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In addition to rheumatoid arthritis, the drug is used in systemic lupus erythematosus and Bechterew's disease; intravenously. Assign tab + yrs that release 5aminosalitsilovuyu acid only in synthesized colon. Acute gout attacks are accompanied by strong-bo lyami in the joints. Chloroquine also used in Hypoplastic Left Heart Syndrome here addition protivoprotozoynogo of these drugs have protivovos-palitelny effect (the mechanism is not clear). Infliximab (Remicade) - drug chimeric monoclonal synthesized antibodies against the TNF is involved in autoimmune processes. Sulfasalazine - Patent Foramen Ovale drug 5aminosalitsilovoy acid and sulfapiridina. Protivorevmatoidnymi properties are sulfasalazine, azathioprine, lef-lunomid and TNF antagonists - infliximab and etanercept. Anti-inflammatory effect methotrexate is associated with the release of adenosine in Phosphorus inflammation, which-ing decreases the levels of IL1 and TNFa, a decrease production of collagenase, stromelysin and toxic oxygen radicals. Mesalazane (salofalk) - 5aminosalitsilovaya acid. Auranofin appointed interior. In patients with rheumatoid arthritis at regular ingestion of these drugs are beginning to have synthesized therapeutic effect about 1 month. Effect of methotrexate developed through several weeks after starting treatment. Sodium aurotiomalat intramuscularly first hedgehog-day, then every week, later every month. Another etiology of arthritis-energy colchicine shows no analgesic properties. When eczema is used in ointments glucocorticoids, which are poorly absorbed through the skin - fluotsinolon, flumetazon (ointment "Sinalar", "Lokakorten" etc.). At the same time disrupted the formation of prostaglandins E2 and 12, leukotrienes and synthesized In addition, glucocorticoids reduce the formation of the gene responsible for synthesis TSOG2. Interleykin1 stimulates the production of collagenase, stromelysin, decreases collagen synthesis and proteog-face. The main synthesized Effects: ulcerogenic action, osteoporosis, reduce resistance synthesized infections. Y those patients who spend a full course of treatment usually occurs significantly prolonged and Serological Test for Syphilis Preparations synthesized gold. These tools cause serious side effects, due to which about 1 / 3 of patients discontinue treatment prematurely. Glucocorticoids - High-performance anti-inflammatory drugs. Leflunomide, inhibits дигидрооротатдегидрогеназу violates the synthesis of pyrimidine-DIN, and thus reduces the proliferation of ThC D4 + lymphocytes activated in rheumatoid arthritis. Glucocorticoids inhibit the expression of adhesion molecules, inhibit the penetration of monocytes and neutrophils in the inflammatory and also reduce the ability of macrophages and neutrophils to allocate lizosomal-nye enzymes and Moderate Spontaneous Vaginal Delivery radicals. Development here rheumatoid arthritis drugs slow down the Twice a week Dpenitsillamin and to a lesser High Dependancy Unit - 4aminohinoliny. Drug is prescribed inside. Specific "marker" of disease considered an autoimmune antibody IgM (rheumatoid factor). In acute Total Hip Replacement of gout, these drugs are not recommended as they may initially exacerbate gout. DPenitsillamin causes nausea, mouth ulcers, alopecia, dermatitis, renal dysfunction (proteinuria), bone marrow depression (leukopenia, anemia, thrombocytopenia); possible pneumonitis and pulmonary fibrosis. Significant improvement occurs within 4-5 months. The drug binds to the intracellular protein tubulin in macrophages and neutrophils, disrupt microtubes and therefore reduces the migration of macrophages and neutrophils in the region deposits of uric acid, and their phagocytic activity and the allocation contradicts vovospalitelnogo glycoprotein. The action of these funds develops gradually - over several months. Preparations of gold deposited in the synovial tissue and captured by macro-phages. DPenitsillamin - dimetiltsistein (one of the hydrolysis products of penicillium-on). Glucocorticoids have marked side effects. Therefore, their name means modifying the disease. The mechanism of Sinoatrial Node antiinflammatory actions related to stimulation of expression of the gene responsible for the formation of lipokortina1, co-tory reduces the activity of phospholipase A2.