Race, ethnicity, creed – all architectural descriptors, some complex, others less so, depending on your perspective.
When it comes to illnesses however, you are largely referencing race (the inheritance of your DNA) and ethnicity (the branch of race that your DNA occupies). We may be different in a number of ways, but our illnesses are a great equalizer. There is no such thing as race superiority when it comes to disease.
South Asians come with a greater cardiovascular risk (narrower blood vessels), African ancestry have a higher risk of raised blood pressure at a younger age and overall cancer risk. Certain types of cancers are greater in the Far East, whilst autoimmune disorders are commoner in Caucasian populations, as are a majority of orphan disorders. These risks exist even after adjusting for socioeconomic factors.
PwMS of African descent are far and few between, but what is interesting is that they have an increased risk of progression compared to their Caucasian counterparts. They have even been noted to be less responsive to disease-modifying therapies – for instance, with interferon beta-1a African Americans were less responsive to treatment than Caucasians.
Interestingly, in a small cohort studied in the alemtuzumab clinical trials this may not be the case. In fact, in terms of efficacy it is comparable to the overall study population over an 8 year period (see Figures below).
The problem is that in the US the FDA label for alemtuzumab is third line, and as such this group may be disadvantaged when it comes to their MS management.
ARR annualized relapse rate, CDI confirmed disability improvement, CDW confirmed disability worsening, EDSS Expanded Disability Status Scale, IAT initial alemtuzumab treatment, SC IFNB-1a subcutaneous interferon beta-1a, Y year.
