Understanding Non-Radiographic Axial Spondyloarthritis - Episode 7
Transcript: Philip J. Mease, MD: When we turn to other comorbidities, the 1 I would start with is cardiovascular disease. There is evidence of increased amount of basic cardiovascular disease, coronary artery disease, hypertension, and so forth in an axial spondyloarthritis population. This is at least partly related to having ongoing inflammation in the body.
We know that information can beget increased or accelerated atherosclerosis. It’s important for patients to be aware of that for their primary care doctors. And if they have a cardiologist, they should be aware of that so that there can be measures taken to control what’s controllable in terms of cardiovascular manifestations, including controlling blood pressure, controlling hyperlipidemia, weight loss, and so forth. I think this is important.
Additionally, in the cardiovascular reader, there’s a special comorbidity that can occur that has to do with conduction defects, arrhythmias that could be related to aortic valve disease. That is, it could be part of the axial spondyloarthritis spectrum. Some of this may have been explained by a mouse model in which we saw that inflammatory changes occurred where entheseal tissue attached to bone, but also the aortic group that was in this model was a place where inflammation occurred.
Another important 1 that’s often overlooked is osteoporosis. You think, “This is paradoxical.” Here we’ve got a disease where there is excessive bone formation, at least in the radiographic form of the disease, not so much in the nonradiographic disease. For osteoproliferation you think, “How could that person have osteoporosis?” But indeed, when you do careful analysis of the bone density of patients with axial spondyloarthritis, including nonradiographic, they have a diminished bone density.
This needs to be attended to. One of the reasons for increased mortality, especially as a patient gets older, is the potential for a fall, a cervical fracture through in the case of radiographic axial spondyloarthritis through syndesmophytes or just because of osteoporosis and all the comorbidities or even mortality that can attend to that. Another that I think is often not attended to properly is 1 we call fibromyalgia or central sensitization. We know that in the general population, somewhere between 4% and 7% of patients can be diagnosed with fibromyalgia.
That’s just in the general population, but if we move over to any of the rheumatic diseases with this chronic pain and inflammation, those numbers go up to 15%, 20%, even 25% of those who may have concomitant fibromyalgia, or the term I tend to prefer, which is central sensitization. This is important to recognize because of the fact that if a patient who was adequately treated—say, with a biologic medication—is continuing to complain of pain, fatigue, sleep disturbance, and you’re thinking, “Oh, we must be inadequately treating them; therefore, we go to switch to a different medication or intensify immunomodulatory treatment,” that may be a mistake.
We don’t really need to switch medications, because if we do, the intensification is going to do harm to the patient. But in fact, we need to be attending to treating fibromyalgia. This may be pharmacologically with certain treatments for that condition or by nonpharmacological methods, such as exercise, physical therapy, and so forth. The converse is very important. There can sometimes be patients with central sensitization that don’t have nonradiographic axial spondyloarthritis, but the clinician will think they do.
Atul was alluding to this previously when he pleaded for us not to over-read imaging studies or to overinterpret and think that the patient has nonradiographic axial spondyloarthritis, so this is a real art to be interpreting the patient’s stiffness experience, fatigue experience, to know how much is being contributed by the nonradiographic axial spondyloarthritis information and a concomitant condition, such as fibromyalgia.
Sergio Schwartzman, MD: If we summarize the comanifestations in the comorbidities, and I love that differentiation in terms of these 2, most of these you can objectively define. You can do a GI [gastrointestinal] work-up and find out whether a patient has inflammatory bowel disease. You could also do a bone density, and you could have an ophthalmologist evaluate the patient for those cold manifestations and comorbidities.
Transcript Edited for Clarity