Rheumatoid Arthritis (RA) is a common condition causing disability in the population of Western countries. The annual incidence is estimated to be about 1% (1). RA affects both the young as well as elderly and, according to some data it was estimated that in 1995, 15% of the U.S. population suffers from this or comorbidities, forecasting for 2020, rising to 18%. Economic impacts associated with RA and associated illnesses in the United States consumed in 1992, a staggering sum of U.S. $ 194,400 million. RA is a chronic, progressive inflammatory process, beginning in the synovium of joints, leading to the destruction of joint tissues, distortion and dysfunction of joints. The disease may result in changes in many organs and systems – including to vasculitis, uveitis, pulmonary.
Despite years of research around the world, has not yet been clearly established and know the cause of RA. Important role in the initiation of the disease process is attributed to genetic predisposition and viral infection. None of the many hypotheses, regarding the association between RA and hereditary factors was not proven. For many years, attempts have been made to find an infectious agent that would be responsible for initiating and fueling the autoimmune process leading to synovial inflammation in RA patients. Among the methods of treatment are varied place pharmacological agents (non-steroidal anti-inflammatory drugs, steroids, immunosuppressive drugs, colchicine, drugs that reduce uric acid, inflammation-modifying drugs, etc.), physical therapy, physiotherapy, spas, psychotherapy and, as a last resort, surgery.
Although a proportion of patients achieved remission of symptoms naturally, so untreated RA progresses, causing disability and sometimes even fatal. Since 1897, when it was first synthesized aspirin derivatives her, otherwise known as non-steroidal anti-inflammatory drugs have become the drug of choice for the treatment of RA. Contrary to the diverse chemical structure, these drugs have not only similar analgesic, antiinflammatory and antipyretic but the same side effects of the gastrointestinal tract and kidneys. Detailed knowledge and to investigate the role of cytokines in the pathogenesis of complex RA led to the manufacture of drugs, which are targeted with these cytokines. Three anti-cytokine biological factors (etanercept, infliximab, and anakinra) are currently available for use. The causal treatment of RA using non-steroidal anti-inflammatory drugs (NSAIDs), also there was some breakthrough with the introduction to the general public of a new class of selective inhibitors and other preferential cyclooxygenase (COX-2). These drugs in some way control the inflammatory processes taking place in the body, providing pain relief at a relatively low toxicity to the digestive system. Non-steroidal anti-inflammatory drugs, which inhibit the formation of pro-inflammatory prostaglandins as antagonistic reaction of cyclooxygenase (COX), have been used in the treatment of RA hundreds, perhaps even thousands, of years. Cyclooxygenase (COX) purified and isolated in 1976 and cloned in 1988, is a key enzyme in the synthesis of prostaglandins (PGs) from arachidonic acid. Their clinical use has, however, been a lot of side effects. It is worth to remind that the discovery of two isoforms of cyclooxygenase (COX-1 and COX-2), which is a NSAID active isoforms led to a breakthrough in the treatment of said. This took place in 1991, when several laboratories also identified the gene responsible for the proper activity of COX and named COX-2. It is now known that it is the inhibition of COX-2 is responsible for the positive and the expected results of the action of NSAIDs (strong anti-inflammatory effect), while the inhibition of COX-1 carries most of the side effects of their actions (mostly toxic effect on the gastrointestinal mucosa. Prostanoids produced by COX-1 plays a physiological role in the body such as the protection of the gastric mucosa, platelet aggregation, vascular homeostasis, control of renal fluid and electrolyte balance and others. In theory, assuming an ideal drug formulation is selectively or at least preferentially inhibits COX-2, resulting in only the desired, a potent anti-inflammatory effects (COX-2) and no effect on the physiological processes of the organic (COX-1). Meloxicam belongs to the group of selective (more precisely – preferential) COX-2 inhibitors. Just as piroxicam, meloxicam is a drug in a row Oxicams. Like other classical NSAIDs, meloxicam provides a unique anti-inflammatory, analgesic and antipyretic activity compared with other competing NSAIDs (inhibitor of COX-1 – called. Classical) as diclofenac, ibuprofen, naproxen. Meloxicam is an effective, which manifests itself especially in the long-term analgesic effect, and improving the so-called called Quality of Life. It is very well tolerated. Cases of side effects (gastrointestinal perforation, ulceration, bleeding, indigestion, abdominal pain, renal dysfunction), there are rare in comparison with classical NSAIDs. Meloxicam is a relatively new non-steroidal anti-inflammatory drug orally and officially accepted in the United States for the treatment of degenerative diseases of the locomotor system, rheumatoid arthritis, Bechterew’s disease and acute pain syndromes in the course of RA. It has been shown in several studies that preferentially blocks the meloxicam, COX-2, in particular using the lowest therapeutic dose, and that it acts by inhibiting the synthesis of strong anti-inflammatory prostanoids in inflammatory cells. As a preferential COX-2 inhibitor should result in better tolerance of the gastrointestinal tract than conventional NSAIDs. COX-2 inhibitors, because of its importance in the treatment of RA, obtained even called the aspirin of the new millennium. In clinical trials demonstrated that meloxicam is as effective as piroxicam, diclofenac and naproxen, causing significantly less symptoms such as pain in the stomach and duodenal ulcers, perforations, constipation or bleeding from the gastrointestinal tract.