(1) First-line disease-modifying treatment for rheumatoid arthritis is based on 
"slow-acting" antirheumatic agents, generally methotrexate. Subsequent options 
include a TNF-alpha antagonist, followed by rituximab or possibly abatacept; (2) 
Tocilizumab, a monoclonal antibody, inhibits interleukin-6 receptors. It is 
licensed in the European Union for patients with rheumatoid arthritis in whom 
other drugs have failed; (3) Clinical evaluation includes 4 placebo-controlled 
trials of the methotrexate-tocilizumab combination, after failure of a 
slow-acting antirheumatic drug (3 trials) or failure of a slow-acting 
antirheumatic drug and a TNF-alpha antagonist (1 trial). An indirect comparison 
suggests that tocilizumab is no more effective than rituximab in patients with 
multiple treatment failure; (4) Tocilizumab, like TNF-alpha antagonists, is an 
immunosuppressant. It carries a risk of serious infections, haematological 
disorders (neutropenia, thrombocytopenia), gastrointestinal bleeding, hepatic 
disorders, and systemic and local reactions during the infusion; (5) the adverse 
effects of long-term tocilizumab therapy are unknown, particularly the risk of 
cancer; (6) Tocilizumab carries a risk of interactions with drugs that are 
metabolised by cytochrome P450 isoenzymes. Clinical consequences cannot be ruled 
out when co-administered drugs have a narrow therapeutic margin; (7) Tocilizumab 
is administered intravenously every 4 weeks, making it slightly more convenient 
that rituximab at the beginning of treatment; (8) In patients with rheumatoid 
arthritis and multiple treatment failure, it remains to be shown whether 
tocilizumab has a better risk-benefit balance than rituximab, a drug with which 
we have more experience. It is therefore better to continue to use rituximab, or 
possibly abatacept.