Are circulating FGF21 and NT-proBNP promising novel biomarkers in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome?, by Prof Joan Carles Domingo, Dr Begoña Cordobilla, Dr Roser Ferrer, Dr Marina Giralt, Dr Jose Alegre-Martin, and Dr Jesus Castro-Marrero in Antioxidants & Redox Signaling, 22 Dec 2020 [doi.org/10.1089/ars.2020.8230]
Research abstract:
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a chronic, disabling, and complex multisystem illness of unknown etiology. The protein FGF21 regulates glucose homeostasis and lipid metabolism, and the protein NT-proBNP is strongly associated with an elevated cardiovascular risk; however, little is known about their role in ME/CFS patients. To address this gap, we explored the association between FGF21 and NT-proBNP and oxidative stress and inflammatory markers in ME/CFS.
Twenty-one ME/CFS patients and 20 matched healthy controls were included in the study. Participants filled out validated self-reported questionnaires on their current health status covering demographic and clinical characteristics. Plasma showed significantly decreased total antioxidant capacity and increased lipoperoxides levels (p = 0.009 and p = 0.021, respectively) in ME/CFS. These ME/CFS patients also had significantly increased levels of inflammatory cytokines (IL-1β, IL-6, IL-10, TNF-α, and C-reactive protein (p < 0.05 for all) but not for IL-8 (p = 0.833) in ME/CFS, indicating low-grade systemic inflammation status.
Circulating FGF21 and NT-proBNP levels were significantly higher (p < 0.0001 and p = 0.005, respectively) in ME/CFS patients than in healthy controls. Significantly positive correlations were found between NT-proBNP levels and IL-1β and IL-6 (p = 0.04 and p = 0.01) in ME/CFS patients but not between FGF21 and these cytokines. In contrast, no significant correlations were found for either FGF21 or NT-proBNP in controls.
These findings lead to the hypothesis that elevated FGF21 and NT-proBNP levels and the association between NT-proBNP and inflammation may be promising novel diagnostic and therapeutic targets in ME/CFS.
