biomarker for response to interferon beta-1b

A forum to discuss research on the origins of MS and its development.
Post Reply
User avatar
frodo
Family Elder
Posts: 1749
Joined: Wed Dec 02, 2009 3:00 pm
Contact:

biomarker for response to interferon beta-1b

Post by frodo »

A long-term follow-up study on biochemical and clinical biomarkers of response to interferon beta-1b treatment in relapsing-remitting multiple sclerosis.

https://europepmc.org/article/med/32500977

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.
Post Reply
  • Similar Topics
    Replies
    Views
    Last post

Return to “MS Etiology and Pathogenesis”