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Rheumatology›Condition·Updated Jun 27, 2026·v1

Ankylosing Spondylitis

Ankylosing spondylitis is a chronic inflammatory disease of the axial skeleton driven by the IL-23/IL-17 axis, presenting with inflammatory back pain, enthesitis, and extra-articular manifestations (uveitis, psoriasis, IBD). Management follows a treat-to-target strategy: NSAIDs first-line, then TNF inhibitors (adalimumab, infliximab, etc.) or IL-17 inhibitors (secukinumab, ixekizumab), with JAK inhibitors (upadacitinib) for refractory cases. Early diagnosis via MRI of sacroiliac joints and HLA-B27 testing is critical. Prognosis is improved with early treatment, but cardiovascular disease and osteoporosis are key comorbidities.

High Evidence401 references·13,543 words·55 min read·v1
ankylosing spondylitisaxial spondyloarthritisspondyloarthritisHLA-B27sacroiliitisenthesitisuveitisinflammatory back painTNF inhibitorIL-17 inhibitorJAK inhibitortreat-to-targetASDAS

Quick Reference

RxDrug of choiceTNF inhibitor (e.g., adalimumab 40 mg SC every other week) after failure of ≥2 NSAIDs.
AltAlternativesIL-17 inhibitor (secukinumab 150 mg SC q4w, ixekizumab 80 mg q4w, bimekizumab 160 mg q4w) or JAK inhibitor (upadacitinib 15 mg PO daily, tofacitinib 5 mg PO BID) for inadequate response or contraindication to TNFi.
⊘AvoidIL-17 inhibitors in active IBD; methotrexate for isolated axial disease; dual biologic therapy; JAK inhibitors in patients with history of VTE, age >65 with smoking history.
DxTest of choiceMRI of sacroiliac joints with STIR and T1 sequences for detection of active sacroiliitis.
ScKey scoreAnkylosing Spondylitis Disease Activity Score (ASDAS); target <1.3 (inactive disease).
→When to referAcute anterior uveitis (same-day ophthalmology); suspected vertebral fracture (imaging/surgery); new IBD symptoms (gastroenterology); inadequate response to first biologic (rheumatology).
Early treat-to-target with NSAIDs then biologics aiming for ASDAS <1.3; TNF monoclonals preferred for uveitis/IBD; IL-17i and JAKi effective after TNFi failure; exercise is essential; screen for TB before biologics and monitor CV risk.
Ankylosing spondylitis (AS) is a chronic, progressive inflammatory disease of the axial skeleton, defined by sacroiliitis, enthesitis, and aberrant new bone formation that can culminate in spinal fusion and functional disability. The disease typically presents in the third decade of life with inflammatory back pain, morning stiffness, and progressive loss of spinal mobility. Extra-articular manifestations, acute anterior uveitis, psoriasis, inflammatory bowel disease, occur in up to 40% of patients. The central effector pathway is the IL-23/IL-17 axis, initiated by HLA-B27 misfolding. Early recognition and treatment with biologic DMARDs (TNF inhibitors, IL-17 inhibitors) can slow radiographic progression and improve outcomes. Management follows a treat-to-target strategy aiming for ASDAS < 1.3, with NSAIDs as first-line, followed by biologics and JAK inhibitors.

Overview and Recommendations

Background

  • •Ankylosing spondylitis (AS) is a chronic, progressive inflammatory disease of the axial skeleton, defined by sacroiliitis, enthesitis, and aberrant new bone formation that can culminate in spinal fusion and functional disability. It is the prototypic member of the spondyloarthritis (SpA) family, sharing genetic (HLA-B27), clinical (axial inflammation, enthesitis, uveitis), and radiographic (sacroiliitis, syndesmophytes) features.
  • •AS affects approximately 0.1-0.5% of the population worldwide, typically presenting in the third decade of life. Males are affected 2-3 times more often than females in radiographic AS, but the sex ratio is smaller when MRI-based criteria are used. Onset after age 45 is rare and should trigger a search for alternative diagnoses.
  • •The central effector pathway is the IL-23/IL-17 axis, initiated by HLA-B27 misfolding and ERAP1-mediated peptide presentation, then sustained by innate immune cells (γδ T cells, neutrophils, ILC3) at entheseal and gut mucosal sites. Syndesmophyte formation is driven by mechanotransduction and Wnt signalling downstream of inflammation, not by TNF alone.
  • •Extra-articular manifestations are integral: acute anterior uveitis occurs in ~26%, psoriasis in ~9%, and inflammatory bowel disease in ~7% of patients. These manifestations often precede the diagnosis of AS and critically influence biologic selection.
  • •Untreated, AS leads to irreversible spinal fusion, reduced quality of life, and increased cardiovascular risk. All-cause mortality is increased by ~36%, driven largely by cardiovascular deaths. Early treat-to-target strategies with NSAIDs and biologic DMARDs have fundamentally altered the expected trajectory, but complete arrest of radiographic progression in high-risk patients remains an unmet goal.

