Am I wasting everyone’s time and online space writing about interferon-beta? The fact of life is that some of you still use it. In some parts of the world it may be the only disease-modifying therapy that is readily available. However, having said this, there needs to be a method to the madness of picking first line treatments for MS, and this at least for the interferon’s is relatively straight forward.
When you inject interferon’s (IFN), a cascade of physiological changes take place in your body that are measurable and predict response to treatment (the so-called interferon inducible proteins: viperin, myxovirus resistance protein(MxA), anti-IFN antibodies, cytokines to name a few). If the mojo is not happening within you, the chances are that you’re in the medium – long term going to experience treatment failure.
In this study from Poland, the researchers studied 4 interferon-inducible proteins (see Table below) in 45 RRMS participants with follow up.
Disappointingly as you would with a treatment that is ~30% efficacious in terms of relapse rate reduction, the proportion with no evidence of disease activity drops over the years (see Figure below). But, all is not lost as a fair number also remain free of disease progression and just below half relapse free and MRI activity free.
So, what are the factors that determine response to IFN-B?
Based on this study, those with no disease activity at follow up tended to have higher levels of USP18, viperin and MxA at baseline and at 24 months of treatment.
The question then begs why are we not using these biomarkers to predict efficacy and switching those that show negligible response?
Adv Clin Exp Med. 2020 Jun 5. doi: 10.17219/acem/121063. Online ahead of print.
A Long-Term Follow-Up Study on Biochemical and Clinical Biomarkers of Response to Interferon beta-1b Treatment in Relapsing-Remitting Multiple Sclerosis
Background: While interferon beta-1b (IFN-β-1b) is still a commonly used disease-modifying drug in the treatment of multiple sclerosis (MS), therapeutic possibilities are expanding, and treatment failure should be identified early. Markers to predict response to IFN-β-1b, either clinical or biochemical, are therefore urgently needed. Interferon-induced proteins, including viperin, suppressor of cytokine signaling 3 (SOCS3), ubiquitin specific peptidase-18 (USP18), and myxovirus resistance protein A (MxA), are possible markers of IFN-β-1b bioavailability and treatment response.
Objectives: To evaluate viperin, SOCS3, USP18 and MxA as markers of treatment response in Polish IFN-β-1btreated patients with MS.
Material and methods: In 45 IFN-β-1b-treated Polish patients with MS, serum concentrations of viperin, SOCS3, USP18, and MxA were assessed before and after 24 months of IFN-β-1b treatment. The patients were followed clinically and with magnetic resonance imaging (MRI) for a median of 6.8 years.
Results: Low viperin, USP18 and MxA at baseline and 24 months and high SOCS3 at 24 months correlated with higher disease activity up to the 6th year of observation, but only baseline MxA and USP18 were independently related to outcome, with higher concentrations predicting less disease activity in the first 3 years and after the 1st year, respectively.
Conclusions: We confirm the predictive value of MxA and propose USP18 as a possible new prognostic biomarker in IFN-β-1btreated MS patients.