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Serum-leptin and adiponectin are associated with neither disease activity nor treatment response in multiple sclerosis (MS), according to a study published in the Journal of Neuroimmunology.
Researchers in this study previously demonstrated that fewer overweight individuals with MS were able to achieve no evidence of disease activity status through interferon-beta (INFB) treatment than their normal weight counterparts. Adipokines are secreted by fatty tissue and have inflammatory properties, and they have been shown to mediate disease activity in autoimmune diseases. Investigators hypothesized that leptin and adiponectin, the most abundantly secreted adipokines, could serve as biomarkers for MS. Adiponectin has anti-inflammatory activity, and low levels are associated with worse autoimmune disease activity. Leptin acts in the regulation of the Th1/Th2-balance and is negatively associated with the number of regulatory T-cells. It, therefore, has pro-inflammatory activity, and high levels are associated with worse autoimmune disease activity.
Investigators recruited 88 patients with MS from an omega-3 fatty acid study in MS (OFAMS). The participants were 18 to 55 years of age, had an Expanded Disability Status Scale (EDSS) score of ≤5, and experienced ≥1 relapses or a new T1-weighted gadolinium-enhancing (T1Gd+) or T2-weighted (T2) lesion on MRI before inclusion.
Participants were given 44 μg IFNB -1a subcutaneous injections 3 times per week during months 6 through 24. Investigators collected serum samples at baseline and after 1, 3, 6, 7, 9, 12, 18, and 24 months. Blinded laboratory technicians measured serum leptin and adiponectin levels using radioimmunoassay. MRIs were performed at baseline and after 1, 2, 3, 4, 5, 6, 7, 8, 9, 12, and 24 months.
At baseline, there was a positive correlation between body mass index and serum-leptin (P <.001) but no significant relationship between body mass index and serum-adiponectin (P =.137). Serum-leptin levels were significantly higher (mean difference 55.7 pmol/L; 95% CI, 14.5-96.9; P =.008) and serum-adiponectin levels were significantly lower (mean difference 0.24 mg/L; 95% CI, 0.01-0.46; P =.037) prior to IFNB treatment than after. No relationship was found between serum-adipokine levels and MRI activity (new T1Gd+ or new/enlarging T2-lesions). Eleven participants experienced clinical relapse during the study. There was no significant difference in baseline serum-leptin and adiponectin levels (P =.70 and P =.20, respectively). There was also no relationship between EDSS score and baseline serum-leptin or adiponectin levels (P =.89 and P =.38, respectively). No evidence of disease activity-3 status was defined as no relapse, sustained disability progression, nor MRI activity during the 24-month study period. Of the participants that received IFNB treatment, 18% achieved no disease activity-3 status. There was no difference between participants who achieved no evidence of disease activity-3 status and those who did not in terms of baseline serum-leptin or adiponectin levels (P =.21 and P =.33, respectively).
Unfortunately, this study could not identify new biomarkers for MS. Further research is necessary to examine the relationship between body mass index and MS disease activity and treatment response.
Disclosures: Multiple authors declare affiliations with the pharmaceutical industry. Please refer to reference for a complete list of authors’ disclosures.
Reference
Kvistad SS, Myhr KM, Holmøy T, et al. Serum levels of leptin and adiponectin are not associated with disease activity or treatment response in multiple sclerosis. J Neuroimmunol. 2018; 323:73-77.
