Endocrine Abstracts

Recent research has suggested mild hypocortisolism in at least some subjects with Chronic Fatigue Syndrome (CFS). For example, our study of 120 well-characterised CFS patients showed a significant reduction in 24-h urinary free cortisol (UFC). Studies of the HPA axis suggest a generally impaired responsivity to challenge, although there is no one specific pattern. Examples include impaired responses to CRH challenge. A randomised, placebo controlled trial of low dose (5-10 mg/day) hydrocortisone replacement therapy found a significantly greater reduction in fatigue in patients on hydrocortisone compared to placebo, suggesting that low cortisol levels may be contributing in some way the fatigue. Furthermore, in those patients who responded to hydrocortisone, there was a reversal of the previously observed blunted responses to CRH. The most effective treatment for CFS is cognitive behavioural therapy; we have now shown that this therapy is also effective at increasing cortisol levels and revering HPA axis changes. This suggests that the HPA axis changes may be secondary to the effects of CFS on factors such as sleep and inactivity rather than a primary feature. Prospective studies of chronic fatigue occurring after glandular fever, in which HPA axis changes are not observed, support this contention. All the above studies received local ethical committee approval.
It is suggested that HPA axis disturbance may be a significant perpetuating factor in fatigue chronicity, but (a) there is no specific pattern of abnormality (b) it is of multifactorial aetiology and (c) it is one of many potential factors responsible for perpetuating fatigue in CFS.