Juvenile chronic arthritis

Juvenile chronic arthritis

    * Introduction
    * Symptoms and Diagnosis
    * Differential Diagnosis
    * Treatment
Juvenile arthritis is a chronic connective tissue disease of unknown origin. Among the security features that remind disease is a chronic synovitis and extraarticular shows systemic manifestations. Some define it as articular disease of unknown origin with onset before 16 years, including four or more joints with pain, swelling and limitation of joint movements. Swelling should last at least three months (like pain).
Clinical Diagnostic Criteria Clinical diagnostic criteria (American College of Rheumatology) are under the age of onset 16 years (juvenile) and undetermined etiology. Another criterion is the failure to comply with any painting such as the autoimmune rheumatic autoimmune hepatitis, panarterita nodosa, eritemmatos lupus (SLE), psoriatic arthritis. Ankylosing anchilopoetica is framed in juvenile chronic arthritis (JCA) is considered to define a particular form of spondylitis in adulthood in Europe, but not in the U.S.. A final criterion, gives no less important is the duration of joint damage over 6 weeks or more than three months.
Regarding the incidence of disease, juvenile chronic arthritis (JCA) is growing in the world, unlike acute rheumatism which falls continuously. In the U.S. 60-120 new cases are recorded annually at 100. 000. The chronic arthritis in children and adults generally appear 8-19 new cases per year to 100. 000.
Causes and pathogenesis in juvenile chronic arthritis In terms of definite etiology is not known pathogenic disease. They know they are incriminated both internal and external factors. Of the nature of external factors such as: viruses (parvovirus B19), chlamydia bacteria (Shigella), but this antigen has not been demonstrated in synovial joints. Internal factors (endogenous) include: glycoprotein 39 of synovial joints. The etiology is "signed" by an external trigger or endogenous factor known to infect synovial genetically predisposed individuals.
There are many histocompatibility antigens that predispose patients to the onset of disease. HLA B27 is best known, his presence causing the risk of developing the disease increase 100-200 times. These patients often have reactive arthritis after gastrointestinal infection. Other classes are present in the form of polyarticular seropositive DR4, DR11 appears in the systemic type, DRW8 this particular shape pauciarticulara with iridocyclitis child.
The etiology is probably multifactorial with genetic autoimmune particularly on land.
There are many physiological theories, but I'm not 100% confirmed. Theory of rheumatoid factor (RF) argues that many patients have rheumatoid factor, but not all. Do not explain, however, the pathogenic process for those without rheumatoid factor (RF). Acting on sinovalei hypothetical antigen stimulates B cells to produce this level of IgG antibodies by the immune system known as non-self (auto-antibodies) with production of IgG antibodies against their own, they are called rheumatoid factor (antibodies against its own structures ). Rheumatoid factor immune complexes formed with normal antibodies, activates complement, the classical and alternative pathway, with production of inflammatory phenomena through chemoattraction, accompanied by destruction of macrophages and neutrophils and release sites of enzymes (acid phosphatase, cathepsin) that amplify inflammation, leading to destruction articular cartilage. Interaction of B and T lymphocytes immune to the release of limfokine to determine, in turn, accumulation of macrophages in the synovium and rheumatoid factor production continues, the self-sustainability. In practice, not in Romania and rheumatoid factor titre May evidenteaza complement in synovial fluid decreased by consumption.
There are present and ragocitele, polymorphonuclear (PMN) or macrophages which includes rheumatoid factor, IgG, anti-rheumatoid factor and anti-complement. Ragocitele only when there are no rheumatoid factor or tuberculosis (TB), they are not pathognomonic for juvenile chronic arthritis. Currently, juvenile arthritis is considered a prototype for cronca imbalances B and T lymphocytes due to a particular genetic field. Hypothetical antigen stimulates a T lymphocyte clone (CD4) lymphocytes, which represent 80% of the joint. Hypothetical antigen is captured by antigen presenting cells and T lymphocyte shows class histocompatibility antigen DR on the surface antigens are considered together. It initiated the formation of a CD clones activated secretion of IL1, and IL2, IL4, IL6 and IF gamma, TNF alpha, which increases the phagocytic activity and transmit signals in B lymphocytes (by IL1, IL2, IL4) resulting in such antibodies and factor with the formation of CIC RF that activates complement and release in the final proteolytic substances that destroy the articular cartilage and perpetuate the inflammatory process. Antigen remains in the patient for life.
Juvenile chronic arthritis and arthritis are chronic diseases of adult life. This disease leads to complete removal of articular joint destruction in its use and pinching: permanent disability. Preferred position is flexion of these joints, so be it by forced extension exercises performed as early as not to hinder maneuvering invalidation strictly necessary. Hot packs or hot baths lead to a worsening of inflammatory processes. Physical therapy is very beneficial from an exacerbation.