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Main –› Health & Hygiene –› Medicines & Remedies
 

How to Treat Rheumatoid Arthritis?

 
Author: Aleksandr Kavokin, MD, PhD
 

Traditionally, non-steroidal anti-inflammatory drugs (NSAIDs) go as the first-line therapy. Aspirin, ibuprofen, naproxen, sulindac, indomethacin, nabumetone, tolmetin relieve symptoms. However, NSAIDs can not prevent joint destruction. Corticosteroids efficiently reduce the symptoms of inflammation. Alas, the side effects of corticosteroids are extremely extensive. They cause weight gain, weak bones, infection, acne, easy bruising, diabetes, facial puffiness, stomach ulcers, eye cataracts and many others.

In case of active rheumatoid arthritis the disease-modifying anti-rheumatic drugs (DMARDs) are used. An example is methotrexate. Doctors often use DMARDS together with corticosteroids and NSAIDs. Gold compounds and anti-malaria drugs are also in use. Other drugs include: azathioprine, cyclosporine A, D-penicillamine, minocycline, sulfasalazine. Majority of these drugs have serious side effects and complications. Currently DMARDs are not well tolerated and have serious side-effects. Corticosteroids are still widely used, but doctors expect development of newer and better DMARDs. Opiates and topical lidocaine relieve pain.

Rheumatoid arthritis cause extra production of pro-inflammatory cytokines (the regulating substances of immunological system) and relative lack of anti-inflammatory cytokines. This imbalance leads to the development of cartilage and bone destruction. The process erodes bone in the joints. Researchers found biologic agents to block some specific cytokines. For, example anti-TNF monoclonal antibodies infliximab and adalimumab block TNF (Tumor Necrosis Factor, one of the most potent cytokines). Another strategy use etanercept (a soluble TNF receptor) that reacts with TNF and prevents attachment of TNF to the real TNF receptors on the target cells. An IL-1 receptor antagonist anakinra prevents another type of inflammatory response. Use of these biological agents made significant and rapid clinical improvements with low toxicity.

Alas, there were some drawbacks after long-term use. One was the need for parenteral administration (needlesticks) which is unpleasant and may lead to infections. Another was that the agents cause an immune reaction of the body and loose efficiency over time. Furthermore, monoclonal antibodies and soluble receptors inhibit on the extracellular level. More effective would be to block intracellular inflammatory pathways. Inhibition of p38 MAPK by oral drugs is the possibility under investigation at present.

Weight loss, physiotherapy, joint injections, and specialized tools for home activity help the patients. In severe case patient may need joint replacement. Some patients benefit form changes of diet and lifestyle. Reducing stress, sleeping well, eating less and highly digestible foods, eating yogurt, garlic, vegetables, drinking sufficient volume of water may help some patients.

 
 
 

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