Fatigue in myasthenia gravis (MG) is likely caused by long-term, low-grade inflammation mediated by a biomarker known as C-reactive protein (CRP), according to a study recently published in Neurology.
Fatigue is one of the most pressing symptoms in MG. Different from fluctuating muscle weakness, it includes physical tirednes, as well as a lack of energy in performing mental and cognitive functions.
There are various theories as to what the primary drivers of fatigue in MG are. Some scientists think it involves inflammatory processes that are commonly associated with autoimmune diseases such as MG. However, it is likely that patients with MG experience fatigue due to a combination of intersecting factors.
The authors of the study sought to better understand the drivers of fatigue in MG. They thus recruited adult patients with MG at a hospital in the Netherlands. Recruited participants consented to take part in one to two visits. In the first visit, patients were asked to fill in questionnaires relevant to the subject of MG-associated fatigue, and blood samples were also collected for analysis. The second visit was optional, but participants who took part had their CRP levels measured, a biomarker of inflammation. A total of 116 patients took part in the first visit; 105 took part in both.
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Fatigue was found to be a significant problem among participants, with severe fatigue present in 64% of participants. Furthermore, fatigue scores rose in the face of increased disease severity.
In terms of biomarkers, researchers confirmed that CRP had a positive correlation with fatigue. In contrast, fatigue had a negative correlation with hemoglobin levels and cells known as basophilic granulocytes, a type of white blood cell important in the immune system.
Researchers also noted a difference in patients who participated in the first and second visits. In the second visit, approximately 18% of patients who had reported severe fatigue in their first visit had fatigue levels below the cutoff point for severe fatigue; however, 38% of patients who did not have severe fatigue during their first visit qualified for this designation at the second visit. This highlights the variability of symptoms in MG.
“Our findings suggest that chronic low-grade inflammation, mediated by CRP, contributes to the pathogenesis of fatigue in MG,” the study concluded. “This aligns with the hypothesis that local peripheral inflammatory processes induce systemic inflammatory cascades responsible for fatigue.”
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