Show Notes
Welcome Back Rheumatology Fans, Another week, another podcast, another new subject to learn all about and this time it is SUPER relevant to us as Physiotherapists and MSK Therapists seeing patients with Lupus. You can listen to the podcast here, it is 12 mins long but I struggled a little with the accents of the guests, there is a full transcript to download (which I did) which solved that very minor issue. Be aware, it is heavily medical, I had to look up quite a few terms! I have sorted some takeaways below which you all seem to be finding useful! For tons of info on Lupus and Connective Tissue Disorders (as well as all the other Rheum disorder) enroll in my online course. Just FYI changes are coming to this in 2026 but currently if you enroll you get lifetime access so do it NOW. Preload deficiency may explain fatigue and exercise intolerance in SLE - even when disease is controlled Clinicians at Johns Hopkins observed a subset of SLE patients whose lupus was well controlled yet who continued to report profound fatigue, dyspnea, heat intolerance, and markedly reduced exercise capacity. These symptoms were not due to active inflammation, cardiac structural abnormalities, or pulmonary disease. Careful haemodynamic testing - including exercise right-heart catheterisation - revealed that these patients failed to generate adequate preload during exertion, limiting cardiac output. This is “functional dehydration” phenomenon and reframes persistent fatigue in SLE. Exercise intolerance in these patients is posture-dependent and quantifiable Patients described a distinctive pattern: they tolerated exercise better lying flat than standing, and they exhibited elevated baseline heart rates. Cardiopulmonary exercise testing (CPET) confirmed objectively reduced exercise capacity despite structurally normal hearts on CT, echocardiography with strain imaging, and MRI. This demonstrates that the limitation is physiologic rather than subjective, separating preload deficiency from nonspecific fatigue. Recognising this pattern - orthostatic worsening, normal imaging, elevated resting HR - can guide clinicians toward targeted evaluation rather than attributing symptoms to deconditioning or psychological causes. Undetectable NT-proBNP levels help rule out other causes and support the diagnosis Across the cohort, NT-proBNP levels were low or undetectable. While not diagnostic of preload deficiency by itself, an undetectable NT-proBNP carries a ~99% negative predictive value for structural heart disease associated with heart failure. This biomarker therefore helps eliminate common cardiac explanations for exercise intolerance. In the appropriate clinical context - controlled SLE, normal structural imaging, reduced exercise tolerance - very low BNP levels increase confidence that the issue is inadequate cardiac filling rather than pressure overload. Treatment focuses on restoring functional blood volume and controlling heart rate Many patients demonstrated “functional dehydration,” meaning that despite drinking normally, they could not retain enough intravascular volume to support preload during exertion. Treatment therefore parallels POTS (postural orthostatic tachycardia syndrome) management: high fluid intake (1–3 gallons/day) and increased sodium consumption (up to 5 g/day). Some patients benefited from electrolyte solutions like Gatorade or Liquid IV to maintain volume. DO NOT DO THIS WITHOUT MEDICAL SUPPORT The pathophysiology remains unknown Though preload deficiency has now been documented, its underlying mechanism is unclear. Dysautonomia was suspected, but formal autonomic testing did not reach diagnostic thresholds. The next steps include determining prevalence, defining risk factors, and pursuing mechanistic studies to identify the affected biological pathways. Further Resources
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Welcome Back Rheumatology Fans, Ooof this is going to rattle some cages. Synopsis below but the best of this is watching the video. A recent news report about a woman with rheumatoid arthritis who was convicted of benefit fraud caught my attention. The case involved footage of her participating in activities including gym classes and running events despite having previously reported substantial limitations in her day-to-day function. I don’t know enough about the individual circumstances to comment on whether the judgement was appropriate. In fact, the reported offence appears to relate specifically to failing to notify the Department for Work and Pensions of a change in circumstances. But the story raises a broader issue that is highly relevant to people living with inflammatory arthritis and the clinicians treating them. Being physically active does not necessarily mean someone is not disabled. Rheumatoid arthritis, psoriatic arthritis, axial spondyloarthritis and other long-term inflammatory diseases can be enormously variable. Symptoms may fluctuate over time, treatments can substantially improve function, and limitations in one activity do not necessarily predict someone’s ability to perform another. Exercise also forms an important part of rehabilitation. I might see someone who currently cannot run, play tennis or golf because their inflammatory arthritis is poorly controlled. Following improvements in medication and a structured rehabilitation programme, one of our explicit treatment goals might be to return them to those activities. For another person, the goal might simply be getting upstairs more comfortably. To achieve that, we may use relatively demanding strengthening exercises in a gym. Seeing that person performing a squat or leg press tells you very little, in isolation, about how easily they can negotiate their stairs later that day. That distinction matters. We should not create an environment where people receiving appropriate financial support become frightened of exercising because they worry that being seen in a gym, lifting weights or participating in sport could somehow be interpreted as evidence that they are no longer disabled. From a clinical perspective, I want people with inflammatory arthritis to be as active as their condition, preferences and circumstances allow. Where possible, that includes meeting general physical activity recommendations and incorporating cardiovascular and resistance exercise. There are good reasons for doing so. Maintaining physical activity can help protect muscle and bone, improve cardiovascular health and support broader long-term health outcomes. For some patients, returning to demanding exercise is itself a major marker of successful treatment. None of this means that changes in someone’s circumstances should not be reported where required. That is a separate issue. The important point is that exercise capacity and disability are not opposites. A person can exercise and still experience meaningful restrictions from inflammatory disease. They can also improve dramatically with treatment while continuing to have limitations elsewhere. As clinicians, we should be encouraging people towards greater function—not inadvertently giving them another reason to be afraid of achieving it.
This is a free preview of a paid episode. To hear more, visit rheumatologyphysio.substack.com
This is a free preview of a paid episode. To hear more, visit rheumatologyphysio.substack.com