Rheumatoid arthritis drugs too slow to stop damage

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A study by New Zealand researchers has questioned the current treatment approaches for rheumatoid arthritis and say they may be too slow in controlling the start of the joint damage the disease causes.

The team at the University of Otago Christchurch say their research raises serious questions about the drug Methotrexate which is commonly used to treat rheumatoid arthritis.

Rheumatoid arthritis is a chronic autoimmune disorder that causes the immune system to attack the joints causing inflammation (arthritis) and destruction - it can also damage organs, such as the lungs and skin. It can be a disabling and painful condition which affects the whole body and leading to substantial loss of functioning and mobility; many who suffer from rheumatoid arthritis are in constant pain and sometimes crippled by the disease because of joint damage. Rheumatoid arthritis affects more women than men, and usually starts at age 25 or older - the cause remains unknown

For their study the researchers measured the active forms of methotrexate in blood cells in patients starting and stopping treatment and discovered that it takes much longer than initially thought for the drug to reach steady blood levels.

Rheumatologist Dr Lisa Stamp says their research raised some serious questions about current methotrexate dosing regimens when starting the drug and it appears that larger doses, more rapid dose escalation, or possibly administration by injection under the skin may lead to more rapid accumulation in the blood and potentially earlier disease control.

Methotrexate is usually taken orally and binds to and inhibits several important enzymes affecting a number of inflammatory pathways thereby limiting or controlling joint inflammation and the subsequent damage. As a rule doses start at low levels, based on the ‘response to treatment’, with amounts increasing until the disease is under control, but the researchers say valuable time may be lost with this method, resulting in unnecessary joint damage.

Dr Stamp says one of the reasons for this approach with methotrexate, the ‘response to treatment’, is based on the number of possible side-effects from the drug including nausea and injecting under the skin may resolve this problem.

The researchers measured methotrexate polyglutamates - active forms of the drug - in red blood cells in 10 patients who were beginning treatment and 10 who were stopping and found in those patients starting treatment the median time until the methotrexate concentrations were nearly stable was 27.5 weeks.

For those patients stopping treatment it took 15 weeks for the drug to be undetectable in their red blood cells, which may relate to the lifespan of red blood cells of about 120 days.

The researchers say it may be necessary to consider either injecting the drug or rapidly increasing oral doses, in order to reach optimum stable levels much earlier, to improve the beneficial effects on joint damage.

This study is published in the November issue of Arthritis and Rheumatism.


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