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:



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.

That's good information SJLC.
I searched around Google and gleaned that calprotectin correlates well with incidence and severity of RA.
But with AS an PsA it is not as good, that is, like ESR and CRP it is raised for only about half of these AS and PsA patients.

David

Thanks for sharing, very interesting. Hopefully study itself is posting.

In my personal case of AS, I truely believe it is linked to gut from my personal experience.

Thanks

Tim

As someone who had no digestive problems 5 years ago...and then suddenly had my colon decide to stop working...I definitely think it is linked. I had absolutely no spondylitis symptoms until a couple years after the digestive stuff began.

Let us know the progress!

what an awesome opportunity to be a part of that study. great info, thanks for sharing.

Kind of sounds like there could be a couple of distinct subpopulations getting the AS diagnosis, eh? My GP says that happens quite often during the stage where the diagnosis is based on symptoms without understanding the disease very well, and it can confuse study results a lot.

Did it seem like your gut problem came first and triggered the rest?

You're right, it is a great opportunity. I also talked my family into participating with me in a study where they will analyze genes of AS patients and first-degree relatives. Who knows what will turn up eventually from that one.

I have come to the belief over the years, that there are subsets of AS - distinct from the other Spondies.

Some of us are HLA-B27-.
Some of us have ESR numbers that don't elevate and our CRP is never very high either, even tho we're in flare.
And a third subset is people for whom starch is a factor; although, that might be more related to Enteropathic or Reactive Arthritis (both Spondies).

As is usual with AS, a person could have one or all of these factors, so really, who the heck knows!!

Hugs,

ahhh the perks of living in cali ..they seem to do all kinds of studies. way way cool SJLC! not only does the study provide valuable info to the study but also to you on this crazy journey. And you get to have all that monitoring of bodily happenings [stool, blood etc] look forward to the conclusion of this one :]