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Ankylosing Spondylitis
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Symptoms Chronic systemic inflammatory disease involving axial skeleton of younger pts Develops in second/third decade Typically dull aching pain of insidious onset in lower lumber/ buttock region Early morning stiffness(ems) and nocturnal pain
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Symptoms Stiffness improves with exercises and recurs after periods of inactivity Some pts present with painful hips, shoulders, asymmetrical arthritis of lower limbs prior to spinal involvement Cervical and thoracic pain and stiffness is frequent
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Symptoms Enthesitis incl chest pain is common- aggravated by manoeuvres increasing intra-thoracic pressure (eg coughing) Peripheral joints: shoulders, hips, costovertebral, costosternal, manubriosternal, sternoclavicular joints commonly symptomatic at presentation M > F. 2-3.
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Symtoms and presentation Males: spine and pelvis more frequently involved with some involvement of hips, shoulders and chest wall. Tend to have a more severe disease than females Females: pelvis, hips, knees, and wrists with less severe inv of the spine Enthesitis-inflammation of ligament and tendon typical in seronegative arthritis. Eg achilles tendonitis, illiac crest pain, chest wall pain-from inv of costochondral, manubriosternal and sternoclavicular joints
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HLA-B27 B27 +ve in 90-95% of AS. Lower prevalence of B27 in african/african-american population associated with a lower prevalence of AS in these populations B27 +ve individuals have a 2-5% chance of developing AS Male sex, B27+ve, FHx of AS + frequent GI infections are all RFs for developing AS
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Pathogenesis ?development in genetically predisposed individuals, triggered by an environmental factor eg gastro-intestinal infection Reactive arthritis has a similar pathogenesis whereby chlamydia trachomatis, yersinia enterocolitica, shigella flexneri, campylobactor jejunii, salmonella typhymurium have been implicated.
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Pathogenesis B27 +ve rats in a germ-free environment do not develop AS There is a high incidence of GI mucosal inflammation (both symptomatic and asymptomatic), this raises the possibility that the gut, with breakdown of the mucosal lining is a triggering event.
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Pathogenesis Activated T-cells and macrophages found at sites of inflammation with expression of IL-1β, tnf-α and IF-γ. These inflammatory cytokines cause erosion of cortical bone, new bone formation and loss of bone mass
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Associated features Extra-articular symptoms eg acute anterior uveitis. Inflammatory bowel disease and/or psoriases may be present AS associated with CD/UC occurs in 5- 10% of individuals Asymptomatic GI inflammation present in 25-49% of AS
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Associated features 50-60% of AS have microscopic inflammatory lesions at any one time Uveitis occurs in 25-40% Osteoporoses is a common feature-look out for this Less frequent-aortic incompetence, cardiac conduction anomalies, progressive, b/l apical cavitation/fibroses Other spondyloarthropathies-ReA, PsA Enteropathic arthritis commoner in relatives
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Examination B/L sacro-illiac joint tenderness (febere manoeuvre) Peripheral joint synovitis-asymmetric, oligoarticular pattern. Dactylitis of fingers and/or toes Enthesopathy-thickened achilles tendon, planter fascitis, chest wall tenderness etc
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Examination Advanced disease; changes in posture- flattening of normal lumber lordoses, thoracic kyphoses may be exaggerated. C-spine-limitation in ROM with fusion in hyper-flexion
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Presentation Chronic low back pain-usually as a teenager Tend to remain active as way to ease pain and stiffness Back pain tends to become more progressive, symptomatic and severe-look for inflammatory back pain symptomatology Look for assoc chest wall tenderness, heel pain, buttock pain.
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Presentation Rarely may present with acute anterior uveitis Look for other features of extra-axial involvement which would aid diagnoses- asymmetrical oligoarthritis, enthesopathy. Sacro-illeitis; present with pain radiating to buttock and radiating to upper posterior thighs. Usually U/L, intermittent or alternate from one to other side and eventually becomes B/L and persistent
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Examination Chest expansion, SIJ Typical spinal ankyloses occurs after ~ 10yrs Osteoporoses more likely in severe advanced, long-standing AS esp in pts with immobile spine. Rigid osteoporotic spine susceptible to vertebral fractures-prophylactic treatment
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Diagnoses + Investigations Based on clinical/blood test and radiological findings Symptoms of inflammatory back pain Family history Extra-articular lesions B/L sacro-illeitis on XR or MRI MRI-STIR sequences show up inflammation with bone marrow oedema and enthesopathy
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Diagnoses and investigations HLA B-27: in whom hx and examination is suggestive of a sero-negative spodyloarthropathy but have normal XRs Should not be used as a routine, diagnostic, confirmatory or screening test. Positive B-27 in the presence of non- inflammatory back pain with –ve XRs does not confirm diagnoses and up to 8% fo normal pop are +ve. Higher in normal relatives. ↑esr/crp in 70% of AS, but no clear correlation with disease activity. Associated with peripheral arthritis rather than axial arthritis
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Management Combination of non-pharmocologic and pharmocological therapy depending on disease stage and symptoms Patient education essential-life long programme of exercise, use of individual, and group therapy as well as self-help groups Functional disability in AS progresses more rapidly in smokers and less so in those with better social support and reg exercises
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Management NSAIDs-essential DMARDs-not recommended for axial disease, however SASP found to be useful in periopheral arthritis Steroids-oral or parenteral not recommended Anti TNF-all three effective in AS in pts with persistently high BASDAI. No need to use MTX with anti-tnf prior to commencing anti-tnf
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Surgery Rare Hip arthroplasty-structuarl damage causing refractory pain Corrective spinal osteotomy. Fusion procedures in patients with segmental instability may be indicated.
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Prognoses Depends on stage at diagnoses Initiation of effective therarpy Worse in smokers, low socio-economic class Worse in pts poorly compliant with exercises Males worse than females
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