Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Recognise axial spondyloarthritis before radiographic damage, use the recommended imaging sequence, combine exercise and anti-inflammatory treatment, and escalate persistent active disease through specialist biologic pathways.
Axial spondyloarthritis includes non-radiographic disease and radiographic axial spondyloarthritis historically called ankylosing spondylitis. The distinction reflects imaging, not symptom legitimacy. Diagnosis integrates onset, inflammatory features, associated disease, examination, HLA-B27, inflammatory markers and imaging. Women and HLA-B27-negative patients can be under-recognised, and normal mobility early in disease is not exclusionary.
Examine posture, spinal movement, chest expansion, sacroiliac provocation, hips, peripheral joints and entheses, while inspecting skin and nails and asking about eye and bowel symptoms. Mobility measures are useful longitudinally but influenced by age, effort, hip disease and damage. A painful red photophobic eye is not managed by routine rheumatology review; it needs same-day ophthalmic assessment.
NICE imaging starts with sacroiliac radiography in skeletally mature people on the relevant adult pathway. If definite sacroiliitis is absent but suspicion persists, request unenhanced MRI using an inflammatory-back-pain protocol and ASAS or OMERACT interpretation. If imaging and clinical suspicion disagree, seek specialist musculoskeletal-radiology review; consider follow-up MRI when suspicion remains high.
HLA-B27 and other immune variants strongly influence susceptibility, but most carriers never develop disease and negative status does not exclude it.
Microbial and mucosal immune signals may activate entheseal inflammation, supported by clinical overlap with inflammatory bowel disease and psoriasis.
Repeated loading at entheses interacts with immune susceptibility, helping explain inflammation at sacroiliac, spinal and peripheral insertion sites.
Innate and adaptive immune pathways drive inflammation where ligaments and tendons attach to bone, including sacroiliac and spinal structures.
Inflammatory bone injury is followed by abnormal osteoproliferative repair, producing syndesmophytes, ankylosis and progressive restriction in some patients.
Shared immune pathways affect uvea, bowel, skin and cardiovascular structures, so disease burden extends beyond measured spinal pain.
Young onset, insidious pain, second-half night waking, morning stiffness, alternating buttock pain and improvement with movement collectively support axial inflammation.
Uveitis, psoriasis, inflammatory bowel disease, enthesitis, dactylitis and family history substantially increase diagnostic probability and guide shared specialty care.
Sacroiliac erosions, sclerosis, joint-space change, syndesmophytes and ankylosis indicate established structural involvement but absence does not exclude earlier disease.
Unilateral eye pain, photophobia, redness and blurred vision requires same-day ophthalmic assessment to prevent sight-threatening complications.
New severe focal pain, deformity or neurological change after minor trauma in an ankylosed spine requires emergency immobilisation, imaging and spinal review.
Load-related pain improving with rest, focal strain and absent inflammatory or extra-articular features favours mechanical disease, although mechanisms can coexist.
Age-related change, postpartum stress, osteitis condensans and infection can mimic sacroiliac abnormalities and require clinical and imaging correlation.
Flowing anterolateral ossification in an older metabolic phenotype differs from inflammatory corner lesions and sacroiliac erosive disease.
Unremitting pain, systemic decline, trauma, neurological change or structural instability requires urgent alternative spinal assessment rather than an inflammatory label.
Rigid osteoporotic spine behaves like a long bone, allowing unstable fractures and delayed neurological injury after seemingly minor trauma.
Acute unilateral painful red eye, photophobia and blurred vision can recur and threatens sight without prompt ophthalmic treatment.
Restrictive chest movement, aortic-root disease, conduction abnormalities, osteoporosis and cardiovascular risk contribute to substantial long-term morbidity.
Pain, fatigue, stiffness and reduced spinal or hip movement can impair sleep, driving, work, exercise and mental wellbeing.
Non-radiographic disease can be highly symptomatic and active; the term describes imaging rather than the reality of inflammation.
Its value depends on ethnicity and phenotype, and it must never be used as a universal screening or exclusion test.
Regular tailored mobility, posture, strength and aerobic work preserves function and complements rather than follows pharmacological treatment.
MRI requires a protocol, recognised interpretation criteria and clinical context; specialist radiology review helps resolve discordance and prevents both overdiagnosis and missed disease.
Long lever arms and poor bone quality produce unstable fractures after low-energy trauma, sometimes with delayed neurological deterioration.
Excluding disease because HLA-B27, CRP or radiography is negative.
Calling all young back pain inflammatory without associated features and examination.
Using MRI marrow oedema without considering mechanical and postpartum mimics.
Neglecting same-day referral for a painful photophobic red eye.
Treating spinal trauma as minor because initial radiographs appear normal.
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A 31-year-old has chronic inflammatory back pain, previous uveitis and heel enthesitis. Sacroiliac radiographs are nondiagnostic. What is the most appropriate next diagnostic step?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Assess ulcer or bleeding, renal, heart-failure, blood-pressure, cardiovascular, anticoagulant and interaction risks and add gastroprotection when indicated. Avoid systemic NSAIDs from 20 weeks of pregnancy unless essential; use the lowest dose for the shortest time and consider fetal monitoring after several days. They are contraindicated after 28 weeks.
Do not start during active serious infection and stop for a new serious infection; screen for tuberculosis and hepatitis and update immunisation first. Avoid live vaccines during treatment, and seek an alternative in demyelinating disease. Adalimumab is contraindicated in NYHA III or IV heart failure. If continued through pregnancy, document exposure and the BSR plan to defer infant live vaccines until 6 months.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes