Major reviewPrimary Open-Angle Glaucoma in Blacks: A Review☆
Introduction
Glaucoma is one of the leading causes of blindness worldwide.20., 30., 48., 107., 124., 125., 129., 134., 160., 169., 170., 194., 200. Although the number of people affected by the primary glaucomas varies in different reports, it is estimated that approximately 66.8 million people are affected worldwide.134 One of the most prevalent forms is primary open-angle glaucoma (POAG), with approximately 33.1 million sufferers around the world.59., 134. In the United States alone, it is estimated that 2.47 million people are affected by POAG, 130,450 of whom have become bilaterally blind.142 POAG has a serious impact on the quality of life ofa large number of people both in the United States and worldwide.4
Blacks in many areas of the world are disproportionately affected by POAG. Large population-based studies such as the Barbados Eye Study showed that 1 in 11 Afro-Caribbeans over the age of 50 years, and 1 in 6 over the age of 70 years had open-angle glaucoma.100 Another population-based study was conducted in St. Lucia (West Indies), an island composed of a relatively homogeneous black population. Higher prevalence estimates of POAG in blacks 30 years of age and older were reported in St. Lucia, compared to the prevalence estimates reported for whites in other population-based studies.114 Similarly, population-based surveys conducted in African countries have shown the devastating impact of POAG in blacks.8., 22., 38., 148., 151., 187.
In the United States, the Baltimore Eye Survey164., 175. and other studies22., 113., 188., 197. have estimated that prevalence in some age groups may be up to six times as high in black Americans, compared to whites. POAG is the leading cause of irreversible blindness in the black American population164., 183. and early studies suggested that black Americans are more likely to become blind as a result of POAG than are white Americans.63., 68., 195. A more recent study showed that black Americans are 16 times more likely than white Americans to develop POAG-associated visual impairment (i.e., best-corrected visual acuity worse than 20/40 but better than 20/200 in the better-seeing eye).126 Furthermore, POAG progresses more rapidly in blacks.195 A follow-up of the St. Lucia cohort, 10 years after the initial study, showed that visual field progression occurred in 52–73% of untreated glaucoma and glaucoma-suspect eyes.193 POAG appears approximately 10 years earlier in this population.33., 57., 63., 113., 128., 164., 188., 195. Consistent with this trend, David et al39 reported that ocular hypertension appears approximately 12 years earlier in blacks. Furthermore, a higher percentage of blacks than whites (18.1% versus 5.4%) with ocular hypertension go on to develop glaucoma.39., 82.
This article reviews the current knowledge on POAG in blacks. Racial differences in diagnostic factors, risk factors, and treatment methods in blacks will be discussed. Other pertinent issues, such as treatment availability and glaucoma awareness in blacks, will also be reviewed.
That disease prevalence and morbidity may differ according to race is well established. What, then, defines “race” and how is it measured?92 Defining race is much more difficult than it would appear.9 To quote Evelyn Brooks Higginbotham, a noted African American historian and writer, “when we talk about the concept of race, most people believe that they know it when they see it but arrive at nothing short of confusion when pressed to define it.”
Biomedical research has long assumed that phenotype traits like skin color and hair texture can be used to categorize people into meaningful genetic subgroups. Yet, many investigators now assert that there is no genetic basis for racial classification, that biologically distinct races do not exist, and that race as used in the United States is a social and political construct with no basis in science and anthropology.60 The Institute of Medicine in their “Report on Cancer and Ethnic Minorities and the Medical Underserved—1999”, concluded that human biodiversity cannot be adequately summarized according to the broad, presumably discrete categories assumed by a racial taxonomy and recommended using the term “ethnic group.”
