Rheumatoid Arthritis and Stroke: is Homocysteine a Linking Factor?

Ever since increase in homocyseteine (hcy) level termed as hyperhomocysteinemia (hhcy) has been recognized as one of causal factors for an independent factor for the atherothromobosis and endovascular injury, it has become an element of great interest of research. Homocysteine (hcy) has close association (between hcy and different diseases) particularly in rheumatoid arthritis (RA) and in cardio and cerebro-vascular diseases. The capability of hcy to the vascular damage and structurally modifying specific proteins, resulting in formation of neo-antigens may also be a triggering factor of autoimmune reactions and thus hcy has probability to present itself as an initiating factor in autoimmune disease like RA. These all circumstances point towards potentially relevant role of hcy in the onset of specific autoimmune disease. Hcy causes or plays a role in the progression of the associated cardiovascular and cerebrovascular damage through its inflammatory property. Immuno-inflammatory activation may contribute to the increase in hcy level which in turn may add up to the injury of the specific organ in specific diseases (like vessel injury in cardio and cerebrovascular disease, synovial tissue in RA). This bi-directional link appears to connect hcy and the auto-immune disease (immuno-inflammatory activation). In this review we have tried to present the potential relation of hcy as a common linking factor between stroke and rheumatic arthritis, through its bi-directional property. Through this current opinion we have tried to put forth our opinion that hcy is one of the common causal factors in stroke well as in rheumatoid arthritis. This carries an interesting clinical importance in control and prevention of these two diseases of different entity at a common point.