I recently participated in a study done by a young medical researcher, Dr. Matzkies. At my last visit to Cedar Sinai, I talked to one of Dr. Matzkies' colleagues who was quite enthused about the results of her first study, which even won an award from a rheumatology foundation. http://www.rheumatology.org/ref/awards/CoreAwards_Grants_2010.pdf
Here is the description I was given during recruitment for the study:
The purpose of this study is:
To collect stool samples, serum and blood samples from 2 groups: patients with ankylosing spondylitis (AS), living in the LA area and "healthy" controls living in the LA area. We will test the stool samples for fecal calprotectin - a marker associated with inflammation of the gut. | We will test the serum samples for the presence of serologic markers associated with inflammatory bowel disease (IBD). We will determine and compare the frequency and concentration of inflammatory stool marker and IBD associated serologic markers in the AS and healthy volunteers groups.
As of right now, there are no inflammatory markers in AS that are associated with activity, prognosis or treatment response. Thus, in this study, we believe that testing the stool of AS patients for calprotectin is a useful starting point and might be a foundation for future studies exploring the utility of calprotectin as a marker for inflammation in AS and the relationship of both diseases (IBD and AS).
Here is what I learned about the results, based on my discussion with Dr. Matzkies' colleague (I believe the paper hasn't been published yet):
* Both AS patients and control group were chosen among people who had no known digestive disorder and reported no symptoms indicating digestive disorders
* The threshold for the inflammation marker was chosen to be "50" (no idea what units); if more than the threshold was measured, "gut inflammation" was considered to be present
* 7% of the control group exceeded the threshold, but only by small amounts (e.g. 55 versus 50)
* 40% of the AS group exceeded the threshold, often by large amounts (the top end of the scale was around "1000"!!!)
* This difference was deemed to be significant because all those AS patients with obvious gut problems (and also any who could not skip NSAIDs for at least a couple days prior) had already been excluded
Since the study succeeded and the marker protein looks relevant to AS, there can be interesting follow-up studies. For instance, does the gut inflammation increase prior to a flare, or is it the other way around? It would also be very interesting to track the levels for patients never on put NSAIDs, to distinguish between inflammation levels caused by disease versus secondary damage from meds treating the AS.