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-. a systemic disease of connective tissue that are not primarily the small joints of the kind of destructive and erosive arthritis of unknown etiology with a complex autoimmune pathogenesis

causes the disease known to this day. Indirect data, such as elevated white blood cell count and (ESR) indicate the infectious nature of the process. It is believed that the disease as a result of an infection that weakens the immune system in genetically susceptible individuals, developed with the formation of so-called. Immune complexes (the antibody, virus, etc.)., Which are deposited in tissues and cause joint damage. But the ineffectiveness of antibiotic treatment of RA is likely to show the inaccuracy of this assumption.

The disease is caused by an inability high (70%), which comes soon enough. The most common causes of death are infectious complications of the disease and kidney failure. Treatment focuses primarily on damage to the relief of pain, slowing the progression of the disease by surgery and recover. Can reduce the early detection of diseases using modern tools, clearly the damage that can be added to the joints and other tissues.For the first time can after strenuous exercise, emotional stress, fatigue, hormonal changes occur during the time that the impact of adverse factors or infections.

rheumatoid arthritis

is distributed worldwide and affects all ethnic groups, prevalence ratio of 0.5-1% (up 5% in older patients) M: F = 1.03 peak beginning – 30-35 years

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hypothetical triggers of diseases of the rheumatic

paramyxovirus – virus, mumps, measles, respiratory infections, viral syncytialHépatite BHerpès virus – simplex virus “herpes, herpes zoster, cytomegalovirus, Epstein Barr virus (much higher in the synovial fluid of patients with retroviruses REQUESTS – T-lymphotropic virus

For women, the duration of breastfeeding reduced the risk of PR breastfeeding for 24 months or more reduces the risk of developing rheumatoid arthritis. by half.

rheumatoid arthritis

proceeds in three phases. In the first stage, the swelling of the synovial fluid sacks pain, heat and swelling around the joints. The second step is the rapid division of cells compression of the synovial membrane leads. In the third stage, let the infected cells, an enzyme which attacks the bone and cartilage, which often deformation of the affected joints, increasing pain and loss of motor function.

The disease progresses slowly to the first, with the gradual introduction of clinical symptoms for months or years, and even acute or subacute at least -. occurs in about two thirds of cases of fever, and the rest – a mono-or oligo-syndrome, joint pain and often no clinical specificity, which makes it very difficult the differential diagnosis of joint syndrome is caused by morning stiffness of more than 30 minutes and similar expressions in the second half of the night -. symptoms of “stiff gloves”, “corset” out; increased during spontaneous pain in the joints, during active movements of the disappearance of rigidity depending on the activity of the process: The more activity, the greater the duration of the restraint for the joint syndrome in rheumatoid arthritis is characterized by the monotony .., duration, preservation of the aftermath after treatment “. distinguish / p> It prodromal to clinical symptoms (mild, transient pain, pain associated with weather, dysautonomia)” joint damage “and rheumatoid arthritis is often combined with other diseases.” be out for the joints. “- arthritis, arthritis, systemic connective tissue diseases

Assign the following options for the clinical course of rheumatoid arthritis

The classic version of the defeat (two symmetrical joints. and small or grand mono-oligoarthritis affecting mainly the large joints, most commonly in knee. outbreak of the disease and the reversibility of all events during 1-1.5 months (arthralgias are migratory in nature, radiological changes are missing, the anti-inflammatory drugs offer relatively positive effect in the second there are all the symptoms of rheumatoid arthritis)

diagnosis of rheumatoid arthritis (RA) -. For many years there was no test which clearly confirms the presence of the disease was present, the diagnosis of diseases on the basis of biochemical analysis of blood are visible changes in the joints on X, and the basic use of clinical markers, but also in conjunction with the general clinical manifestations – fever, malaise, weight loss examined in the analysis of blood ESR, rheumatoid factor, platelet count, etc. The most advanced analysis is the title of the anti- citrulline-containing cyclic peptides -. PCAC, anti-CCP, anti-CCP specificity of this indicator is 90%, while it is in 79% of sera from patients with RA.

diagnosed clinically important, the lack of discoloration of the skin and inflamed joints, the development of flexor or extensor tenosynovitis of the fingers and the formation of muscles, the typical loads on the brush, so-called “wrist arthritis

The criteria for poor prognosis are:.

injuries early large joints and lymphatic nodules rhumatoïdesganglions enflésparticipation new seals in the subsequent exacerbation, systemic disease, disease activity continues without remission for more than a year, the continuing increase in the ESR, early onset (of the first year) and high titers of factor rhumatoïdeprécoce (up affected to 4 months), radiographic changes in the joints – a rapid destructive changes, detection of antinuclear antibodies and LE cellulesTransporteur HLA-DR4

rheumatoid arthritis, all common, but usually comes from small joints of the fingers start, hands and wrists. Typically, joint damage is balanced, if affected, for example, the painful joint in his right hand, then sick the same joint on the left. The joints at later stages of the disease.

Other common symptoms are morning stiffness . FatigueLa general, the restriction of the activities maladie.La faiblesseSymptômes flu-like, accompanied température.La including low pain when sitting prolongéeLes burst of activity by rémission.Douleurs musculairesPerte loss of appetite, depression, weight loss, anemia, cold and / or humid hands and piedsViolation glands near the eyes and mouth, resulting in insufficient production of tears and saliva.

require, in the presence of an infection, a treatment appropriate antibacterial. In the absence of extra-articular manifestations of light (such as high fever, Felty’s syndrome .. or polynervopathy) treatment of common syndrome begins with the selection of non-steroidal anti-inflammatory drugs (NSAIDs) at the same time in the inflamed joints injected with corticosteroids is an important point in the treatment of rheumatoid arthritis is the prevention of osteoporosis – the restoration of calcium balance in the direction of increasing its absorption in the intestine and excretion reducedthe sources of calcium are dairy products (especially cheese, which contains 600 to 1,000 mg of calcium per 100 g of product as well as cheese, to a lesser degree of curd, milk, sour cream) almonds, hazelnuts and walnuts, etc., and calcium in combination with vitamin D or its active metabolite.

importance in the treatment of therapeutic exercises to maintain maximum joint mobility and maintain muscle mass.

