In rheumatoid arthritis, the build up of fibrin within the joint may be re­sponsible for some form of chronic in­flammation and joint manifestations in­cluding pannus formation and polymorph induced cartilage destruc­tion (Belch et al., 1984). An elevated plasma fibrinogen is a well recognised feature of active rheu­matoid arthritis (RA), and the pres­ence of large amount of fibrin in the synovial fluid and membrane is also well documented in this disease (Back Anderson & Gormsen, 1976). Defective fibrinolytic activity has been demonstrated in many inflamma­tory conditions such as: rheumatoid arthritis (Belch et al., 1984), systemic fupus erythema to sus (SUE) {Chu et al., 1988) and Behcet's syndrome (Guntifie, 1973). However, the exact clinical implication of defective fibrino­lytic activity in various rheumatic con­ditions is still as yet a controversy. Therefore, we have decided to study the fibrinolytic activity of the per­ipheral blood in patients with RA in re­lation to some clinical and laboratory manifestations in those patients.