Rheumatoid Arthritis Treatment

There is no known cure for rheumatoid arthritis, but many different types of treatment can alleviate symptoms and/or modify the disease process.

The goal of treatment is two-fold: alleviating the current symptoms, and preventing the future destruction of the joints with the resulting handicap if the disease is left unchecked. These two goals may not always coincide: while pain relievers may achieve the first goal, they do not have any impact on the long-term consequences. For these reasons, most authorities believe that most RA should be treated by at least one specific anti-rheumatic medication, also named DMARD, to which other medications and non-medical interventions can be added as needed.

Cortisone therapy has offered relief in the past, but its long-term effects have been deemed undesirable.. However, cortisone injections can be valuable adjuncts to a long-term treatment plan, and using low dosages of daily cortisone (e.g., prednisone or prednisolone, 5-7.5 mg daily) can also have an important benefit if added to a proper specific anti-rheumatic treatment.

Pharmacological treatment of RA can be divided into disease-modifying antirheumatic drugs (DMARDs), anti-inflammatory agents and analgesics.

Treatment also includes rest and physical activity.

Disease modifying anti-rheumatic drugs (DMARDs)

The term Disease modifying anti-rheumatic drug (DMARD) originally meant a drug that affects biological measures such as ESR and haemoglobin and autoantibody levels, but is now usually used to mean a drug that reduces the rate of damage to bone and cartilage. DMARDs have been found both to produce durable symptomatic remissions and to delay or halt progression. This is important as such damage is usually irreversible. Anti-inflammatories and analgesics improve pain and stiffness but do not prevent joint damage or slow the disease progression.

There is an increasing recognition among rheumatologists that permanent damage to the joints occurs at a very early stage in the disease. In the past it was common to start with just an anti-inflammatory drug, and assess progression clinically and using X-rays. If there was evidence that joint damage was starting to occur then a more potent DMARD would be prescribed. Ultrasound and MRI are more sensitive methods of imaging the joints and have demonstrated that joint damage occurs much earlier and in more sufferers than was previously thought. People with normal X-rays will often have erosions detectable by ultrasound that X ray could not demonstrate. The aim now is to treat before damage occurs.

There may be other reasons why starting DMARDs early is beneficial as well as prevention of structural joint damage. From the earliest stages of the disease, the joints are infiltrated by cells of the immune system that signal to one another in ways that may involve a variety of positive feedback loops (it has long been observed that a single corticosteroid injection may abort synovitis in a particular joint for long periods). Interrupting this process as early as possible with an effective DMARD (such as methotrexate) appears to improve the outcome from the RA for years afterwards. Delaying therapy for as little as a few months after the onset of symptoms can result in worse outcomes in the long term. There is therefore considerable interest in establishing the most effective therapy with early arthritis, when they are most responsive to therapy and have the most to gain.

Traditional small molecular mass drugs

Chemically synthesised DMARDs:

azathioprine
ciclosporin (cyclosporine A)
D-penicillamine
gold salts
hydroxychloroquine
leflunomide
methotrexate (MTX)
minocycline
sulfasalazine (SSZ)

Cytotoxic drugs:

Cyclophosphamide

The most important and most common adverse events relate to liver and bone marrow toxicity (MTX, SSZ, leflunomide, azathioprine, gold compounds, D-penicillamine), renal toxicity (cyclosporine A, parenteral gold salts, D-penicillamine), pneumonitis (MTX), allergic skin reactions (gold compounds, SSZ), autoimmunity (D-penicillamine, SSZ, minocycline) and infections (azathioprine, cyclosporine A). Hydroxychloroquine may cause ocular toxicity, although this is rare, and because hydroxychloroquine does not affect the bone marrow or liver it is often considered to be the DMARD with the least toxicity. Unfortunately hydroxychloroquine is not very potent, and is usually insufficient to control symptoms on its own.

Many rheumatologists consider methotrexate to be the most important and useful DMARD, largely because of lower drop-out rates for reasons of toxicity. Nevertheless, methotrexate is often considered as a very 'toxic' drug. This reputation is not entirely justified, and at times can result in people being denied the most effective treatment for their arthritis. Although methotrexate does have the potential to suppress bone marrow or cause hepatitis, these effects can be monitored using regular blood tests, and the drug withdrawn at an early stage if the tests are abnormal before any serious harm is done (typically the blood tests return to normal after stopping the drug). In clinical trials, where one of a range of different DMARDs were used, people who were prescribed methotrexate stayed on their medication the longest (the others stopped because of either side-effects or failure of the drug to control the arthritis). Methotrexate is often preferred by rheumatologists because if it does not control arthritis on its own then it works well in combination with many other drugs, especially the biological agents. Other DMARDs may not be as effective or as safe in combination with biological agents.

Biological agents

Biological agents (biologics) are produced through genetic engineering, and include :

tumor necrosis factor alpha (TNFα) blockers - etanercept (Enbrel), infliximab (Remicade), adalimumab (Humira)
Interleukin 1 (IL-1) blockers - anakinra (Kineret)
monoclonal antibodies against B cells - rituximab (Rituxan)
T cell costimulation blocker - abatacept (Orencia)
Interleukin 6 (IL-6) blockers - tocilizumab (an anti-IL-6 receptor antibody) (RoActemra, Actemra)

Anti-inflammatory agents and analgesics

Anti-inflammatory agents include:

glucocorticoids
Non-steroidal anti-inflammatory drug (NSAIDs, most also act as analgesics)

Analgesics include:

paracetamol (acetaminophen in US and Canada)
opiates
diproqualone
lidocaine topical

The Prosorba column blood filtering device was approved by the FDA for treatment of RA in 1999 However, the results have been very modest.

Historic treatments for RA have also included: rest, ice , compression and elevation, acupuncture, apple diet, nutmeg, some light exercise every now and then, nettles, bee venom, copper bracelets, rhubarb diet, rest, extractions of teeth, fasting, honey, vitamins, insulin, magnets, and electroconvulsive therapy (ECT).. Most of these have either had no effect at all, or their effects have been modest and transient, while not being generalizable.

Other therapies

Other therapies are weight loss,orthoses, occupational therapy, podiatry, physiotherapy, immunoadsorption therapy, joint injections, and special tools to improve hard movements (e.g. special tin-openers). Regular exercise is important for maintaining joint mobility and making the joint muscles stronger. Ayurveda, mostly in southern India, is another source of treatment, and while it is popular in India there are no studies to show that it benefits patients with RA.

Radon therapy, popular in Germany and Eastern Europe, can induce beneficial long-term effects for rheumatoid arthritis.

A survey in the United Kingdom between 1998 and 2002 found arthritis to be reported among the five most common reasons for the medicinal use of cannabis.

The resulting effectiveness of treating RA with acupuncture is inconclusive, and "more rigorous research seems to be warranted" according to one study. Severely affected joints may require joint replacement surgery, such as knee replacement.