With the large selection of drugs for MS therapy, the question often arises as to which drug is the right one for the individual patient. We lack reliable biomarkers for an assignment. The term biomarker usually refers to a laboratory value/blood value, the magnitude of which indicates to what extent a response to a drug is to be expected and recorded. The identification of such biomarkers is always a very important topic at congresses, and ideas and innovations in this area are of great interest. At the AAN Congress in Vancouver, a research team from the Czech Republic and the USA was able to show (P3.019) that after the administration of interferon beta-1 a, there is a reduction in the HDL cholesterol level and that the absence of this initial decrease is associated with a poorer response to the administration of interferon beta-1a. The patients in question had a greater loss of brain volume and a higher lesion branch after 4 years of observation. The authors therefore suggest that the HDL cholesterol value is a simple parameter with which the response to an interferon preparation can be estimated.
In addition to the response to therapies, biomarkers can also be important to better define the course of the disease. The aim here is to have an indication from the outset whether an MS is more mild or progressive. Based on the basic data of the EXPAND study, a study on the effect of siponimod (a follow-up substance of fingolimod) in secondary chronic progressive MS (SPMS), the immunological basic profile of the study patients was examined (P3.046). The colleagues were able to show that patients with SPMS had more CD8 lymphocytes and more B-cells in the peripheral blood, whereas fewer Th2 CD4 cells were found. The finding that SPMS has a different immunological profile could in the future lead to this course of the disease being better identified and thus a targeted selection of therapies can be made.
American researchers from Salt Lake City have focused on a completely different type of biomarker (P2.088). John Foley and colleagues addressed the problem of lymphopenia under therapy with dimethyl fumarate (DMF) and were able to show that age and the associated immunosenescence is a risk factor for therapy-related lymphopenia. The higher age could thus also be a risk factor for the development of PML under DMF therapy.
After these examples of the lively discussion about biomarkers, I would like to go into some works on questions in practical MS therapy. A research group from Boston investigated the value of hormone therapy in postmenopausal women with MS and was able to show that the group with hormone replacement therapy had a better quality of life. Also from Boston, a paper was presented (P2.187) that was able to demonstrate a connection between type I allergies and increased disease activity in MS. The authors hold the cell population of mast cells responsible for this, as their mediators mediate an activation of T cells and macrophages, as well as an increased permeability of the blood-brain barrier. Finally, a very interesting paper on discontinuing disease-modifying therapy was presented by a Spanish working group (P3.113). The authors were able to show that patients who stopped their therapy in consultation with their doctor often remained stable after discontinuation than patients who discontinued their medication on their own initiative, without discussing it with the treating doctor. This observation is a clear argument for a joint approach by the doctor and patient, even when it comes to ending therapy.
