1.
Role of mitochondria, oxidative stress and the response to antioxidants in myalgic encephalomyelitis/chronic fatigue syndrome: A possible approach to SARS-CoV-2 'long-haulers'?
Wood, E, Hall, KH, Tate, W
Chronic diseases and translational medicine. 2021;7(1):14-26
-
-
-
Free full text
Plain language summary
Cases of chronic fatigue have been reported following recovery from Covid-19, in what is termed ‘Long Covid’, with symptoms likened to that of sufferers from chronic fatigue syndrome (CFS) and myalgic encephalomyelitis (ME). How CFS/ME develop and treatments may help to further understand Covid-19. This review study of 111 studies aimed to identify where urgent research is required to help understand the potential of chronic fatigue therapies in Covid-19. The study first reviewed disrupted cellular energy production in ME/CFS and increased presence of damaging oxidants. Current therapies for improving cellular energy production in CFS/ME were then reviewed and Ritalin, ubiquinone and mitoquinol mesylate were heavily featured. Antioxidant therapies in CFS/ME were reviewed and observations would suggest that trials in patients with long covid are needed. It was concluded that research in cellular energy production in CFS/ME has been increasing, however remains contradictory due to a lack of a definitive diagnosis, differing disease severity and the huge differences between patients who suffer from CFS/ME. Further research is required in ME/CFS and Covid-19. This study could be used by health care professionals to understand the importance of monitoring symptoms of fatigue post Covid-19 infection and the possible use of ME/CFS treatments.
Abstract
A significant number of SARS-CoV-2 (COVID-19) pandemic patients have developed chronic symptoms lasting weeks or months which are very similar to those described for myalgic encephalomyelitis/chronic fatigue syndrome. This study reviews the current literature and understanding of the role that mitochondria, oxidative stress and antioxidants may play in the understanding of the pathophysiology and treatment of chronic fatigue. It describes what is known about the dysfunctional pathways which can develop in mitochondria and their relationship to chronic fatigue. It also reviews what is known about oxidative stress and how this can be related to the pathophysiology of fatigue, as well as examining the potential for specific therapy directed at mitochondria for the treatment of chronic fatigue in the form of antioxidants. This study identifies areas which require urgent, further research in order to fully elucidate the clinical and therapeutic potential of these approaches.
2.
Will COVID-19 Lead to Myalgic Encephalomyelitis/Chronic Fatigue Syndrome?
Komaroff, AL, Bateman, L
Frontiers in medicine. 2020;7:606824
-
-
Free full text
Plain language summary
In people who have contracted COVID-19, many do not return to full health. Some may develop permanent dysfunction of damaged organs such as the brain, heart and kidney. Others report ongoing lingering symptoms despite tests no longer detecting the virus. This condition is being called ‘long covid.’ Patients post-COVID-19 can develop a post-viral syndrome that is very similar to Myalgic Encephalomyelitis/Chronic Fatigue syndrome, (ME/CFS). This short review looks at how common a post covid illness is and what implications this has for the U.S. and globally. The review concludes that the U.S. and the world will see a substantial growth in the number of people with ME/CFS. We can’t predict at this stage how long lasting that will be.
3.
Clinical symptoms and markers of disease mechanisms in adolescent chronic fatigue following Epstein-Barr virus infection: An exploratory cross-sectional study.
Kristiansen, MS, Stabursvik, J, O'Leary, EC, Pedersen, M, Asprusten, TT, Leegaard, T, Osnes, LT, Tjade, T, Skovlund, E, Godang, K, et al
Brain, behavior, and immunity. 2019;80:551-563
-
-
-
Free full text
Plain language summary
Epstein-Barr virus (EBV) can trigger chronic fatigue (CF) and chronic fatigue syndrome (CFS) in individuals who are predisposed. However, how fatigue develops and how infections may trigger this is not fully understood. This exploratory cross-sectional study of 200 fatigued and non-fatigued adolescents 6 months after EBV aimed to understand symptoms and potential markers for disease. The results showed that all symptoms (not just fatigue) were more pronounced in those individuals suffering from fatigue, despite no increases in viral load. Those with fatigue only had slight changes in immune, nerve and hormonal markers and none correlated with severity of symptoms. It was concluded that there is a discrepancy between symptoms and viral load and alterations to several markers were only marginal. This study could be used by healthcare professionals to understand the possible limitations of using several biomarkers as a diagnostic tool for CF and CFS.
Abstract
INTRODUCTION Acute Epstein-Barr virus (EBV) infection is a trigger of chronic fatigue (CF) and Chronic Fatigue Syndrome (CFS). The aim of this cross-sectional study was to explore clinical symptoms as well as markers of disease mechanisms in fatigued and non-fatigued adolescents 6 months after EBV-infection, and in healthy controls. MATERIALS AND METHODS A total of 200 adolescents (12-20 years old) with acute EBV infection were assessed 6 months after the initial infectious event and divided into fatigued (EBV CF+) and non-fatigued (EBV CF-) cases based on questionnaire score. The EBV CF+ cases were further sub-divided according to case definitions of CFS. In addition, a group of 70 healthy controls with similar distribution of sex and age was included. Symptoms were mapped with a questionnaire. Laboratory assays included EBV PCR and serology; detailed blood leukocyte phenotyping and serum high-sensitive C-reactive protein; and plasma and urine cortisol and catecholamines. Assessment of autonomic activity was performed with continuous, non-invasive monitoring of cardiovascular variables during supine rest, controlled breathing and upright standing. Differences between EBV CF+ and EBV CF- were assessed by simple and multiple linear regression adjusting for sex as well as symptoms of depression and anxiety. A p-value ≤ 0.05 was considered statistically significant. This study is part of the CEBA-project (Chronic fatigue following acute Epstein-Barr virus infection in adolescents). RESULTS The EBV CF+ group had significantly higher scores for all clinical symptoms. All markers of infection and most immune, neuroendocrine and autonomic markers were similar across the EBV CF+ and EBV CF- group. However, the EBV CF+ group had slightly higher serum C-reactive protein (0.48 vs 0.43 mg/L, p = 0.031, high-sensitive assay), total T cell (CD3+) count (median 1573 vs 1481 × 106 cells/L, p = 0.012), plasma norepinephrine (1420 vs 1113 pmol/L, p = 0.01) and plasma epinephrine (363 vs 237 nmol/L, p = 0.032); lower low-frequency:high frequency (LF/HF) ratio of heart rate variability at supine rest (0.63 vs 0.76, p = 0.008); and an attenuated decline in LF/HF ratio during controlled breathing (-0.11 vs -0.25, p = 0.002). Subgrouping according to different CFS diagnostic criteria did not significantly alter the results. Within the EBV CF+ group, there were no strong correlations between clinical symptoms and markers of disease mechanisms. In a multiple regression analysis, serum CRP levels were independently associated with serum cortisol (B = 4.5 × 10-4, p < 0.001), urine norepinephrine (B = 9.6 × 10-2, p = 0.044) and high-frequency power of heart rate variability (B = -3.7 × 10-2, p = 0.024). CONCLUSIONS In adolescents, CF and CFS 6 months after acute EBV infection are associated with high symptom burden, but no signs of increased viral load and only subtle alterations of immune, autonomic, and neuroendocrine markers of which no one is strongly correlated with symptom scores. A slight sympathetic over parasympathetic predominance is evident in CF and might explain slightly increased CRP levels.