Sammendrag
Cytokines, Chronic Fatigue Syndrome and associations with Depression –a pilot study
Purpose of the study
Chronic Fatigue Syndrome (CFS/ME) is a deliberating syndrome with unknown aetiology. Some studies point towards a dysfunction of the immune system, findings are however inconclusive. Also, patients with CFS/ME shows increased scores on depressive parameters though not fulfilling the criteria for depression. Cytokines are regulatory signal proteins of the immune system, also affecting neurons. Thus, cytokines may influence the brain and behavioural patterns. There are several studies finding altered immune activity in psychiatric patients and studies reporting psychiatric effects of immune stimulation. The potential role of immunology and psychiatry together in CFS/ME has not been explored. The objective of this study was to examine the possibility of immunological abnormalities related to psychiatric parameters in CSF/ME. By understanding the underlying mechanisms behind CFS/ME it may be possible to detect subgroups and learn more about the syndrome, and hopefully prevent and treat this syndrome.
We therefore hypothesised a cytokine abnormality/difference in a CFS/ME patient group compared to a healthy control group, and that there were correlations between levels of cytokines and other psychometric and somatic symptom data, such as depression, fatigue or pain.
Method
20 well defined female CFS/ME patients (age 18-42) and 20 healthy age-matched female controls were included in this study. Venous blood plasma was immediately separated and stored at -80˚ C until analysis. ELISA was used to measure the plasma concentration of the following cytokines: IL-4, IL-6, IL-10, IFN-γ, and TNF-α. For psychometric evaluation, Hospital Anxiety Depression Scale (HADS) and SCL-90-R, were used; for fatigue and pain symptoms, Chalder fatigue scale and a self-evaluating pain scale (NRS), respectively, were used. This study was approved by the local Regional Committee for Medical and Health Research Ethics.
Summary of results
A substantial finding was the difference between the CFS/ME group and healthy control group in the plasma concentration of TNF-α (p = .056). Levels of TNF-α correlated with HADS depression scores in the whole population group (p = .003). The two groups differed significantly on scores of fatigue, pain, depression (HADS) and anxiety (HADS) (p = .000, p = .000, p = .000, p = .026), and SCL-90-R parameters of somatisation (p = .000), obsessive-compulsive (p = .000), interpersonal sensitivity (p = .010), depression (p = .000), anxiety (p = .016), hostility (p = .012), psychoticism (p = .012), additional items (p = .000) and GSI (p = .000).
Conclusions
Differences were found between the CFS/ME patients and the control group in plasma levels of TNF-α. Significant differences in pain, somatisation, and depressive symptoms between CFS/ME patients and the control group also were found. Increased TNF-α correlated with symptoms of depression. Further studies including a greater number of subjects are needed to explore the relationship between immune activity and CSF/ME.
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