Future trends in the treatment of rheumatoid arthritis in the light of current etiopathogenetic theories.
The current treatment of rheumatoid arthritis is based on the use of synthetic chemical compounds, the mechanism and action of which have been more or less unknown. Usually this therapeutic effectiveness was discovered accidentally. Often the initial use of such compounds was motivated on the basis of generally diffuse ideas about the eventual pathogenesis of rheumatoid arthritis. The main site of action of most of these drugs has recently been elucidated. Depending on their multiple sites of action the polypharmacy frequency relied upon at present seems also to be theoretically motivated. Many new possibilities for treatment which have appeared recently have resulted from the amission of page limitation. These include various thymic (46), steroid and other hormones (67) and various vehicles or new modes of application, e.g. percutaneous, for directing the effects of drugs selectively to the target tissue, organ and cells. The use of specific T cell clones in therapy (68) has been only briefly dealt with in this article, and the development of operative techniques, endoprosthesis technology and orthopedic devices have not been dealth with at all. Chemical synovectomies with 165Dy-FHMA and other agents (69) will be developed further etc. This overview mainly deals with future trends in the treatment of rheumatoid arthritis based on advances made in the evaluation of the etiopathogenesis. Due to advances in basic sciences and medicine, the pathogenetic mechanisms effective in rheumatoid arthritis are better known today than ever before. The same progress in science has for the first time in history provided us with a potential means of producing bioactive mediators and reagents in sufficient amounts to enable their use also for therapeutic trials and treatment. In addition to the need to develop better methods of treatment for the patients crippled by this chronic disease, studies on the pathogenesis will also be of great benefit to our ideas about exactly what is involved in the complex process clinically known as rheumatoid arthritis.
Konttinen
Y T
YT
Helsinki University Central Hospital, Fourth Department of Medicine, Finland.
Honkanen
V E
VE
D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000503:physiopathology* / Q000628:therapy; D001323:Autoantibodies / Q000276:immunology; D004789:Enzyme Activation; D005122:Exudates and Transudates / Q000276:immunology; D006684:HLA-DR Antigens / Q000235:genetics; D015804:HLA-DR4 Antigen; D006801:Humans; D007130:Immunoglobulin Idiotypes / Q000276:immunology; D010740:Phospholipases / Q000378:metabolism; D013585:Synovitis / Q000276:immunology / Q000503:physiopathology
D001323:Autoantibodies; D006684:HLA-DR Antigens; D015804:HLA-DR4 Antigen; D007130:Immunoglobulin Idiotypes; D010740:Phospholipases