Katrine B. Norheim1, Grete Jonsson2 and Roald Omdal1,3
Correspondence to: Roald Omdal, Department of Internal Medicine, Clinical Immunology Unit, Stavanger University Hospital, PO Box 8100 Forus, 4068 Stavanger, Norway. E-mail: email@example.com
Fatigue is a disabling phenomenon with potentially serious consequences not only for patients, but also for society in terms of health-care expense and loss to the work force. Fatigue is common across a number of diseases, and is highly prevalent in RA, SLE and pSS. Mood disorders strongly contribute to the multifactorial aetiology of fatigue.
However, a substantial percentage of patients suffering from fatigue are not depressed, and in these patients other explanatory mechanisms must be found.
Sickness behaviour in animals, induced by pro-inflammatory cytokines and IL-1β in particular, parallels fatigue in several aspects.
Induction of fatigue by cytokine injections in humans, and relief of fatigue in RA after treatment with biologics, support this hypothesis, and may give rise to future fatigue-specific treatment. Exploration of oxidative stress and gene studies in relation to fatigue offers hope for further understanding of this complex phenomenon.
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MY PS sickness behaviour explained: Pro-inflammatory cytokines, such as TNF-α, IL-1, IL-6, IL-12 and IL-17, are important players in the inflammatory response, and are crucial both in defence against infection and in development of autoimmune disease. Pro-inflammatory cytokines in animals act on the brain during infection and other inflammatory states to cause a behavioural response entitled sickness behaviour (Fig. 1). This phenomenon is characterized by drowsiness, loss of appetite, decreased activity and withdrawal from social interaction [54, 55], and represents a change of behaviour theorized to enhance survival of infection. Fatigue in humans could be considered a part of this biologically triggered coping mechanism.