Plasma concentrations of tumor necrosis factor-α (TNF-α) and soluble TNF receptors in patients with bulimia nervosa

BACKGROUND Tumor necrosis factor-alpha (TNF-alpha) is a cytokine with numerous immunological and metabolic activities. In addition, TNF-alpha can stimulate a variety of physiological, neuroendocrine and behavioural responses of the central nervous system. In experimental animals, TNF-alpha induces changes in physiological and behavioural parameters which have also been observed in eating disorders. The biological activities of TNF-alpha are mediated by two structurally related, but functionally distinct receptors, TNF-RI and TNF-RH. Since injection of TNF-alpha results in increased shedding of TNF-alpha receptors, it is likely that TNF-alpha release is reflected by soluble TNF-receptors (sTNF-Rs) levels. AIMS We studied plasma concentrations of TNF-alpha and two sTNF-Rs (sTNF-RI and sTNF-RII) in female patients with bulimia nervosa. DESIGN AND PATIENTS Twenty female patients with bulimia nervosa (BN) and 20 age-matched normal women (N) were studied, MEASUREMENTS Plasma TNF-alpha concentrations were measured by enzyme immunoassay kit and plasma concentrations of sTNF-RI and sTNF-RII were measured by enzyme-linked immunosorbent assay. RESULTS Plasma TNF-alpha concentrations in BN were significantly higher than those in N (4.7 +/- 0.5 ng/l vs. 1.6 +/- 0.1 ng/l; P< 0.01). Although no significant difference was observed in plasma sTNF-RI concentrations between the two groups, plasma sTNF-RII concentrations in BN were significantly higher than those in N (2080.0 +/- 107.5 ng/l vs. 1569.5 +/- 84.0 ng/l; P<0.01). Plasma TNF-alpha concentrations were significantly related to plasma sTNF-RI concentrations (r=0.511, P<0.05) and to plasma sTNF-RII concentrations (r=0.532, P<0.05) in bulimic patients. However, plasma TNF-alpha concentrations were not related to body fat mass or to bulimic behaviours in these patients. CONCLUSIONS Our present findings suggest that the adipose tissue may not be the immediate source of TNF-alpha in bulimic patients but the increase in plasma TNF-alpha in these patients may be derived from the central nervous system sources. The elevated sTNF-RII may reflect different shedding kinetics compared with sTNF-RI in bulimic patients.