Practical Strategies for Improving Outcomes in Diverse MS Populations was the Symposium that started the second day of the annual Consortium for MS Centers meeting in Indianapolis. This is a topic of special interest to many people because of the differences in how people react to treatment, depending on their ethnic and genetic background. It was a panel presentation and these are the topics of each presenter and my summation of their text and comments.
Trends in the Epidemiology of Multiple Sclerosis (MS)
Aliza Ben-Zacharia, DrNP, ANP, MSCN
There is an increase in the prevalence of MS numbers worldwide and it can be partially attributed to people with MS living longer, thanks to available therapies, and also migration patterns. People are moving around the globe with greater ease, and also inter-mingling genes. The disease profile used to be there was a greater prevalence in people with Northern European genetic roots, Caucasian, and female.
It used to be that latitude of where the person was raised and lived had an effect on their rate of MS likelihood. The higher latitudes used to be associated with higher MS rates, but that has changed. Before 1980, for each 10 degrees of latitude the incidence of MS increased by 31%. That number after 1980 is down to 15% increase for each 10 degrees in latitude change.
A number change that is even more significant is the increase in the women to men with MS ratio. In 1955, the ratio was 1.4:1, meaning for every one man, there were 1.4 women with MS. In 2000, the ratio changed to 2.3:1. Most recently in 2010, the ratio was 3:1. What is causing this increase in the number of women with MS is unknown, but some factors being looked at include occupation, smoking, obesity, pregnancy, and birth control.
Dr. Ben-Zacharia cited the study Incidence of multiple sclerosis in multiple racial and ethnic groups, 2013, with numbers that challenge the perception that MS is a white women’s disease. This study looked at 496 newly diagnosed people and found the risk of MS in black women was higher than in white, Hispanic or Asian women. Black men in this study had the same risk ratio as white men. Again, the reasons for this difference are not known, but deeper looks are being made at the role of genetics and environment.
Special Considerations in African-American and Hispanic Populations with MS
Bruce Cree, MD, PhD
Dr. Cree’s focus was on understanding the phenotypes of MS among the various populations is at least partially due to genetics. Cases of MS among Africans are very rare, the same cannot be said about African Americans who have European genes along with the African genes.
The time from the beginning of MS to disability milestones of advancing to secondary progressive MS (SPMS) and the use of assistive devices for African Americans was shorter than for whites. The phenotype summary Dr. Cree gave was-
“African Americans are more likely to have
- An older age of onset
- Multiple-symptom onset
- Transverse myelitis
- Optospincal MS
- Secondary progressive MS
- Ambulatory impairment
- Lower vitamin D levels”
When comparing MRI imaging, African Americans with MS have higher T-2 lesion load and gadolinium –enhancing lesions and lower brain magnetization transfer ratio (MTR) than whites.
With these differences, Dr. Cree shared the therapy responses for each group. According to the study results in the EVIDENCE study, “African Americans appeared to not respond as well as whites to treatment with IFN as well as whites in all clinical and MRI outcomes.” IFN is any of the interferons, including Betaseron, Rebif, Avonex and Plegridy.
African American response to therapy with natalizumab (Tysabri) was looked at in the SENTINEL and AFFIRM studies. The conclusion is African Americans ‘respond to treatment with natalizumab with statistically significant reductions in relapses, time to next relapse, contrast enhancing lesions, new lesions and burden of disease on weighted imaging.” He says the immune suppression mechanism of Tysabri appears to be better for this group over that of the interferons.
He also touched briefly on the MS patterns of Hispanic whites, which he said studies show compared to whites, they have a younger age of onset, have a greater incidence of optic neuritis and transverse myelitis, and similar rates of ambulatory impairment. Hispanics with MS have a lower level of vitamin D than whites, and like African Americans, also respond better to natalizumab than interferons.
How Do We Customize Therapy, Improve Adherence, and Enhance Quality of Life for These Patients With MS?
Mary D. Hughes, MD
Dr. Hughes focused on how to personalize treatments to make it meaningful for African Americans and began by saying adherence to therapy is the holy grail of MS. Medication adherence includes taking it as prescribed for the timing, doses and how often.
She cited studies that show overall, 20-30% of prescriptions written are never filled, and 50% of all prescription drugs are not taken as prescribed. Her example of not finishing all the days of antibiotics and saving a few for ‘just in case’ hit home with me and the rest of the audience as an example of not taking drugs as prescribed.
There is a drastic difference in rates between whites at 80% and African Americans at 62% adherence for prescription drugs. Four primary reasons cited for non-adherence are; lack of understanding how the medicine works, forgetfulness, the cost of the prescription, and concern about side effects.
For Hispanic/Latino people with MS, there are additional considerations for adherence, including a possible language barrier, and cultural needs of the social group vs individuals. The challenge for the clinicians is to understand the concepts of treatment for the culture of the patient and find ways to respect the culture while delivering appropriate care.
Dr. Hughes uses strategies based on shared communication. She particularly favors the teach back method, where the patient is asked to repeat back to her what the instructions and information about MS and their treatment is given and she can then correct any errors. She told the audience it is important that her patients are not passive, but active partners in their own care.
The panel question and answer session yielded more information and it was unfortunate they had limited time because the exchange was fast.
A question was asked about what treatment to begin for African Americans newly diagnosed with MS.
Dr. Hughes called to “increase awareness of disease progression and set a lower threshold for disease progression”
Dr. Cree said all patients the “escalation approach is not necessarily the way to go; should we take the newly diagnosed and treat them with the most efficacious drugs?” He said part of the problem is insurance companies want to see failed therapies for patients before escalating treatments.
Dr. Hughes said she has found success with starting people on greater efficacy treatments, but “you need to be aggressive with the insurer and provide the information” to demonstrate the need.
Dr. Cree said at first he was skeptical of the data about the overall lack of response to interferons for African Americans, but there has since been consistent data to back this thought, including clinical data, and MRI evidence of relapses. “Before we had the newer agents there weren’t a lot of options but to use off label types of drug” but now there are additional options besides the interferons, Dr. Cree said.
Have researchers looked at genetic mix for clues to disability progression?
Dr. Cree said to understand the genomics they would need large samples of subjects. “Metabolism is a new area of study. In the new genetic map of MS there are over 150 snips of MS susceptibility genes which might help us understand better the effects of metabolism” on MS. He added he believes there “has to be an environmental factor on top of genetics.’
Dr. Hughes answered the final question about adherence and talked about an interest in “literacy toolkits. How do we assess patients to where they are and how can we meet their needs? We need to design our communication techniques to them, and we don’t currently do that.”
She closed the comments by adding “We’ve talked about adherence a long time. Now we need to find what are the practical things we can do to improve these (adherence) rates?”
The question of why is your MS different than my MS appears to be rooted in our diverse genetic pool. This Symposium gave me plenty to think on and I hope this transcript of the proceedings does the same for you.
Wishing you well,