The most recent treatment of rheumatoid arthritis (RA) has been the development of drugs called biologic response modifiers (BRMs). They are a subset of the class of drugs known as disease modifying anti-rheumatic drugs (DMARDs), which are a variety of arthritis medications known to treat arthritis symptoms and slow down progression of joint destruction.
BRMs are medicines which are based on compounds that are made by living cells. Some of BRMs are used to treat rheumatoid arthritis by targeting specific component of the immune system called TNFα, which can increase inflammation and tissue damage.
Enbrel® (entercept) is a TNFα blocker that contains man-made protein and binds to TNF-alpha. It acts like a sponge to remove the TNF-alpha molecules from the joints and blood. It has proven effective at preventing the progressive destruction of the joints in patients with rheumatoid arthritis. Enbrel is given by self-injection once or twice per week. Studies show it may cause irritation at the injection site. Other common side effects include headache, dizziness and nasal and throat irritation. There have also been reports linking Enbrel to multiple sclerosis inflammation of the optical nerve.
BRMs are not for everyone, in some people, they may not work at all. For others, one biologic may not work but another may be effective. BRMs can cost at least $10,000 and more per year.
http://nydailynews.healthology.com/arthritis/arthritis-treatment/article4150.htm?pg=2
Its interesting that some of these medications don't work. Not to long ago, I talked to a Grad student from the Chem-biochem department who told me about a particular literature that explained that cellular receptors can be expressed with great variation between different individuals.
ReplyDeleteIf this is true, then it would make sense for BRMs to be more ineffective with certain individuals than others - strictly based on a particular expression of ones genotype.
It was interesting reading about these medications. I read that similar to other medicines it can cause many flu-like symptoms. In addition, the patient needs to remain in the hospital during the course of the treatment which can become very expensive. So hearing many cons about how this treatment may not work seems disappointing.
ReplyDeleteI don’t think we should be so pessimistic about anti-TNF drugs! While they don’t work for everyone, they have been a godsend for many others, especially patients with rheumatoid arthritis and inflammatory bowel diseases like Crohn’s.
ReplyDeleteOne aspect that was not mentioned in this string (but may have been mentioned elsewhere in the posts – apologies if I am repeating someone) is the effect of anti-TNF drugs on risk for tuberculosis (TB) and non-tuberculosis mycobacteriae (NTM).
We know that mycobacteriae are very effective at evading killing by the immune system. They are contained within granulomas which is a carefully orchestrated collection of macrophages, giant cells and lymphocytes. TNF alpha appears to be critical for recruiting and maintaining these leukocytes as an organized granuloma.
Therefore, when a patient with latent TB is administered an anti-TNF drug, the risk of mycobacterial escape from containment increases dramatically! The rate of TB among patients on an TNF alpha inhibitor like infliximab is >10-fold higher than persons not taking these drugs. And when patients on anti-TNF drugs do develop TB, they develop severe disseminated forms rather than localized pulmonary disease.
So while these drugs can provide great benefits in terms of reducing joint destruction and improving quality of life, they come with some significant risks. It is key to check these patients for latent TB infection and treat it if present before giving an anti-TNF alpha agent.