Physiotherapy

(electrophoresis of anti-inflammatory drug, hydrocortisone phonophoresis) and spa treatments. With single and persistent oligoarthritis includes the introduction of isotope of gold, yttrium, etc., with persistent strains of joints is the reconstructive surgery performed

Systemic drug therapy involves the use of four classes of medications:..

1, nonsteroidal anti-inflammatory drugs (NSAIDs),

2 basic medicines

3 glucocorticosteroids (GCS)

4 biological agents.

NSAIDs remain the first line of therapeutics that are directed primarily at relieving the acute symptoms of the disease, and to ensure a stable clinical remission and laboratory. <

p are in the acute phase of illness from the use of NSAIDs, corticosteroids, pulse corticosteroid therapy or in combination with cytotoxic immunosuppressive therapy.

NSAIDs a current net-inflammatory effect by inhibiting the activity of cyclooxygenase (COX ) -. a key enzyme in the metabolism of arachidonic acid is caused, is particularly interesting, the discovery of two isoforms of COX, which are identified as COX-1 and COX-2 play different roles in regulating the synthesis of prostaglandins (PG). shown that NSAIDs, the activity of the isoforms inhibit COX, but their anti-inflammatory activity based on inhibition of COX-2.

Most of the known NSAIDs inhibit COX-1, the appearance of complications including gastropathy, renal failure, encephalopathy , hepatotoxicity.

explains Sun, depending on the blocking COX-selective and nonselective NSAIDs in COX-2 inhibitors.

are representative of the selective COX-2 inhibitors are divided meloxicam, nimesulide, celecoxib. These drugs have minimal side effects and maintaining a strong anti-inflammatory and analgesic. COX-2 inhibitors can be used in all programs of treatment of rheumatoid arthritis that the use of NSAIDs. meloxicam (Movalis) in the early treatment of inflammatory activity attributed to 15 mg / day and then transferred to 7.5 mg / day as maintenance therapy at a dose of nimesulide 100 mg given twice a day

celecoxib (Celebrex) -. A specific inhibitor of COX-2 -. is at 100 attributed to selection 200 mg twice daily for the determination of the older drug is not necessary, however, patients with a body weight below the median (50 kg ..), it is advisable to begin treatment with the minimum recommended dose.

you should avoid the mixing of two or more NSAIDs remain unchanged because of their effectiveness, and to play the risk of side effects

basic drugs increases a central role in the treatment of rheumatoid arthritis, but now there was a new approach to its target compared to the familiar tactics of treatment of progressive rheumatoid arthritis (“the pyramid principle”), is now advocated aggressive treatment of essential drugs immediately after diagnosis, the purpose of -. the flow changes of rheumatoid arthritis and maintenance of remission, the reason for this situation are the lack of early rheumatoid arthritis, deformities, osteopenia, and severe complications created by autoimmune mechanisms, the likelihood of remission

The most important basic therapy of rheumatoid arthritis.. methotrexate, sulfasalazine, gold preparations, D-penicillamine, through the Reserve include cyclophosphamide, azathioprine, cyclosporine A The new group consisted of the following drugs: Remicade …

replaces inefficient for 1.5 to 3 months or basic drugs, when combined with corticosteroids in low doses, thus activity of rheumatoid arthritis before the start of the first six months -. a critical phase, the latest efficiency-based therapy should be discontinued.

The best preparation for the start of treatment in severe rheumatoid arthritis based and RF-positivity, the presence of extra-articular manifestations of monitored cytotoxic immunosuppressant that is extended for use tolerated and has fewer side effects than other drugs in this group

carefully in the treatment of essential drugs, the activity of the disease and side effects

A new approach – Methotrexate is.. The use of high doses of corticosteroids (pulse therapy) in combination with slow-acting tools that can improve the efficiency of the latter, with combinations of methotrexate with gold salts, sulfasalazine, and a selective immunosuppressant cyclosporin A.

with a high degree of inflammatory activity of corticosteroids are used, and if systemic manifestations of rheumatoid arthritis is a form of pulse therapy is used. corticosteroids alone or in combination with cytotoxic drugs cyclophosphamide -.. SCS also used anti-inflammatory therapy after failure of other medications support

In some cases, corticosteroids are used as local treatment indications for use. essentially mono-or oligoarthritis of large joints,

In rheumatoid arthritis the synovial membrane, for some reason which secrete large quantities of the enzyme that destroys the disulfide bonds in the cell membrane. In this case it is “leakage” of proteolytic enzymes of cellular lysosomes, which reacts. cause damage to bones and cartilage around the body with it, including a Cascade -.. these reactions triggered in cells by cytokines, aggravated the symptoms associated with chronic inflammatory arthritis with TNF-α, often resulting in damage to cartilage and joints, which to a physical disability.

The treatment uses a monoclonal antibody ‘s, the effect with a high affinity to TNF, both in the soluble and transmembrane forms, resulting from the neutralization of TNF activity.

During the progression of rheumatoid arthritis, joint damage in patients with rheumatoid arthritis is a narrowing of the joint space between the bones and the erosion of bone observed in the joint space. Clinical studies with the monoclonal antibody is its use as shown slow erosion and narrowing the space between the bones.