الفهرس 
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Abstract
JIA is not a single disease but encompasses all subtypes of idiopathic arthritis in childhood with disease onset prior to age 16, and persistence for more than 6 weeks (Ravelli and Martini, 2007).
The etiology of JIA remains poorly understood. Both genetic and environmental factors may play a role in the pathogenesis of JIA. A single causative gene defect for all JIA subtypes appears very unlikely, since the distinct clinical entities are minimally overlapping. A genome-wide scan in affected families suggested that several genes are associated with the development of JIA (Thompson et al., 2004).
The treatment of JIA is specifically targeted to each JIA subtype. The management of JIA encompasses pharmacological interventions, physical and occupational therapy, and also psychosocial support (Hashkes and Laxer 2005).
Poor outcome predictors can help determine patients requiring early aggressive therapy. Patients with polyarthritis and positive rheumatoid factor, antibodies to cyclic citrullinated peptides, the presence of HLA-DR4, nodules, and early onset symmetric small joint involvement have a poor prognosis (Ferucci et al ., 2005).
The last 10–15 years have witnessed an explosion in the development and application of medicines designed to target specific cytokines or cell surface receptors, therapies broadly referred to as biologics (Cohen et al., 2006).
Biologics are routinely used in adult and pediatric arthritis; overall, they have been remarkably effective, changing the outlook for a generation of patients afflicted with these disorders. Most of the studies on biologics have focused on TNF inhibitors, but emerging evidence, particularly in adults, has suggested that other therapies may be effective as well, even in patients who have failed TNF inhibitors (Cohen et al., 2006).
Aside from the TNF inhibitors, there is minimal published pediatric data for these therapies, although anakinra and tocilizumab have both shown promise in the population of children with SOJIA (Yokota et al., 2008) and several data suggest that abatacept may be effective JIA (Lovell et al., 2006).
Tocilizumab may have an important role in both RA and SOJIA (Smolen et al., 2008). Abatacept represents a successful transition from basic science research to clinical applications. It appears to be safe and effective in RA, showing success even in patients refractory to TNF inhibitors (Genovese et al., 2005). Preliminary data likewise reveals effectiveness in JIA (Lovell et al., 2006c). Rituximab shows a strong effectiveness record in RA, and has been safely used in a variety of other pediatric and adult rheumatological conditions (Scheinberg et al., 2006).
IL-1 blockade by anakinra interferes with the pro-inflammatory cascade important in the pathogenesis of chronic arthritis. Although its role in the therapy of RA and polyarticular JIA is undefined, anakinra is generally well-tolerated and does appear to be very effective in treating the systemic features of SOJIA (Pascual et al., 2005).
The side effects of biological therapy depend on the type of treatment. Often, these treatments cause flu-like symptoms such as chills, fever, muscle aches, weakness, loss of appetite, nausea, vomiting, and diarrhea. Some patients develop a rash or hypersensitivity reactions. Depending on how severe these problems are; patients may need to stay in the hospital during treatment. These side effects are usually short-term and they gradually go away after treatment stops. There have been concerns about the side effects of monoclonal antibodies, but these are rare. Early side effects include the risk of allergic reactions (including anaphylaxis), and reactions to the infusion. These are often treated with medications given before treatment. Biologics also carries a risk of worsening infection, and can cause reactivation of old infections, like tuberculosis. Over time, there is the risk of serum sickness, which is a delayed hypersensitivity response to the medication. Later complications may include multiple sclerosis and lymphoma. Finally, the medication is quite expensive, with treatment costs ranging from US$3000 to $8000 per infusion (Lovell et al., 2006).