Experimental arthritis is an animal model of chronic inflammation that is associated with a decrease in body weight gain, growth hormone (GH) and insulin-like growth factor-I (IGF-I). Cyclooxygenase enzymes (COX) are responsible for prostaglandin (PG) production. COX-1 is responsible for the physiological production of PGs and COX-2 for the elevated production of PGs that occurs in sites of disease and inflammation. The aim of this work was to analyze the role of COX-1 and COX-2 in arthritis-induced decrease in GH and IGF-I. For this purpose, arthritis was induced in male Wistar rats by an intradermal injection of Freund’s adjuvant (1mg) in the sole of the right paw. Fifteen days after adjuvant injection control and arthritic rats were divided in three groups. One group was daily injected for 8 days with saline; another one was injected with 4mg/kg s.c. of indomethacin (unspecific inhibitor of COX) and a third group of rats was injected with 1 mg/kg s.c. of meloxicam, a specific inhibitor of COX-2. Arthritis induced a decrease in body weight gain (12.2 ± 3 vs 39.4 ± 1.9 g (± SEM), P<0.01, n=10-12), pituitary GH gene expression (43 ± 6 vs 100 ± 22, % over control values, P<0.01, n=7-9) and IGF-I serum levels (730 ± 38 vs 109 ± 32 ng/ml, P<0.01, n=10-12), whereas it increased the serum levels of PGE2 (6.94 ± 0.3 vs 6.558 ± 1.6 ng/ml, P<0.05, n=10-12). In arthritic rats, indomethacin and meloxicam treatments markedly decreased the arthritis score and the swelling of the paws (P<0.01), and totally prevented the decrease in body weigh gain (P<0.01). Meloxicam injection did not have any effect in control rats but indomethacin induced a decrease in IGF-I serum levels in control rats. In arthritic rats, both COX inhibitors prevented the decrease in IGF-I serum levels as well as in pituitary GH gene expression. All these data suggest that, during chronic inflammation, prostaglandins have an inhibitory effect on body weight, GH and IGF-I, since treatment with COX inhibitors reverses these harmful effects in arthritic rats.