IntroductionAdherence to treatment, including early treatment discontinuation, in patients with multiple sclerosis or clinically isolated syndrome can be affected by: treatment tolerability, route of drug administration, patient age, disease duration, comorbidities, medical care, and support from their caregivers.AimThis study aimed to identify the risk factors for poor adherence to Betaferon® treatment, including early discontinuation and omitting doses.Materials and Methods852 adult patients treated with Betaferon participated in this 24-month study. All patients were interviewed using the Risk of Drop-out Questionnaire, the Center for Epidemiologic Studies Depression Scale and the Kurtzke Expanded Disability Status Scale.ResultsPatients who stopped therapy were younger (p = 0.003) had a higher mean EDSS score (p = 0.022), higher mean number of relapses (p = 0.017), and reported more often fear of injection (p = 0.027) and adverse events (p = 0.007) than those who did not stop treatment. Comparing patients who stopped therapy in the first and the second year, patients who stopped therapy in the first year of treatment more frequently reported flu-like symptoms and fever, and those who stopped therapy in the second year reported—ineffectiveness of treatment and disease progression. Multivariable logistic regression models confirmed that young age, short disease duration, advanced and progressing disease, and poor Betaferon tolerability were related to premature treatment discontinuation. The risk of omitting a dose during therapy was increased in patients who were working or studying, who had more advanced disease or more adverse events, and in patients who received less support from their caregivers.ConclusionsSeveral reasons may lead to problems with adherence to Betaferon treatment. Patients at higher risk of discontinuing treatment need to be identified early to make caregivers’ support available to them.

Objective: Adipocytokines are cytokine-like mediators that link adipose tissue function with inflammatory and autoimmune processes, and have a suggested role in the pathogenesis of multiple sclerosis (MS). The aim of this study was to analyze the effects of methylprednisolone, interferon-1b (INF) and glatiramer acetate (GA) on leptin, resistin, and adiponectin concentrations in relapsing-remitting MS (RRMS) patients. Methods: The study included 154 RRMS patients who were hospitalized in the Department of Neurology, Poznan University of Medical Sciences. The comparison group included 31 patients with myasthenia gravis (MG) and 39 healthy controls. Serum levels of leptin, adiponectin, and resistin were evaluated before treatment initiation. In the RRMS patients treated with methylprednisolone, adipocytokine evaluation was performed one day after the therapy. Patients treated with INF or GA were evaluated at 1 month and 6 months. Routine neurological examination and expanded disability status scale (EDSS) scoring were performed, and MRI scans were analyzed for the localization of demyelinating plaques. Body mass index, glycemia, and insulin levels were evaluated and homeostatic model assessment insulin resistance index (HOMA-IR) was calculated. Results: Adiponectin and resistin levels in RRMS and MG patients were increased compared to controls, but adiponectin levels were lower in RRMS than MG patients. Intravenous methylprednisolone in RRMS with relapse caused an elevation of leptin concentration. INF treatment caused a significant, time-dependent effect on resistin concentration. GA administration influenced only resistin concentration as a long-term effect. No relationship between adipocytokines and metabolic status or insulin resistance was found. Conclusions: We identified resistin as the most important adipocytokine associated with RRMS. Its concentrations are reduced by first line immunomodulatory treatment, which produces a milieu of beneficial inflammatory and metabolic processes. On the other hand, the routine treatment of MS relapses with methylprednisolone induces harmful metabolic and inflammatory effects that may be mediated by elevated leptin levels.

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