The pathogenesis of multiple sclerosis (MS) is a complex and multifaceted process characterized by an autoimmune response. Effective treatment is essential, as the primary aims are to suppress disease activity and significantly reduce long-term disability (Ng et al., 2024). While current therapies provide significant clinical benefits, it is crucial to consider their safety profiles when making treatment decisions.

Fingolimod (Gilenya®, Novartis Pharma AG, Basel, Switzerland), is a sphingosine-1-phosphate receptor modulator that prevents lymphocytes from exiting lymphoid tissues and infiltrating the central nervous system (CNS) (Cohen and Chun, 2011). It is widely used for MS management due to its effectiveness in reducing inflammation and relapse rates (Biolato et al., 2021). However, its association with elevated liver enzyme levels necessitates close monitoring, potential dosage adjustments, or even discontinuation in severe cases (Joni et al., 2020; Rae-Grant et al., 2018). Although hepatoxicity is typically mild, the risk of significant adverse effects must not be underestimated, underscoring the need for safer treatment alternatives.

Cladribine, an oral DMT, selectively depletes lymphocytes and offers durable disease suppression with a short treatment regimen (Clavelou et al., 2023; Tallantyre et al., 2024). In addition to its efficacy, cladribine demonstrates a more favorable safety profile compared to fingolimod, with a lower risk of hepatotoxicity and minimal liver function test (LFT) abnormalities (Butzkueven et al., 2023; Butzkueven et al., 2022).

However, there is a notable lack of data regarding the safety and efficacy of transitioning patients from fingolimod to cladribine, especially for those with elevated liver enzymes (Leist et al., 2023). This study aims to address this gap by demonstrating recovery of liver enzymes during cladribine therapy and thus identify safer treatment strategies for patients with MS (pwMS).