Tumour necrosis factor production and cell-mediated immunity in anorexia nervosa.

Fourteen patients with anorexia nervosa (AN) were studied for the production of tumour necrosis factor (TNF), the activation of the interferon (IFN) system and cell-mediated cytotoxicity (CMC) and the results were compared with 16 age-matched healthy women. AN patients had significantly increased spontaneous TNF production by peripheral blood mononuclear cells (PBMC) in vitro (16 +/- 5 U/ml versus 4 +/- 3 U/ml in the control group; P less than 0.05), although no TNF was detectable in the plasma from either group. TNF production in vitro, following stimulation of PBMC by phytohaemagglutinin (PHA) or tumour cells, was similar in AN patients and controls; however, lipopolysaccharide (LPS) induced TNF production was found to be lower in AN (P less than 0.1). CMC was significantly lower in AN patients (4 +/- 2 versus 10 +/- 3 in controls, expressed as lytic units/10(6) cells; P less than 0.05), but no difference could be found between AN and controls in IFN activity as reflected by the level of the IFN-induced enzyme 2'-5' oligoadenylate synthetase (2-5A) in PBMC. Beta-endorphins in the plasma were higher in the AN group (P less than 0.05) but these levels could not be correlated to those of IFN, CMC or TNF. Defective CMC and increased TNF production by PBMC in patients with anorexia nervosa may possibly result from the nutritional deficiencies and neuroendocrine abnormalities associated with the disease, and may contribute to the pathophysiology of AN.