data were age-standardized, the overall incidence in Mexican
Americans in the LALES population remained lower for early AMD (0.95
vs 1.73) and late AMD (0.11 vs 0.18) than in whites in the BDES.
Recognizing the need for more data regarding AMD in different
racial/ethnic groups, VanderBeek and associates report differences in
the prevalence and incidence of nonexudative and exudative AMD between
whites and non-Hispanic blacks, Hispanics, and Asian Americans using
health care claims data from a large, national managed care network.
While adjusting for confounders (but not smoking status), they found
at age 60 years that non-Hispanic blacks had a 25% lower prevalence of
having nonexudative and 30% lower prevalence of having exudative AMD
coded in their medical claims record compared to whites. At age 80
years, the comparable prevalences were 44% and 55% that of whites.
Similar comparisons for Hispanics demonstrated at age 60 years a
similar risk for nonexudative AMD to that in whites but a 28% higher
risk of exudative AMD than whites, while at age 80 years there was an
18% reduced lower risk for nonexudative AMD and a similar risk of
incident exudative AMD in Hispanics compared to that found in whites.
Compared to whites, Asian Americans showed a 28% increased risk for
nonexudative AMD at 60 years but a 46% decreased risk for exudative
AMD at age 80 years. The authors are well aware of the significant
limitations in using claims data to estimate prevalence and incidence
in making these and other estimates that appear in their paper.
Readers of this and other epidemiologic papers must be cautious when
interpreting the comparisons between racial/ethnic groups; studies
differ in methods of ascertainment of the study cohort, in
participation, and in ascertainment and definitions of the presence
and severity of AMD.
Assuming that the data in the Vanderbeek paper reflect accurate
estimates of the prevalence of early and late AMD, the reasons for the
differences among racial/ethnic groups are not known. Jampol and
Tielsch speculated that melanin, "acting as a free radical scavenger
or in some other way, may protect the pigment epithelium, Bruch's
membrane, choroid, or the outer retina from degeneration changes
predisposing the patient to choroidal neovascularization." More
recently, differences in distributions of deleterious and protective
genes for AMD among the different racial/ethnic groups suggest that
these may explain the differences in risk of developing AMD. In the
MESA, whites, blacks, and Hispanics who were homozygous for the CFH
Y402H CC variant genotype had the highest prevalences of early AMD
compared to those with the CFH Y402H TT wild genotype. The CFH Y402H
CC variant genotype distributions varied among these racial/ethnic
groups and explained some of the difference in early AMD prevalence
for Chinese and for Hispanics, but not for blacks. It was postulated
that differences in distributions of other protective (CFH-related
1/3c deletions, C2/BF haplotype) and deleterious genotypes (eg, ARMS2)
and their interactions with environmental/host factors (eg, smoking,
inflammation, oxidative stress, diet) among the different
racial/ethnic groups would further explain these differences. In the
LALES, the homozygous CFH Y402H CC variant polymorphism was present in
only 3% of the study population compared to 9% to 21% of non-Hispanic
whites. Even within a racial/ethnic group (eg, Mexican American),
there is great diversity in racial/ethnic origins and likely
differences in gene distributions attributable to this heterogeneity.
What do these data tell us about AMD? They suggest that genetic, and
possibly genetic and environmental, interactions play a role in the
pathogenesis of AMD. Understanding these differences may indicate the
possibility of successful preventive approaches for this disease.
Also, late AMD, while less common in blacks and Hispanic whites than
non-Hispanic whites, is still frequent enough to warrant identifying
those at greatest risk of progression, and they, too, would likely
benefit from interventions to reduce noxious exposures (eg, cessation
of smoking) and use of potential preventive therapies (eg, use of
antioxidant zinc multivitamins) in those at highest risk of
progression to late AMD.
Am J Ophthalmol. 2011 Aug;152(2):153-4
http://www.ncbi.nlm.nih.gov/pubmed/21784191
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