The Young and the RA

As I explained in my ABOUT page, I started this blog for a grad school class. Now the time has come for my final project for the class, and I need to learn more about my readers, get advice for improving my blog, etc. So please help!!! Only 10 questions, and I’d really appreciate any input you can give.

Click here to take survey

Thanks,

S.P.

I witnessed an incident the other day that really hit me, and I wanted to share it with you.

So, to set the scene, I was getting blood drawn at the university hospital I go to for my doctor appointments. As I was sitting there, I noticed a woman going around to individuals in the waiting room to ask them if they would be willing to donate blood to a gene bank that was being started by the university to be used in research.

Now, I was a little surprised that no one was willing to step up and give an extra vial of blood. I mean they were already getting it drawn; how hard is it to give a little more? So when she finally made it to me, I told her, “Yes, I would love to help.” She seemed a little taken aback. I guess after so many no’s, you aren’t ready for the yes.

As I got up to follow her to get the survey they needed filled out to go along with my donation, a man sitting near me pipes up, “So do you pay for giving blood? I’ll do it if you pay.” ARE YOU KIDDING ME?

While it is true that some researchers give reimbursements for participation in studies, I have to imagine those studies involve a little more than a one-time survey and a tube of blood. To only help researchers when money is involved is selfish. The research that is being done now is going to help provide better healthcare for us in the future, not to mention our kids, grandkids, great-grandkids, etc. 

I very strongly believe in participating in as many research opportunities as possible. There is no cure for RA currently, and the treatments currently available don’t work for about 40 percent of those with RA. I want to do all I can to assist researcher in finding treatments for these people. 

Now, I know not everyone goes to a rheumatologist at a research university as I do, but if you do, it is not hard to get involved in research. There are flyers up all over the lobbies (next time take a long look while waiting for your doctor), and often your rheumatologist will ask if you would be interested in participating in some study or another. It’s really not hard to get involve.

For those of you that don’t see doctors at a research hospital, there are other ways to get involved in studies if you are interested. Check out researchra.com or centerwatch.com your local university hospital for research opportunities.

Until next time,

S.P.

Tumor-necrosis factor (TNF) modifiers are some of the latest major breakthroughs in treating RA. The current TNF modifiers on the market are infliximab (Remicade), etanercept (Enbrel) and adalimumab (Humira). These drugs are genetically engineered and work by interfering with your bodies TNF, an immune factor that plays an important part in the disease-fighting process.

Studies done on TNF modifiers, a type of biologic drug, have shown that they all work fairly quickly and show significant improvements for those with RA. Often, as with other biologics, TNF modifers are combined with methotrexate to help increase their effectiveness. Combining a biologic with methotrexate also has the benefit of showing fewer side effects than using a higher dose of methotrexate alone.

While Remicade, Enbrel and Humira block TNF, they do differ in some ways, and it is important to know about them and realize what works best for you.

“Enercept (Enbrel) is a protein made from the fusion of two TNF receptors. The end product mimics their effects, which neutralize TNF. A 2002 two-year study suggested it is superior to methotrexate in slowing RA disease progression and has fewer side effects. It has been approved for RA, juvenile RA, and psoriatic arthritis.

“Inflixamab (Remicade) and adalimumab (Humira) are both monoclonal antibodies (MAbs), which are specially designed antibodies that target TNF. In one study, infliximab was superior to methotrexate, gold, corticosteroids, and a interleukin-1 receptor antagonist. Humira, the latest TNF modifier is the first fully human anti-TNF MAb, which may reduce some of the problems of infliximab” (About.com).

Like other RA drug, TNF modifiers do not cure RA — it is important to realize that there is currently no cure for RA. TNF modifiers have shown some evidence that they slow and may even halt joint erosion. These drugs are fairly expensive, however, and can cost over a thousand dollars a month.

There are side effects of TNF modifiers, though, and it is important to be aware of them. TNF modifiers can increase the risk of certain fungal and mycobacterial infections, including tuberculosis, because these drugs work by inhibiting the immune system. But since TNF modifiers target precise molecular targets, they don’t have as many widespread effects on the body. The side effects of the three drugs I mentioned above are similar, but can differ:

• “The most common adverse effects of all three are minor reactions at the injection site, but there are few other immediate side effects.
• Because these agents affect immune factors, there is some risk for severe infections particularly in susceptible individuals, such as those with uncontrolled diabetes, people taking other immunosuppressants, or anyone with a current active infection. For example, cases of tuberculosis and histoplasmosis (a fungal infection in the lungs) have been reported in patients taking TNF-modifiers. (While millions of healthy people unknowingly carry the TB organism, it rarely becomes active in those with healthy immune systems.) RA patients should be tested for TB before initiating treatment. It is not yet known if adalimumab poses as high a risk as infliximab.
• There have been a few reports of aplastic anemia.
• In rare cases, both etanercept and infliximab have been associated with nerve damage that resembles the disease process in multiple sclerosis. This involves demyelination (the loss of myelin, the insulation coat over nerve fibers) and can result in confusion, numbness, changes in vision, and difficulty walking.
• According to some experts, patients with multiple sclerosis should avoid these agents until further research is complete. (The effects of adalimumab are not known yet.)
• There have been reports of a lupus-like symptoms in a few patients taking etanercept, which resolved when the drug was stopped.
• Many patients develop an immune reaction to infliximab itself, which makes the drug less effective overtime. Nevertheless, in one study, benefits persisted for at least two years after stopping the drug.
• Although adalimumab is a similar agent, it is a fully human molecule and, therefore, may not provoke the immune response that infliximab does. Long-term studies are needed to confirm this.
• Infliximab has been linked to a few deaths in patients with pre-existing congestive heart failure.
• There is some suggestion that anti-TNF drugs increase the risk for lymphomas” (About.com).

So now you have all the information you need to know about TNF modifiers. It is important, however to be aware that there are other biologics out there, such as Kineret and Orencia, but I’ll talk more about them another time.

Until next time,

S.P.