Axial spondyloarthritis emerged as the missed cause of back pain in a patient with systemic lupus erythematosus
A 54-year-old woman already living with systemic lupus erythematosus developed a second autoimmune disease that can easily be overlooked when chronic pain is attributed to one diagnosis alone. She arrived with persistent low back pain that had continued for a year, despite ongoing immunomodulator and glucocorticoid therapy for lupus. The overlap between these two disorders created a genuine diagnostic trap: the back pain could have reflected inflammatory spine disease, but it also could have represented avascular necrosis, osteoporotic vertebral injury, or another musculoskeletal complication associated with long-term steroid exposure.
The eventual diagnosis was ankylosing spondylitis, confirmed after imaging of the hips and bilateral sacroiliac joints. In a patient with established lupus, that sequence matters because the symptom pattern is easy to misread. Low back pain in someone receiving corticosteroids often triggers concern for structural damage, while inflammatory axial disease may be delayed when joint symptoms are assumed to fit within the broader lupus picture. Here, the imaging findings redirected the workup away from the more common steroid-related differentials and toward axial spondyloarthritis.
Imaging changed the differential when clinical examination was not enough
History and physical examination raised suspicion for axial spondyloarthritis, but clinical impression alone could not settle the question. Magnetic resonance imaging of the hips with bilateral sacroiliac joint assessment provided the decisive evidence and ruled out competing explanations such as avascular necrosis of the hip and osteoporotic vertebral fractures. The case illustrates how important cross-sectional imaging can be when inflammatory back pain appears in a patient with overlapping autoimmune disease and treatment-related risks.
A single swollen or tender joint can mislead; bilateral sacroiliac involvement points to a different biology.
The underlying pathophysiology of lupus and ankylosing spondylitis is not identical, which is exactly why coexistence is so diagnostically challenging. SLE is classically associated with systemic autoantibody-mediated inflammation, while axial spondyloarthritis targets the sacroiliac joints and spine through a distinct inflammatory pathway. When both occur together, the clinician has to separate drug toxicity, mechanical pain, osteoporotic injury, and inflammatory sacroiliitis before treatment can be rationalized. The MRI result in this case did that work by anchoring the diagnosis to the axial skeleton rather than to the hip joint alone.
Sulfasalazine improved pain and mobility alongside lupus-directed therapy
Treatment was layered rather than replaced. The patient received sulfasalazine for ankylosing spondylitis while continuing hydroxychloroquine, prednisolone, and mycophenolate for lupus. After three months, she reported less lower back pain and greater range of motion in the hip joint, and examination showed only mild sacroiliac tenderness. In practical terms, that response suggests the inflammatory component of her pain was at least partly reversible once the correct diagnosis was treated.
Sulfasalazine remains a conventional disease-modifying option in spondyloarthritis, and this case supports its use when axial disease coexists with lupus. The medication does not solve every inflammatory spine presentation, but it can blunt peripheral and some axial symptoms without forcing an immediate move to more aggressive therapies. In a patient already balancing immunosuppression for lupus, that sort of conservative escalation has real bedside value. It allows the clinician to address the newly recognized spondyloarthropathy while preserving the regimen that had already been selected for the original autoimmune disease.
Why coexistence of lupus and ankylosing spondylitis creates a diagnostic blind spot
The coexistence of SLE and AS is described as extremely rare, and that rarity itself contributes to under-recognition. Most rheumatology clinics see both conditions regularly, but usually in separate patients, not in the same one. Once a patient has a known autoimmune diagnosis, new musculoskeletal complaints are often interpreted through that existing label. In this case, persistent low back pain might have been dismissed as nonspecific pain, steroid-related bone disease, or another lupus-associated complication if imaging had not been pursued.
This is where the clinical lesson becomes concrete. Patients with lupus can still develop a second inflammatory rheumatic disorder, and the differential diagnosis of back pain should stay open when symptoms persist or the pattern suggests inflammatory axial involvement. MRI is especially useful because plain clinical examination may not distinguish sacroiliitis from degenerative disease or steroid-related injury. The case also shows that the presence of one autoimmune disorder does not exclude another, even when the coexistence is unusual enough to feel counterintuitive.
A rare case, but one with clear bedside implications
The follow-up at three months is encouraging, but the report remains a single-patient account. It cannot define a standard regimen, predict long-term radiographic progression, or establish whether sulfasalazine will control axial symptoms durably in all patients with the same overlap syndrome. What it does establish is the need for diagnostic discipline. Persistent back pain in a patient with lupus deserves evaluation for axial spondyloarthritis, particularly when imaging can identify sacroiliac inflammation and exclude more familiar steroid-associated complications.
For rheumatologists, this case argues for a broader diagnostic frame when autoimmune disease seems to explain everything but does not fully account for the pain. For patients, it reinforces a more basic point: chronic back pain is not always a side effect of the disease they already know they have. Sometimes it is a second inflammatory disorder hiding in plain sight.