The concept of ethnicity is more concerned with cultural distinctions and learned behavior and thus carries less of a biological connotation. However, the use of ethnicity in classifying people in medical research has its own problems with ambiguity.161 For example, there is no single black culture in the United States. A recently emigrated taxi driver from Haiti, a slave-descendent farmer from rural Mississippi, and a young Republican politician from a mixed marriage may all classify themselves as “black,” but will likely have distinct cultural experiences.190
The distinction between race and ethnicity is often blurred in medical research. From the standpoint of health differences, what is measured with the variable “race” is likely to be some combination of culture, genes, and external societal influences.165 The concepts of race and ethnicity are complex, and while acknowledging that self-report is imperfect,5., 185. clinical studies have relied on this method.15., 62. In this article, we use the term “race” rather than “ethnic group” because we believe that the concept of biological race does have some usefulness in clinical medicine, particularly in the assessment of phenotypic differences in attributes that define a particular disease. However, we caution that a strictly biological connotation of race focuses too narrowly on only one of many factors that are likely to be operational in explaining the disparity in the prevalence and morbidity of specific diseases.189
Large population-based studies provide important information on the prevalence of POAG and on risk factors for the disease in blacks. Clinical observations suggesting racial differences in POAG date back to the 1930s.119., 183. However, solid evidence regarding these differences could only be obtained through large population-based studies. These studies offer several advantages over other study designs, including reduced possibility of selection bias, thus providing more accurate prevalence estimates. One of the first population-based surveys was conductedin St. Lucia, in 1989, and it included 1,679 Afro-Caribbeans.114 The Baltimore Eye Survey (5,308 subjects 40 years of age or older, of whom 45% were black Americans) and the Barbados Eye Study (4,631 subjects 40 years of age or older, 93% of whom were Afro-Caribbeans) were later conducted to characterize vision in people of African descent. The two most recent prevalence surveys were conducted in Africa, on Bantu-derived populations. One was conducted in the district of Kongwa, central Tanzania and included 3,268 black East Africans.22 The other was conducted in South Africa, in the Hlabisa district (Northern KwaZulu–Natal Province). This survey examined 1,005 subjects in rural Zululand.
Although the prevalence estimates of POAG reported in these population-based surveys do vary (Table 1), all have reported higher prevalence estimates of POAG in people of African descent compared to whites in other population-based studies. The variability in the prevalence estimates may be due to differences in the definitions, criteria and/or testing methods used to define, diagnose and classify POAG.54 Table 2 provides an overview of such differences that arise between the population-based studies included in Table 1, in making a POAG diagnosis.
Section snippets
OPTIC NERVE
Racial differences in optic nerve parameters between blacks and whites are well documented (Table 3). Larger optic disk areas have been observed in normal,29., 110., 178., 180. post-mortem,136 and glaucomatous113 eyes of blacks. This finding is robust and the differences remain significant after adjusting for the effect of different fundus cameras and topographers.120 Racial differences in other optic disk parameters have also been reported and are listed below; however, they should be
Racial Differences in Risk Factors
Age, elevated IOP, and family history of glaucoma are the most important risk factors for POAG, and diabetes, systemic hypertension, and refractive error are potential risk factors.168 There is evidence suggesting that blacks and whites differ with respect to these factors.10., 81., 87., 102., 150., 172., 198.
Treatment Methods and POAG Management
Glaucoma treatment is aimed at reducing IOP through either drug therapy, surgery, or by a combination of the two methods. There is evidence that blacks may have poorer response to treatment than whites to both methods of treatment.
ACCESSIBILITY TO TREATMENT
Glaucomatous visual loss is often preventable with current drug regimens and surgical techniques, provided that intervention occurs in the early stages of the disease. Although black Americans are a high-risk group, they are less likely than white Americans to initiate POAG treatment.58 Ontiveros et al showed that black Americans are also less likely than white Americans to have a primary care physician and to undergo glaucoma screening, even though all their respondents were eligible for
Conclusion
Noting differences in phenotypic characteristics and responses to treatment between blacks and whites should prove useful in providing optimal ophthalmic care to black populations. It should be noted that blacks have larger disks and thinner RNFL than whites. Although there are conflicting reports, a number of studies have reported elevated IOP levels in untreated blacks compared to whites. Furthermore, blacks have thinner CCTs than whites and thus their recorded IOPs may underestimate their
Method of Literature Search
A search of the MEDLINE database was conducted using the following search words: glaucoma, POAG, African-American, race, racial differences, blacks, prevalence, optic nerve, optic disk, neuroretinal rim area, cup-to-disk ratio, RNFL, intraocular pressure, central corneal thickness, treatment, drugs, medication, surgery, glaucoma awareness, and risk factors. The search covered the years 1967 to July 2002 and articles published in English and in French were included. Additional sources included
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The authors wish to thank Dr. Tarek El Beltagi for reviewing earlier versions of the manuscript and Ms. Shannon Kleinhandler for her assistance. This article was supported by NIH grants EY08208 (PAS) and EY11008 (LZ), and the Glaucoma Research Foundation (PAS). The authors reported no proprietary or commercial interest in any product mentioned or concept discussed in this article.