This raises the question most people who suspect at home or close this chronic disease or already sick. The goal of treatment in rheumatoid arthritis is a slowing of disease progression, reduction of pain, improved mood and mental condition of the patient, providing the ability to perform work and independence in everyday life. Rheumatoid arthritis can’t be cured. However, you can inhibit the disease and prevent its further development. The earlier it is diagnosed, the sooner you will be used intensive care, the better the prognosis for a smooth life.
Available rheumatoid arthritis treatment
Treatment of rheumatoid arthritis includes pharmacotherapy, rehabilitation and patient education. The main goals of treatment rheumatoid arthritis are:
- alleviate pain, swelling and fatigue
- improvement in function of the pond
- inhibition of progression of joint
- prevention of disability
- preventing deaths subsidiary of rheumatoid arthritis
Drugs used in rheumatoid arthritis is traditionally divided into 2 groups: 1 Soothing the pain and symptoms of the second disease-modifying drugs (DMARDs), which are divided into: – non-biological DMARDs formerly called conventional DMARDs – biological DMARDs Despite the division between non-biological and biological DMARDs DMARDs commonly used abbreviation for drugs classical (non-biological) and biological DMARDs are called in short biological agents.
Medicines to relieve pain and symptoms of inflammation
This group includes non-steroidal anti-inflammatory drugs and glucocorticoids.
Non-steroidal anti-inflammatory drugs (NSAIDs) were for many years the basic drugs used to relieve pain and symptoms of inflammation in RA. NSAIDs do not inhibit progression of the joint and do not limit tissue damage. The mechanism of action of NSAIDs is the inhibition of the enzyme cyclooxygenase (COX), which in turn prevents the conversion of arachidonic acid (building block of cell membranes) to prostaglandins – mediators of inflammation. Operation of the NSAID is only symptomatic: reduction of pain, swelling and inflammation. The above-mentioned Cyclooxygenase enzyme (COX) has two isoforms: COX-2 and COX-1. COX-2 is an enzyme that is produced in the process of inflammation. It produces inflammatory mediators and its inhibition by NSAIDs determines the efficacy of the drug. COX-1 isoenzyme is an enzyme present in the body at normal conditions. Its inhibition is associated with side effects, especially in the gastrointestinal tract and kidney. In the nineties of the twentieth century developed a group of NSAIDs selectively inhibiting COX-2 (rofecoxib, celecoxib). The selective COX-2 inhibitors hopes are pinned on a perfect NSAIDs: effective (inhibiting COX-2) and safe (not inhibiting COX-1). These hopes have not been fulfilled, because the treatment with a selective COX-2 appeared to complications of the cardiovascular system, increase mortality in patients with heart attacks and strokes. This sparked a lively discussion in and out of the registration of all NSAIDs include warnings against the adverse effects of cardiovascular NSAIDs cause numerous side effects, especially when used chronically. The most serious complications are of the gastrointestinal tract, resulting from the action of COX inhibition, and the production of prostaglandins (PG). In the stomach, the PG have a beneficial effect, since the gastric mucus secretion, stimulate the protection forming the highly acidic gastric environment (pH 1-2). The weakening of the mucosal barrier exposes the gastric mucosa to hydrochloric acid and damaged. Consequently, there is a complication abbreviated to CSP – perforations, ulcers, bleeding. These complications lead to pain in the left upper abdomen (ulceration), anemia (bleeding) and may even be life-threatening (massive hemorrhage, perforation – perforation of the stomach). To some extent, it can be prevented with an NSAID with drugs inhibiting gastric acid secretion in the stomach (such as proton pump inhibitors). Other complications of NSAIDs is fluid retention (fluid retention in the body, adverse effects for patients with heart failure and hypertension), attenuation of the antihypertensive drugs, impaired renal insufficiency inclusive. All NSAIDs are metabolized in the liver and can cause damage (hepatotoxic). In older patients are common side effects in the central nervous system: disorientation, confusion, depression. NSAIDs can cause headaches. NSAIDs inhibit COX-1 strongly reduce aggregation (clumping) platelet used in high doses increase the risk of bleeding, used in small doses reduce the risk of heart attack and stroke (platelet aggregation and reduce the risk of blood clots in the vessels of the heart and brain). One such drug is aspirin (acetylsalicylic acid). The active substances belonging to the group of NSAIDs include aspirin, ibuprofen, ketoprofen, diclofenac, naproxen, meloxicam, nimesulide, nabumetone, rofecoxib, celecoxib.
Glucocorticoids are used to treat synthetic equivalents of naturally occurring hormones produced by the adrenal gland (glands located on the upper portions of the kidney). Glucocorticoids are the drugs with very potent anti-inflammatory and immunosuppressive, and therefore are used in the treatment of many rheumatology inflammatory diseases and autoimmune diseases. GKS strongly than anti-inflammatory NSAID, as they operate at a higher level, the formation of the inflammatory process. GKS inhibit the activity of the enzyme phospholipase A2 called, thereby preventing the release of arachidonic acid from cellular membranes. Arachidonic acid is not converted to mediators of inflammation (PG).