2 Measurements of prostaglandin E₂ (PGE₂), thromboxane (TX) B₂, 6-keto-PGF_1α and PGF_2α were performed by radioimmunoassay techniques in synovial effusions obtained from 23 patients, and validated by thin-layer chromatographic analysis of the extracted immunoreactivity.

3 PGE₂ and TXB₂ accounted for more than 60% of the total immunoreactivity in untreated patients. The absence of any constant ratio between the different arachidonic acid metabolites detected in synovial fluid is consistent with a heterogeneous cellular origin of these compounds.

4 Indoprofen treatment was associated with a consistent reduction of synovial prostaglandin and thromboxane concentrations, ranging from 36% in the case of 6-keto-PGF_1α to 90% in the case of PGE₂.

5 In contrast, 6-MeP caused opposite changes on different metabolites originating via the cyclo-oxygenase pathway. Thus, 6-keto-PGF_1α concentrations were reduced by 35%, PGF_2α concentrations were increased by 30%, while PGE₂ and TXB₂ were unchanged following 6-MeP.

6 Although the mechanism(s) underlying the failure of 6-MeP to reduce synovial PGE₂ and TXB₂ levels are uncertain, the results of the present study clearly indicate that therapeutic doses of steroidal and nonsteroidal anti-inflammatory drugs cause quite distinct changes in arachidonic acid metabolism, which might be relevant to their specific therapeutic actions and side-effects.