Fatigue Syndromes and the Ætiology of Autoimmune Disease
A. Poteliakhoff, Jnl CFS, 1998, 4(4):31-49
In the last decade or so, an impairment of Hypothalamic-Pituitary-Adrenal (HPA) axis activity has been observed in fatigue syndromes. Elevated levels of glucocorticoids help to prevent the immune system from over-reacting and generating a damaging autoimmune process. The corollary should be that reduced activity of the HPA axis and diminished levels of plasma cortisol could be associated with autoimmune (AI) disease. Experimental work in mice and rats supports this view. Furthermore, plasma levels of cortisole have been found to be low in the early stages of rheumatoid arthritis. There is some clinical evidence that connective tissue disorders (many of which are regarded as autoimmune diseases) occur approximately one year after the onset of prolonged or chronic fatigue, with the implication that fatigue is not merely a symptom of these disorders but precedes them. Many workers have found changes in the immune system of subjects suffering from CFS (mainly immune activation) which could be conducive to the development of the AI disease. It has recently been found that there is, in the CFS, some deficiency of another adrenal steroid, namely that of dehydroepiandrosterone. This steroid exerts a regulatory activity on the immune system and a deficiency may well be an additional factor in the genesis of AI disease.
If an association can be established between fatigue syndromes and autoimmune disease then these syndromes will need to be addressed in a more concerned manner and prophylactic measures undertaken to forestall AI disease.
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