JRA (Juvenile Rheumatoid Arthritis)

JRA (Juvenile Rheumatoid Arthritis)

Introduction

Juvenile rheumatoid arthritis - a chronic inflammatory joint disease in children under 16 years of unknown etiology and pathogenesis of complex, characterized by steadily progressive course, and accompanied in some patients, involvement of internal organs, often ending disability.

Among the rheumatic diseases of childhood juvenile rheumatoid arthritis is most common the first place. The disease is observed in different regions of the globe with a frequency of 0.05 to 0.6% in the population. Primary disease and varies widely, ranging from 6 to 19 cases per 100,000 child population (Wilkinson, 2001).

JRA affects about 1 in 1000 children (150,000 to 250,000 in the US alone) with overall incidence twice as high in females and is the most common form of arthritis in childhood. At least five subgroups are recognized. SYN: Still's disease; juvenile idiopathic arthritis (Varni et al., 1994).

Etiology

The etiology of juvenile rheumatoid arthritis is unknown to date. Among its reasons for considering, there are a set of different environmental factors (viral and bacterial infections, trauma, joint, chill, insulation, the introduction of protein drugs, etc.). The basis of an inadequate response in patients with juvenile rheumatoid arthritis is their "hypersensitivity to various environmental factors," results in a complex immune response that leads to the development of progressive disease. Family and a family history of rheumatic diseases plays a role. Studies in recent decades have linked juvenile rheumatoid arthritis in patients with the presence of DR-locus HLA DR4 with a predominance of patients with systemic forms of the disease, and DR5 - with mainly articular variant of the disease (Rennebohm, 1994).

Pathogenesis

The pathological process in juvenile rheumatoid arthritis begins in the synovium of the joint microcirculation disturbances and destruction of cells lining the synovial membrane. In response to the above changes in the patient in a modified IgG, which are perceived by its own immune system as autoantigens (Beales et al., 2003). Immunocompetent cells, including plasma cells, synovial joint, in response to produce antibodies - anti-IgG. These antibodies, called rheumatoid factor, in the presence of complement interaction with the autoantigen, and there is a formation of immune complexes. CEC have a damaging effect on both vascular endothelium and the surrounding tissue. The first to suffer the synovium of the joint, resulting in developing arthritis. In the synovial fluid and joint tissues with the formation of excessive amounts of cytokines, macrophage origin - interleukin-1 and inetrleykin-6, tumor necrosis factor (TNF-a). Interleukin-1 induces inflammation and destroy cartilage. The same is true of tumor necrosis factor (TNF-a). Interleukin-6 promotes the overproduction of acute phase proteins of inflammation - C-reactive protein and fibrinogen. There is a further activation of enzyme systems that destroy cartilage. Increased tumor blood vessels, or angiogenesis, which arises from the action of cytokines on the tissue, and enhances the degradation of cartilage (Jay et al., 2002).

Symptoms

The clinical picture of juvenile rheumatoid arthritis is varied. The beginning of the disease may be acute or subacute. At an acute the beginning of the is usually the body temperature raises, appears soreness ...