Evaluation

  • •Suspect axial spondyloarthritis (axSpA) in any patient under 45 years with chronic back pain (>3 months) that is insidious in onset, worse with rest, and improves with exercise. Nocturnal pain (waking the patient in the second half of the night) and morning stiffness lasting ≥30 minutes are cardinal features.
  • •Ask about peripheral joint pain, heel pain (Achilles tendinitis, plantar fasciitis), and extra-articular symptoms: eye redness with photophobia (uveitis), chronic diarrhea or abdominal pain (IBD), and skin or nail changes (psoriasis).
  • •Examine for spinal mobility: modified Schober test (lumbar flexion <5 cm is abnormal), chest expansion (≤2.5 cm in men, ≤2.0 cm in women is abnormal), and occiput-to-wall distance. Perform SI joint provocation tests (FABER, Gaenslen, direct compression) and assess for enthesitis at the Achilles tendon, plantar fascia, and costochondral junctions using the Maastricht Ankylosing Spondylitis Enthesitis Score (MASES).
  • •Order HLA-B27 testing: present in 85-95% of radiographic AS patients. A positive test in a young adult with typical IBP strongly supports the diagnosis (LR+ ~9.0). Rheumatoid factor and anti-CCP are characteristically absent.
  • •Measure CRP and ESR: CRP is elevated in only 40-60% of patients; a normal CRP does not exclude active disease. However, an elevated CRP increases the probability of active inflammation on MRI and doubles the odds of response to TNF inhibitors.
  • •Obtain MRI of the sacroiliac joints (SIJ) with STIR and T1-weighted sequences as the gold-standard imaging modality. A positive MRI requires the clear presence of bone marrow edema (BMO) on STIR suggestive of active sacroiliitis (ASAS definition). The combination of BMO plus structural lesions (erosions, fat metaplasia, ankylosis) substantially increases specificity.
  • •Plain radiography of the SIJ remains first-line for classification: the modified New York criteria require definite radiographic sacroiliitis (grade ≥2 bilaterally or grade 3-4 unilaterally). However, radiography has poor sensitivity in early disease (delay to detection typically 5-10 years).
  • •Apply the ASAS classification criteria for axSpA: in a patient with IBP (age <45 years), the diagnosis requires either (a) sacroiliitis on MRI or radiography plus ≥1 SpA feature (uveitis, psoriasis, IBD, dactylitis, enthesitis, good response to NSAIDs, family history, HLA-B27, elevated CRP), or (b) HLA-B27 positivity plus ≥2 other SpA features. These criteria are for classification, not diagnosis; interpret in clinical context.
  • •Distinguish AS from non-radiographic axSpA (nr-axSpA): the key difference is the presence of definite radiographic sacroiliitis in AS. Both forms share similar levels of pain, stiffness, and MRI inflammation, but radiographic AS carries a worse functional prognosis due to irreversible structural damage.
  • •Consider alternative diagnoses: diffuse idiopathic skeletal hyperostosis (DISH) lacks sacroiliitis and HLA-B27 association; fibromyalgia frequently co-occurs and can confound disease activity assessment. Red flags for urgent action include acute-onset severe spinal pain with neurological deficit (vertebral fracture), acute painful red eye (uveitis), and severe bloody diarrhea (IBD flare).

