The present diagnosis of this disease centres on biochemical blood analysis with an x-ray to check for noticeable joint changes using clinical markers. This is done with observations of some other signs like loss of weight, sickness and fever. For the blood analysis, the platelet count, rheumatoid factor and ESR are studied. Another examination is the antibodies titer to cyclic citrulline. The conditions for poor diagnosis are:
Timely impairment of large joints and the form of rheumatoid nodules
Inflamed lymph nodes
New joints involved in later exacerbation
Stubborn activity of the disease with no reduction for more than 12 months
The ESR constantly increasing
High titers of rheumatoid factor within the first year
Radiographic alterations in the affected joints within the first few months
Noticeable LE-cells and antinuclear antibodies
It starts at any joint but often times at small joints in the wrists, hands and fingers. The affected joints are symmetric, for example, the same joint damaged on the right hand will be damaged on the left. If more joints are damaged, the stage of the disease has advanced. Some more symptoms are: Tiredness Morning painfulness and paleness Flu symptoms Pain after long sitting Remission from disease activity occurrence Muscle ache Loss of appetite Downheartedness Loss of weight Anemia Cold Wet palms and feet Damage of glands around the eyes and mouth
Treatment of RA
Here are some treatments: There is a need for a proper antibacterial therapy. In the absence of symptoms like fever, non-steroidal anti-inflammatory drugs (NSAIDs) are used to treat the joint syndrome. Corticosteroids are injected to highly inflamed joints. There is need to avoid osteoporosis and restore calcium balance. Therapeutic exercise is important so that maximum joint motion and muscle mass can be maintained. There is also need for physiotherapy and spa. Isotopes of gold, yttrium are introduced for stubborn mono-and oligoarthritis. Reconstructive surgery is used for stubborn joint strains.
Four classes of medications can be used for complete drug treatment: Nonsteroidal anti-inflammatory drugs (NSAIDs) Basic medications Glucocorticoid drugs Biological agents.
Non-Steroidal Anti-Inflammatory Drugs
This is the first line of therapeutic treatments used for the aid of severe signs of the disease while also making sure that lab and clinical remission are stable. NSAIDs are known to have an anti-inflammatory effect that results from COX (cyclooxygenase) activity inhibition. COX is a basic enzyme from the metabolism of acid and arachidonic. The use of two or more NSAIDs should be avoided as it doesn't change its effectiveness but will rather increase the risk of side effects.
The following are the key drugs for basic RA therapy: D-penicillamine Gold preparations Sulfasalazine Methotrexate In a reserved way, includes: Cyclosporine A Azathioprine Cyclophosphamide There is a new group that comprised Remicade drug. If the drugs are ineffective after one and a half to three months it can be substituted with or used together with corticosteroids in low doses. This reduces RA activity. Cytotoxic is an immunosuppressive agent that can be endured for a long-lasting use and its side effects are less compared to other drugs in this group.
This is corticosteroids and is used for high inflammatory activities and in systemic signs of RA, it is used in the form of pulse therapy. Pulse therapy is a new method that utilizes high doses of corticosteroids together with a slow-acting tool. Methotrexate is also used with cyclosporine, sulfasalazine and salts of gold. Sometimes corticosteroid serves as a local treatment mostly for mono-or oligoarthritis in large joints
In RA the synovial membrane, for reasons ambiguous, release a huge amount of enzyme glucose-6-phosphate dehydrogenase. This enzyme terminates the disulphide bonds of cell tissue. The proteolytic enzymes leak from cell lysosomes that injure the adjoining bones and cartilage. The body creates cytokines to respond to this. The therapy utilizes a monoclonal antibody to the cytokine which has tumour necrosis factor (the A TNF). Its effectiveness has a high affinity in a tie to TNF. This is in it's soluble and transmembrane forms that bring about the TNF activity being neutralized. As RA progresses, joint damages are viewed as a tightening of the gap between bones and its erosion in the articular area. Clinical tests of monoclonal antibody presented its use as unhurried erosion and contracting of the gap between the bones.
90 Prestwick Road
INGRAM, NE66 2AE
070 7086 1436