Hi, Platypus:
Certainly, the key really is whether the AS is active when the blood was drawn and, as you suggested, whether the inflammatory markers are modified by the action of drugs like NSAIDs.
Most people with AS will have increased lymphocytes during disease activity, according to Ebringer, et al, since the IgA (IgA-Kp) is the (proposed) provocative AS agent. If it is found in elevated amounts (as the monomer) in whole blood, it is orders of magnitude more plentiful as the dimer in lymph. A rare complication of AS is IgA amyloidosis due to increased IgA circulation. I don't know if or whether ANA readings are affected, or how this possibly relates (another question for my medical friends).
CRP is apparently the one to worry about since it could be linked to aortitis or other cardiovascular conditions and there might be an extra caution to better control cholesterol levels, so that is another test in which we should be interested.
Since FM is a common "co-diagnosis" (to be polite) with AS, I contacted some doctors who claimed good results treating this condition, but learned along the way that FM is non-inflammatory and always symmetrical and there are (were?) 18 body points, the majority of which must be painful, to obtain a diagnosis. Well, if you press hard enough, I suppose that ANY point will hurt and then we can make even AS appear symmetrical, but the problem in AS is still the negative inflammation markers that so many people (especially women, since 'AS is a man's disease' is still the prevailing wisdom) are stuck with--often preventing valid diagnosis. A nuclear bone scan is often better than mri or X-rays, but a simple blood test should, by now, have been devised to provide correct information.
The differences between AS and FM are significant enough that that nobody should be diagnosed with FM when they really have AS. Those who do not indicate can have a tough time not being 'typical,' but chronic and recurrent inflammation of right (only) hip for example, plus positive antigen status, should not warrant a misdiagnosis of FM over AS, despite the lack of elevated ESR or CRP. Such a misdiagnosis is regrettably not uncommon.
I have no doubt that FM can be secondary to AS, and I have the basis for a new thesis: Fibromyalgia, AS, and Global Warming
It goes something like this: I noticed the diagnostic points in FM are similar (albeit not exactly the same) to symptoms experienced by mixture divers whose mixture is not quite right--oxygen content wise. The possibility of oxygen deprivation as a cause for many cases of FM is not unreasonable, based upon one fact that FM relents in a significant percentage of those patients who have been 'treated' by doing aerobics, and another fact that in many cities oxygen levels are much lower than normal, displaced by 'greenhouse gasses.' In certain locations, the O2 levels are an estimated 50% lower than they were just 100 years ago. The fact that we who suffer with AS do not like to breathe very much, or even move very much sometimes if at all, might make us prime targets for FM, if there is any validity to this hypothesis.
I know FM just cannot be this simple--in total--but these are some interesting observations that may be useful.
As the disease progresses (or in my case 'accelerates' due to NSAID usage), the ESR can become elevated where it was earlier not. After I began taking NSAIDs my ESR increased from a range 28-48 to often over 100; certainly, I was always an indicator.
Best Regards,
John
