Immunosuppressive actions of prostaglandins and the possible increase in chronic inflammation after cyclo-oxygenase inhibitors.
A method is described to examine the activity of potential antirheumatic drugs on the release and activity of lymphokines and interleukins in vitro, using human peripheral blood mononuclear cells and synovial cells. The enhancement of lymphocyte-mediated effects brought about by non-steroid anti-inflammatory drugs has been shown to be the result of inhibition of a prostaglandin negative-feedback mechanism. Since the underlying features of rheumatoid arthritis and related diseases are almost certainly brought about by mononuclear cell activation, their enhancement by non-steroid anti-inflammatory drugs might well have serious clinical implications. The possibility is discussed that aspirin-like drugs, administered in large doses to patients suffering slight joint pain, might well exacerbate, perpetuate or even initiate a chronic arthritic condition. We suggest that, as soon as the disease has been diagnosed, patients should be treated with a disease-modifying drug and, if necessary, an analgesic which does not inhibit cyclo-oxygenase.
D002455:Cell Division / Q000187:drug effects; D016861:Cyclooxygenase Inhibitors; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007249:Inflammation / Q000276:immunology*; D007376:Interleukin-2 / Q000494:pharmacology; D009000:Monocytes / Q000378:metabolism*; D010835:Phytohemagglutinins / Q000037:antagonists & inhibitors; D011458:Prostaglandins E / Q000096:biosynthesis / Q000502:physiology*; D013601:T-Lymphocytes / Q000187:drug effects*
D016861:Cyclooxygenase Inhibitors; D007376:Interleukin-2; D010835:Phytohemagglutinins; D011458:Prostaglandins E; D007213:Indomethacin