Changes in Serum Ceruloplasmin Levels Based on Immunomodulatory Treatments and Melatonin Supplementation in Multiple Sclerosis Patients

نویسندگان

  • Monika Adamczyk-Sowa
  • Paweł Sowa
  • Sebastian Mucha
  • Jacek Zostawa
  • Bogdan Mazur
  • Maciej Owczarek
  • Krystyna Pierzchała
چکیده

BACKGROUND The cause of multiple sclerosis (MS) is currently unknown, but it is thought that oxidative damage and iron metabolism mechanisms are involved. The aim of this study was to examine ceruloplasmin concentration in MS patients based on various immunomodifying therapies and to test the effect of antioxidative melatonin on ceruloplasmin levels. MATERIAL AND METHODS This prospective study included 102 MS patients and 15 healthy controls. Patients were divided into groups according to different immunomodifying therapies: interferons beta 1a, interferons beta 1b, glatiramer acetate, mitoxantrone, and immunomodifying pre-treatment (A, B, G, Mx, and P groups, respectively), and the relapse R group. MS patients were supplemented with melatonin for 3 months. Serum ceruloplasmin concentrations, EDSS, brain MRI, serum C-reactive protein level, and white blood cell count were examined. RESULTS The results indicated significantly increased levels of ceruloplasmin in MS patients. No differences in ceruloplasmin concentrations between the relapse group and controls were observed. In A and G groups, ceruloplasmin levels before and after melatonin were similar to levels in controls. In group B, ceruloplasmin concentration was significantly higher vs. control and relapse groups. After melatonin administration in group B, ceruloplasmin levels decreased. Ceruloplasmin concentrations in the Mx group were significantly higher compared to controls. CONCLUSIONS We found for the first time that ceruloplasmin concentration in MS patients varies depending on different immunomodulatory treatment and decrease after 3 months of melatonin administration. Ceruloplasmin could be a valuable serum marker for the chronic demyelinating process participating in oxidative stress mechanisms, as well as a neurodegenerative marker, but not a marker of acute-phase MS.

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عنوان ژورنال:

دوره 22  شماره 

صفحات  -

تاریخ انتشار 2016