Contents lists available at ScienceDirect Multiple Sclerosis and Related Disorders journal homepage: www.elsevier.com/locate/msard Clinical trial Immunoglobulin G index as a biomarker of relapse response to corticosteroids during early stages of multiple sclerosis Farouk Talaat (MD in neurology), Ismael Ramadan (MD in neurology), Eman Hamdy (Master Degree of Neurology) ⁎ , Amira Sayed, Amr M Elfatatry Department of Neurology and psychiatry, Faculty of Medicine, Alexandria University, Egypt ARTICLE INFO Keywords: Acute relapse Biomarker IgG index Multiple sclerosis Response to steroids ABSTRACT Background: Despite the considerable advances in disease modifying therapy in multiple sclerosis (MS), man- agement of acute MS relapses remains understudied. The response to relapse therapy is heterogenous among patients, and the exact reason behind such response remains elusive. Identification of a reliable biomarker for relapse responsiveness would contribute considerably to optimizing the relapse outcome. Objectives: to explore whether the immunoglobulin G (IgG) index during acute relapse contributes to relapse response to corticosteroid therapy or not. Methods: A prospective study was conducted on 46 MS patients attending MS clinic in relapse with a baseline EDSS≤3 before the relapse. IgG index was measured in all patients before corticosteroids therapy, and their EDSS was re-assessed after 3 months. Results: The mean age of the recruited patients was 26.89 ± 4.19 years, with females constituting 71.7% of the sample. IgG index was significantly higher in patients who recovered fully after relapse (1.44) than those who were partially recovered (0.95)(P<0.001), and it was inversely correlated with EDSS increase after the relapse (r=-0.390, P = 0.007). On regression analysis, the OR of IgG index to relapse response was 0.05 (CI: 0.07–0.31, 95%)(P = 0.003). Conclusions: IgG index can be a promising biomarker of relapse response to steroids in early stages of MS. 1. Introduction Despite the considerable advances in management of multiple sclerosis (MS) during the past few decades, the vast majority of these advances focused mainly on disease modifying therapy (DMT) (Cerqueira et al., 2018), and less researches were concerned with the management of acute relapses and the therapeutic measures of opti- mizing the relapse response to acute treatment. Acute multiple sclerosis relapses contribute considerably to long- term disability, and it is estimated that up to 49% of acute MS relapses result in a residual increase in Expanded Disability Status Scale (EDSS) of at least 0.5 point (Lublin et al., 2003). As it is well-established that the progression of MS continues once the EDSS reaches 3(3), optimal treatment of acute relapses – particularly at early stages of the disease - is fundamental to prevent long-term progression and disability. Even though, the primary focus of the current literature researches in the field of MS is to prevent further relapses rather than to treat the acute relapses. Several lines of management are used to treat acute MS relapses, with corticosteroids being on the top of the list (Kong et al., 2017). Intravenous corticosteroids are considered the mainstay and the first line of management of acute MS relapses (Miller et al., 2000). Patients who do not respond to corticosteroids are offered other treatment modalities such as plasma exchange and/or intravenous im- munoglobulins (Roed et al., 2005; Cortese et al., 2011). According to data from NARCOMS registry, up to 50% of acute MS relapses respond inadequately to steroids (Nickerson and Marrie, 2013). To date, the exact reason behind the non-homogenous relapse response to corti- costeroids among MS patients remains elusive. Some researchers stu- died the clinical predictors of relapse recovery, and despite the ex- istence of some conflicting results, high EDSS before the relapse seemed to be the major predictor of poor response to relapses (West et al., 2006). Other reported risk factors for poor recovery after relapses in- cluded male gender, high relapse severity and progressive stages of the disease (Hirst et al., 2012; Leone et al., 2008). This could probably be due to the change in the pathologic mechanisms of MS and the al- teration in synaptic plasticity, inflammatory changes and structural damage (Kalincik, 2015). https://doi.org/10.1016/j.msard.2019.101495 Received 15 August 2019; Received in revised form 10 October 2019; Accepted 1 November 2019 ⁎ Corresponding author. Eman Hamdy. Assistant lecturer of Neurology, Faculty of Medicine, Alexandrai University, Egypt. E-mail addresses: farouktalaat@yahoo.com (F. Talaat), ismramadan@hotmail.com (I. Ramadan), e_hamdyameen@yahoo.com (E. Hamdy). Multiple Sclerosis and Related Disorders 38 (2020) 101495 2211-0348/ © 2019 Elsevier B.V. All rights reserved. T