Arthritis Treatment: Why Do Rheumatoid Arthritis Patients Stop Treatment?
Rheumatoid arthritis (RA) is the most common form of inflammatory arthritis, affecting more than 2 million Americans. It is a systemic autoimmune disease that has the potential for significant damage to internal organs. One of the biggest issues when it comes to treating rheumatoid arthritis is the high rate of discontinuation of therapy.
The primary reason for medication discontinuation is not side effects. Rather, it is lack of efficacy.
When patients discontinue medication due to lack of efficacy, they run the risk for developing many of the systemic complications of the disease. These include cardiovascular disease, lung issues, leg ulcers, and inflammation of arteries leading to organ damage.
One temptation has been to push the dose of disease modifying anti-rheumatic drugs (DMARDS) such as methotrexate to higher and higher doses when a patient doesn’t respond. This can lead to liver toxicity.
One option has been to use lower doses of the DMARD and combine it with a biologic medication. Biologic medications are antibody-based medications that act on the immunologic abnormalities that cause RA.
They act with laser-like precision. The biologic medicines that are used first-line are the tumor necrosis factor inhibitors. Tumor necrosis factor is considered to be an important cause of the chronic inflammation and destruction in rheumatoid arthritis.
Multiple studies have shown that the addition of a biologic drug to a DMARD is particularly effective in inducing remission in RA.
Because of the results of these trials, it is important to understand the essential need for early introduction of a biologic medicine in patients who are not doing well on their DMARD alone.
One conundrum that can occur is the development of non-response to a biologic. This non-response can be due to either lack of effectiveness or to drug intolerance.
Once a patient has failed one tumor necrosis factor inhibitor, the likelihood of their failing another TNF inhibitor is high. And patients who fail two TNF inhibitors are at even higher risk for not responding to another TNF inhibitor. This means that once a patient has failed one TNF inhibitor, many feel that perhaps a medication with a different mode of action should be considered.
On the other hand, there is evidence that some patients will respond to another TNF inhibitor despite failing the first. The upshot is that most patients will receive a trial of at least two of these kinds of medicines before being switched to a drug with a different mode of action.