COMMENTARY

EULAR 2010 Highlights From Joseph Markenson, MD

Joseph Markenson, MD

Disclosures

June 28, 2010

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Hello; my name is Joseph Markenson, Professor of Clinical Medicine at Weill Medical College of Cornell University, Hospital for Special Surgery, in New York. I'm presently in Rome at the EULAR [European League Against Rheumatism] Congress. This is a large meeting, with over 15,000 rheumatologists. Let me tell you a little bit about what I think is kind of interesting, or what has come out of this meeting so far that is worthwhile learning about.

We've had a lot of studies on new therapies over the years, and I can't tell you that there's anything new now about a novel therapy. There are some interesting pieces of information, subanalyses of many of the therapies that we already know about, such as the B-cell antagonists, rituximab, abatacept, and TNF [tumor necrosis factor] inhibitors. But what I found interesting is that there is a lot of information, not only about the new therapies, but how to use them, and I think that is becoming important.

We're learning more and more about rheumatoid arthritis, disease activity, comorbidities, and how we should treat patients. We're getting data to say that if we do things according to algorithms, we may be getting better outcomes. Now, nobody likes an algorithm, but we know that you really need to treat to a target; you need to treat to a number.

And so, the first thing that came out of the ACR [American College of Rheumatology] and EULAR were new criteria for diagnosis. These criteria advance us a little bit beyond the 1987 criteria, and they will begin to tell a little bit about how to diagnose early disease. We're all learning that if we diagnose early disease and we're aggressive, the patient is going to do much better. The studies are now are looking at not only the 20% response, the 50% response, and the 70% response, but they are beginning to ask questions like how many new patients that you start on therapy can you put into remission at the end of a year, with remission being defined as a DAS [disease activity score] of less than 2.6. You need to measure it. How many patients can you put into low disease activity?

For example, there was a study with abatacept[1] that talked about the fact that in patients who were able to drop to low disease activity within 3 months with their particular medication, were able to maintain that level for up to 4 years. There was a little more evidence from the COMET [COmbination of Methotrexate and ETanercept in Active Early Rheumatoid Arthritis] study, and the study of early RA [rheumatoid arthritis] with etanercept vs methotrexate in combination. What was interesting about that study, and what we learned a couple of years ago, was that -- no question -- you could put 1 out of every 2 patients into remission by using the combination of methotrexate and etanercept. But what they are showing us now is that they are dissecting that information, and they are looking at very early disease vs later disease (albeit still within the realm of being early disease). They were able to demonstrate better outcome measures, less destruction, if they treated people very early. How do you treat people early? You measure their activity of disease. You recognize them. You use the criteria.

So, to me, this is very exciting. I know most of us don't want to do measurements, but I think certain things like the Rapid 3 are easy to do, and the data definitely show that we're able to get people into remission -- surprisingly, 50% of patients with new-onset disease -- and maintain them. So what I'm learning here is that our medications not only put people into remission at a single point in time, but the new bar, if you will, is how long they keep them in remission. Remember, this is a disease that goes on for many years, so we want to know about more than just a single point in time.

Thank you very much. I'm Joseph Markenson, Professor of Clinical Medicine at Cornell University Medical College and Hospital for Special Surgery at EULAR in Rome.

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