A prospective study of 62 patients with relapsing-remitting multiple sclerosis (RRMS) treated with Glatiramer acetate (GA) was conducted to evaluate the value of baseline and treatment-modulated cytokines in predicting the clinical response to the drug after 2years of therapy. There were 32 responders and 30 non-responders. GA upregulated Th2/regulatory cytokines and inhibited Th1 cytokines in sera or PBMC supernatants 3 and 6months into treatment. We found two prognostic models with clinical utility. A model based on IL-18 at baseline, the change in TNFa from baseline to 3months, the change in IL-4 from baseline to 6months, and the change in the log of the ratio of TNFa/IL-4 from baseline to 6months had an area under the curve (AUC) of 0.80. A high IL-18 level at baseline and a reduction of TNF-alpha over time are associated with a response to GA. Although the study identified predictive biomarkers of clinical response to GA, the results will need to be validated in other data sets.
Can you predict who will respond to glaterimer acetate and if you are non-responder you can switch. This study finds a few cytokines that may give a clue to who responds, which seems to be those with less evidence of inflammatory activity in their blood..go figure:-).
However, it is not sufficiently descriminatory as per ususal, even if it is repeated and so the way people will work out the failures is by the actual failure, I suspect.
The good side effect profile makes this a popular approach, but as time is brain and in this group of sixty we had about 50% failures, one may ask if this. Is the way to go?