Axial Spondyloarthritis Flashcards
Definition and epidemiology of AxSpA
-A chronic inflammatory disease mainly affecting the spine, and sacroiliac joints
-Prevalence of AxSpA approximately 0.6% in UK population
-May be a history of PsA or inflammatory bowel disease and iritis
=Overlapping immunogenetic basis
-Peak incidence late teens to early 20’s, 45 yrs or younger
-Men affected more commonly than women (3.5:1)
Pathophysiology of AxSpA
-Genetic predisposition
=HLA-B27 – positive in 90% of patients
=Other loci include ERAP, IL-23R, IL-12, IL-12R
-Environmental trigger
=Infectious trigger, alteration in microbiome?
-Increased production of IL-23
-Activation of Th17 cells
-Increased IL-17 and TNF production
-Inflammatory infiltrate of joints and tendons at enthesis
Clinical features of AxSpA
-Inflammatory low back pain with insidious onset
=Night pain and morning stiffness (sacroiliac region sometimes radiating to buttocks, 30 mins+)
=Pain and stiffness improved by exercise
=Good response to NSAID
=3 months, insidious onset
-Large joint arthritis
-Uveitis
-Psoriasis
-Osteoporosis and vertebral fractures
-Aortic regurgitation
-Upper lobe fibrosis
-Enthesitis
Physical examination in AxSpA
-Limited range of spine movements in all directions (lateral flexion)
=Abnormal Schrober’s test (reduced forward flexion): a line is drawn 10 cm above and 5 cm below the back dimples (dimples of Venus). The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as possible
=May be normal in early disease
-Reduced chest expansion
=Normal in early disease
-Anterior Uveitis (acutefully painful red eye with photophobia or blurred vision)
-Aortic regurgitation (very rare)
-Apical fibrosis
-Achilles tendonitis
-AV node block
-Amyloidosis
-Arthritis (peripheral, asymmetric, 25%, more common if female)
-Cauda equina syndrome?
-Fixed flexion deformity in advanced disease
Investigations in AxSpA
-Imaging
=plain X-ray lumbar spine and pelvis: Sacroileitis (subchondral erosions, sclerosis), syndesmophytes, vertebral fractures, may be normal in early disease, squaring of lumbar vertebrae, bamboo spine (late and uncommon)
=MRI: Marrow oedema - more sensitive for early disease, if x-ray negative for sacroiliac involvement but suspicions high
=DEXA: Osteoporosis
-CXR: apical fibrosis
-Routine bloods
=ESR and CRP may be raised but may be normal
-Immunology
=Autoantibodies negative
=HLA B27 positive but not diagnostic (90% patients with AS, 10% normal)
-Spirometry may show restrictive defect (pulmonary fibrosis, kyphosis and ankylosis of the costovertebral joints)
Management of AxSpA
-NSAID
=Trial of at least two NSAID for 2-4 weeks, full dose
-Progress to biologic therapy if inadequate response
-Immunosuppressive therapy
=MTX, Sulfasalazine, Leflunomide for peripheral synovitis
=Not effective for axial disease
=Anti-TNF therapy is persistently high disease activity despite conventional treatments
-Corticosteroids
=Ineffective for axial disease (may worsen osteoporosis)
=Intra-articular steroids for peripheral synovitis
Role of biologics in AxSpA
-Indicated for active disease which has responded inadequately to DMARD
=BASDAI score >4.0
-Licensed treatment options are:
=Anti-TNF therapy
=Secukinumab (IL-17)
-Investigational (unlicensed) drugs
=IL-23 blockers, JAKi)
Non-pharmacological treatment for AxSpA
-Physiotherapy
=Very important in AxSpA (regular exercise like swimming)
=Back exercises to prevent flexion deformity
=Maintain good posture
-Occupational therapy
=May play role in those with peripheral arthritis
-Orthopaedic surgery
=Arthroplasty (especially THR)
=Spinal surgery seldom used (osteotomy, spinal decompression)
Main differential of AxSpA
-Prolapse intervertebral disc = Pain follows nerve root distribution.
-Mechanical back pain = Worse on movement, relieved by rest