How is MS different in blacks?
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Multiple sclerosis (MS) affects different populations in various ways, as seen by the varying rates of the disease around the world. As a general rule, MS becomes increasingly common as you move away from the equator. This “geographic effect” has been attributed to genetic variations as well as environmental factors such as sun exposure.
Small differences in genetics may explain in part why MS is more common in people with northern European ancestry and less so in other groups. Other variations in genetic factors may also be the reason why the symptoms and severity of MS differ from one person to the next, and from one ethnic group to another.
Does MS behave differently in blacks?
A number of studies have found that MS symptoms are often more severe and disabling in African-Americans. Across the life span, from adolescence to adulthood, African-Americans have a greater risk that MS relapses will be more frequent and more severe (Boster and colleagues. Pediatr Neurol 2009;40:31-33; West and colleagues. Neurology 2006;67:809-813).
Inflammatory flare-ups in the brain also appear to be more damaging in blacks (Weinstock-Guttman and colleagues. Neurology 2010;74:538-544), which could suggest some impairment in neurological repair mechanisms. As a result, African-Americans have a two-fold higher risk of primary-progressive MS compared to whites (Naismith and colleagues. Mult Scler 2006;12:775-781). And the more common relapsing-remitting form appears to progress more rapidly, resulting in disability at an earlier age (Kister and colleagues. Neurology 2010;75:217-223).
One reason for this disability is that African-Americans are more likely to develop muscle weakness affecting posture and walking (called pyramidal symptoms), and difficulties in coordinating muscle movements (called cerebellar symptoms) (Kaufman and colleagues. Am J Phys Med Rehabil 2003;82:582-590; Naismith 2006).
But a few other issues are worthy of consideration. The first is uncertainty about the diagnosis. There are several demyelinating conditions that can resemble MS, such as ADEM (mentioned above). Another is optico-spinal MS (OSMS), which primarily affects the optic nerve and spinal cord. This variant is twice as common in African-Americans compared to white Americans (Cree and colleagues. Neurology 2004;63:2039-2045). Also important are transverse myelitis (TM), an attack of inflammation that affects the spinal cord that is typically caused by a viral infection; and neuromyelitis optica (NMO), which causes both transverse myelitis and optic neuritis. Both TM and NMO are more common in African-Americans compared to white Americans (Oh & Levy. Neurol Res Int 2012;460825; Cree 2004).
Since these demyelinating conditions are often more disabling than MS because they target the spine, it’s possible that some of the studies looking at MS disability among African-Americans have included people with these other conditions, which may have skewed the results somewhat. But getting the diagnosis right is critical because current MS therapies are often ineffective in treating these other demyelinating diseases.
Another issue – and a recurrent concern – is socioeconomic factors. A Mississippi State University study found that African-Americans with MS were less likely than whites or Hispanics to have been treated at an MS clinic, or to have been seen by a neurologist specializing in MS – fair indications that African-Americans were not receiving the best care (Buchanan and colleagues. Ethn Dis 2010;20:451-457).
In addition, a study by the Cleveland Clinic found that African-Americans were more likely to suffer some types of impairment, such as problems with vision, hand movements and mobility compared to whites (Marrie and colleagues. Neurology 2006;66:1235-1240). However, these differences between blacks and whites were much less pronounced once socioeconomics had been factored in.
Are MS treatments effective?
The perception that MS is uncommon in African-Americans has been challenged in recent years. A Veterans Administration study published last year looking at military personnel serving from 1990-2007 – the Gulf War generation – found that the incidence of MS was actually higher in African-Americans compared to white Americans (Wallin and colleagues. Brain 2012;135[pt 6]:1778-1785).
Unfortunately, perceptions are accompanied by realities. Blacks may not be diagnosed because their doctors aren’t expecting to find it. And once diagnosed, they are typically not recruited into clinical trials. When looking at whether MS therapies are equally effective in everyone, most of the information is based on the results seen in white females – who typically make up about three-quarters of the subjects treated in clinical trials. For example, in the initial Avonex trial, only about 7% of the study subjects were black (Jacobs and colleagues. Ann Neurol 1996;39:285-294). In the U.S. trial of Copaxone, whites made up 94% and 6% were “Other” races, which weren’t defined (Johnson and colleagues. Neurology 1995;45:1268-1276). More recent studies are much the same. Among the 1,234 people enrolled in the DEFINE trial of Tecfidera, only 26 (2%) were black (Gold and colleagues. N Engl J Med 2012;367:1098-1107). The recent trend of conducting more trials in eastern Europe is unlikely to change this. Research is needed to determine if there are barriers to recruiting African-Americans into clinical trials.
So there is limited information on MS treatments in African-Americans but a few studies have made the attempt. In the EVIDENCE trial comparing Avonex and Rebif, a post-hoc analysis found that African-Americans taking an interferon-beta (two-thirds on Avonex) had more relapses, and were more likely to continue having relapses on treatment than whites (Cree and colleagues. Arch Neurol 2005;62:1681-1683). A second study found that African-Americans continued to progress more rapidly despite taking an interferon (Klineova and colleagues. Ethn Dis 2012;22:221-225). So these findings suggest that interferons may be less effective in African-Americans, or may be less able to control the more aggressive MS symptoms seen in blacks. Another factor is whether the person takes the drug – with one study finding that African-Americans were less likely to keep taking their medication, which may in turn be influenced by the high cost of medications (Lafata and colleagues. J Am Pharm Assoc 2008;48:752-757).
The only other study of drug response specifically in African-Americans looked at Tysabri (Cree and colleagues. Arch Neurol 2011;68:464-468). It found that Tysabri was highly effective, although somewhat less so than it was in whites. The obvious limitation is that only 49 people out of the two thousand in the Tysabri trials were black, and any analysis of 2% of a study population is less than robust.
Unfortunately, this is all that’s known about MS drugs in the black population. There is limited information suggesting that interferon-beta drugs may be less effective, and equally limited information that Tysabri may be a better choice. Clearly there is a need for more studies to investigate the MS disease process in different populations, and to address the very real challenges and needs of people of African ancestry living with MS.
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