Characterization of pituitary function with emphasis on GH secretion in the chronic fatigue syndrome

OBJECTIVE Previous studies have revealed that hormonal disturbances may acc ompany the chronic fatigue syndrome (CFS), Changes in the secretion of the pituitary-adrenal axis have been demonstrated, as well as abnormalities in the GH-IGF-I axis. However, data have not always been well characterized an d were sometimes conflicting. The small number of CFS patients investigated in earlier studies may have played a role in the interpretation of the res ults. SUBJECTS AND DESIGN Hormonal testing was performed in 73 nonobese CFS patie nts and nonobese 21 age-and gender-matched healthy controls. We investigate d GH, ACTH and cortisol responses to insulin-induced hypoglycaemia. In a su bgroup of patients arginine and clonidine stimulation for GH was also perfo rmed. Nocturnal secretion of GH, ACTH and cortisol were determined. Serum l evels of IGF-I, prolactin, TSH, and free thyroxine were also measured. Visc eral fat mass was assessed by CT scanning. RESULTS GH response to insulin induced hypoglycaemia assessed by peak value (17.0 +/- 13.1 mu g/l vs. 22.1 +/- 9.8 mu g/l; P=0.01) and by AUC (450.0 /- 361.3 mu g/l vs. 672.3 +/- 393.0 mu g/l; P=0.002) was significantly decr eased in CFS patients vs. controls. Nocturnal GH secretion assessed by GH p eak value (5.4 +/- 3.7 vs. 9.0 +/- 5.1 mu g/l; P=0.44) and by AUC (34.4 +/- 20.2 vs. 67.4 +/- 43.1; P=0.045) was also significantly impaired in CFS pa tients. Arginine and clonidine administration showed no differences in GH s ecretion between CFS patients and controls, In the CFS group, GH peak value s were significantly higher after ITT than after arginine (P=0.017) or clon idine (P=0.001). No differences in serum IGF-I levels were found between CF S patients and controls. Except for a significantly lower nocturnal cortiso l peak value, no differences were found in ACTH and cortisol secretion betw een CFS patients and controls. Significantly higher serum prolactin revels (7.4 +/- 4.7 mu g/l vs. 4.4 +/- 1.3 mu g/l; P=0.004) and significantly high er serum TSH levels (1.6 +/- 1.0 mU/l vs. 1.0 +/- 0.4 mU/l; P=0.011) were f ound in CFS patients. Serum free thyroxine was comparable in both groups. V isceral fat mass was significantly higher in CFS patients (86.6 +/- 34.9 cm (2) vs. 51.5 +/- 15.7 cm(2); P<0.001). CONCLUSIONS We observed a significant impairment of GH response during insu lin-induced hypoglycaemia and a low nocturnal GH secretion in CFS patients. These changes did, however, not read to different concentrations in serum IGF-I. The clinical expression of this inadequate GH secretion can thus be questioned, although the alteration in body composition may be related to t his relative GH deficiency. Significantly increased prolactin and TSH level s were found when compared to controls. These findings give support to the hypothesis of a decreased dopaminergic tone in CFS. Further investigations are required in order to identify specific adaptations within the neurotran smitter system in CFS and to determine the clinical importance of the impai red GH homeostasis.