1. Leptin inhibits food intake and is an important regulator of long-term energy balance. In rodents, plasma concentrations of leptin are increased by administration of interleukin-1 and tumour necrosis factor. Hyperleptinaemia may mediate the anorexia and weight loss which is observed in chronic infections and inflammatory conditions.

2. Plasma leptin and soluble tumour necrosis factor receptor (sTNF-r55) concentrations were measured in patients with inflammatory bowel disease and acquired immunodeficiency syndrome (AIDS), and healthy controls.

3. The patients with AIDS were severely wasted [% body fat 12 (9–16); median (interquartile range)] compared with those with inflammatory bowel disease (25.1 (19–31.5)] and control subjects [29.4 (23.6–37.8)]. Leptin concentrations were highly correlated with percentage body fat in controls (r = 0.74, P < 0.001) and patients with IBD (r = 0.73, P < 0.001) but not in the patients with AIDS (r = −0.024). Leptin concentrations were similar in the inflammatory bowel disease (4.8 (2.6–10.1) ng/ml] and control groups [8.0 (3.1–14.1) ng/ml] but were significantly lower (P < 0.05) in patients with AIDS (1.8 (1.5–2.3) ng/ml] after 23 patients were matched for sex and percentage body fat in patients with inflammatory bowel disease (2.4 (1.8–4.1) ng/ml]. Plasma concentrations of sTNF-r55 were higher in both the patients with inflammatory bowel disease [0.19 (0.16–0.23) ng/ml] and those with AIDS [4.8 (2.8–7.3) ng/ml] compared with controls [0.14 (0.09–0.16) ng/ml] but were not correlated with either percentage body fat or plasma leptin concentrations.

4. Hyperleptinaemia does not appear to mediate the anorexia and weight loss associated with inflammatory bowel disease and AIDS. In patients with AIDS with extreme wasting there was no relationship between body fat and leptin and this may be related to the rapid weight loss which occurs in these patients.

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