Management

  • •Initiate a non-steroidal anti-inflammatory drug (NSAID) at the maximum recommended anti-inflammatory dose as first-line pharmacotherapy for all patients with active axSpA. Continuous NSAID therapy may be preferred over on-demand use; the CONSUL trial showed that continuous celecoxib 200 mg twice daily plus golimumab reduced 2-year radiographic spinal progression compared to golimumab alone.
  • •Do not routinely use conventional synthetic DMARDs (methotrexate, sulfasalazine) for isolated axial disease; their efficacy is limited to peripheral arthritis. Methotrexate at doses of 7.5-10 mg weekly is no better than placebo for axial symptoms.
  • •Initiate a tumor necrosis factor inhibitor (TNFi) in patients with active axSpA who have failed ≥2 NSAIDs. Five TNFi are approved: adalimumab 40 mg SC every other week, certolizumab pegol 400 mg SC at weeks 0,2,4 then 200 mg every 2 weeks, etanercept 50 mg SC weekly, golimumab 50 mg SC every 4 weeks, and infliximab 5 mg/kg IV at weeks 0,2,6 then every 8 weeks. The NNT for ASAS40 is 4 in biologic-naïve patients.
  • •Choose TNFi based on extra-articular manifestations: adalimumab, certolizumab, golimumab, and infliximab reduce uveitis flares and are effective for IBD; etanercept does not prevent uveitis and is not effective for IBD. For patients with recurrent uveitis, a TNF monoclonal antibody is preferred.
  • •Perform screening for latent tuberculosis (TB) using tuberculin skin test or interferon-gamma release assay before starting any biologic DMARD. Also screen for hepatitis B (HBsAg, anti-HBc) and hepatitis C. Administer pneumococcal, influenza, and COVID-19 vaccines before starting therapy.
  • •Switch to an IL-17 inhibitor (secukinumab, ixekizumab, bimekizumab) in patients with contraindications to TNFi or inadequate response to one or more TNFi. Secukinumab 150 mg SC at weeks 0,1,2,3,4 then every 4 weeks; can increase to 300 mg monthly. Ixekizumab 160 mg SC loading dose then 80 mg every 4 weeks. NNT for ASAS40 is 3.5 for secukinumab and 3.3 for ixekizumab.
  • •IL-17 inhibitors are contraindicated in patients with active inflammatory bowel disease (IBD); they can exacerbate IBD. Mucocutaneous candidiasis (mostly grade 1-2) is more frequent with IL-17i than TNFi.
  • •For patients who fail one or more bDMARDs, consider a JAK inhibitor: upadacitinib 15 mg PO daily or tofacitinib 5 mg PO twice daily. In the SELECT-AXIS 2 trial, upadacitinib achieved ASAS40 in 45% vs 18% placebo after bDMARD failure (NNT = 3.7).
  • •Perform baseline CBC, LFTs, renal function, fasting lipid panel, and TB screening before starting a JAK inhibitor. Avoid JAK inhibitors in patients with a history of VTE, age >65 years, and current or past smoking due to increased risk of MACE and malignancy.
  • •Reassess disease activity every 3-6 months using ASDAS (or BASDAI + CRP). Target ASDAS <1.3 (inactive disease) or at least <2.1 (low disease activity). If the target is not achieved within 3-6 months, escalate therapy.
  • •For a disease flare (ASDAS increase ≥0.9 units), consider a short course of high-dose prednisolone: 60 mg PO daily for 1 week, then taper by 10 mg weekly to 10 mg, then 5 mg daily for 2-4 weeks (COBRA-AS regimen). NNT for BASDAI50 = 4.
  • •In patients who achieve sustained remission (ASDAS <1.3 for ≥6 months), gradual tapering of bDMARD dose or extension of dosing interval can be attempted, but the ACR conditionally recommends against routine dose reduction: the ABILITY-3 trial showed that withdrawal of adalimumab led to flare in 63% vs 35% with continuation (NNT = 3.6 to prevent one flare).
  • •Prescribe regular, supervised exercise therapy for all patients with axSpA. Exercise programs improve BASDAI (MD -1.0, 95% CI -1.5 to -0.5) and BASFI (MD -0.8, 95% CI -1.3 to -0.4) compared to no exercise.
  • •Do NOT use systemic glucocorticoids (≥10 mg prednisone/day) for long-term disease control; they have no proven efficacy for spinal disease and cause corticosteroid-related AEs.
  • •Do NOT combine two biologic DMARDs (e.g., TNFi + IL-17i); this increases risk without additive benefit.
  • •Refer for surgical evaluation if there is evidence of spinal fracture, pseudarthrosis, or spinal stenosis causing neurological compromise. Total hip arthroplasty is commonly needed for advanced hip involvement; preoperative optimization of disease activity and perioperative discontinuation of TNF inhibitors (typically 1-2 weeks before surgery) is recommended.
  • •Discharge criteria: a flare is considered resolved when ASDAS-CRP returns to <1.3 or <2.1 and the patient reports no more than mild pain. Step down glucocorticoids to 0 if possible and re-establish maintenance therapy.

Board Review — High Yield

  • •HLA-B27, Present in ~90% of AS patients; odds ratio for disease ~50-100; strongest genetic risk factor.
  • •Syndesmophyte, Hallmark radiographic finding; driven by Wnt signaling and mechanotransduction, not TNF alone.
  • •ASDAS, Preferred composite disease activity score integrating CRP and patient domains; target <1.3 for remission.
  • •MRI sacroiliitis, Bone marrow edema on STIR sequence is gold standard for early diagnosis; can detect disease years before plain films.
  • •Uveitis, Most common extra-articular manifestation (~26%); TNF monoclonal antibodies (adalimumab, infliximab) reduce flares; etanercept does not.
  • •TNF inhibitors, First-line biologic after NSAID failure; NNT for ASAS40 = 4; adalimumab 40 mg q2w, infliximab 5 mg/kg q8w.
  • •IL-17 inhibitors, Effective for axial and skin disease; contraindicated in active IBD; secukinumab 150 mg q4w, ixekizumab 80 mg q4w.
  • •JAK inhibitors, Upadacitinib 15 mg daily or tofacitinib 5 mg BID after bDMARD failure; screen for VTE risk, herpes zoster.
  • •Modified New York criteria, Require definite radiographic sacroiliitis (grade ≥2 bilateral or 3-4 unilateral) for AS diagnosis.
  • •COBRA-AS regimen, Prednisolone 60 mg daily tapered over 6 weeks for severe flares; NNT = 4 for BASDAI50.

Deep Dive — Evidence Details

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