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Ankylosing Spondylitis

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Ovid: 5-Minute Sports Medicine Consult, The


Ankylosing Spondylitis
Catharine Mayer
Eugene Hong
Basics
Description
  • Ankylosing spondylitis (AS) is a chronic inflammatory, seronegative autoimmune arthritis characterized by inflammatory back pain.
  • It is the most common and potentially severe subtype of the spondyloarthritis (SpA), which includes:
    • Reactive (Reiter) arthritis
    • Arthritis/spondylitis with inflammatory bowel disease (IBD)
    • Arthritis/spondylitis with psoriasis
    • Unspecified spondylitis
  • AS causes inflammation of the sacroiliac joints, peripheral joints, and entheses (sites where ligaments or tendons attach to bone).
  • Common sites for enthesopathy include:
    • Calcaneus
    • Patella
    • Tibial tubercle
    • Vertebral bodies
  • The involvement of vertebral body entheses leads to the characteristic findings of ankylosis (fusion) and syndesmophytes (vertical bony growths) responsible for the classic radiographic “bamboo” appearance of the spine in advanced disease.
  • Synonym(s): Axial spondyloarthritis; Inflammatory spine disease
Epidemiology
Incidence
  • Overall incidence: 0.5–8.2/100,000/yr (1)
  • Incidence rate varies directly with prevalence of HLA-B27 in given population.
  • Commonly presents in young adulthood
  • Predominant age:
    • 80% of patients with AS develop symptoms before age 30.
    • <5% of patients with AS present after age 45.
  • Predominant gender: Male > Female (∼3:1).
Prevalence
  • Prevalence of AS in a given population depends on HLA-B27 prevalence in the population.
  • Overall prevalence in U.S. is 0.10–0.12% for AS and 0.21% for all SpAs including AS.
  • Higher in Alaskan Eskimos and some Native American populations owing to higher than average HLA-B27 rate
  • Lower in African Americans secondary to a lower HLA-B27 rate
  • Up to 5% of patients evaluated for chronic low back pain are ultimately diagnosed with AS.
Risk Factors
  • Positive family history of SpA or HLA-B27
  • 90% or more of individuals with AS are HLA-B27-positive.
  • Reactive arthritis triggered by Chlamydia trachomatis and certain enteric infections (eg, Shigella, Salmonella, Yersinia, and Campylobacter spp.) predisposes to development of AS.
  • 10–20% of HLA-B27-positive patients with reactive arthritis develop AS.
Genetics
  • Expression of HLA-B27 antigen is clearly linked to the development of AS, but the exact mechanism is unknown.
  • Prevalence of HLA-B27 in African Americans is 2–4% and in Caucasians is 8%.
Etiology
  • A clear etiologic pathway has not been established.
  • Research suggests that some interplay among environmental/infectious exposure, genetic predisposition, and immune response is responsible for the development of AS and all SpAs.
  • It is likely that an autoimmune response triggered by an immunologic event causes an inflammatory cell infitrate (predominately T cells and macrophages) in the sacroiliac joints, peripheral joints, and entheses leading to ongoing inflammation that results in bony proliferation, erosions, sclerosis, and destruction.
Commonly Associated Conditions
  • Uveitis/iritis
  • IBD
  • Psoriasis
  • Rarely, cardiac valve/aortic root involvement
Diagnosis
  • Must recognize the features of inflammatory back pain (IBP) to distinguish from mechanical back pain. New York criteria are the traditional diagnostic criteria for AS. New criteria to diagnose all causes of IBP, not just AS, have been developed by the Assessment for SpondyloArthritis International Society (ASAS).
  • ASAS-endorsed criteria for IBP (SOR-A: Validated clinical rule) (2):
    • Age of onset <40 yrs
    • Insidious onset
    • Improvement with exercise
    • No improvement with rest
    • Nighttime pain with improvement on getting up
  • Requires 4 of 5 parameters
  • 77% sensitive, 92% specific for IBP (not only AS)
  • Modified 1984 New York criteria for AS:
    • Clinical criteria:
      • Low back pain and stiffness of at least 3 mos' duration that improves with exercise but is not relieved by rest
      • Limited lumbar spinal motion in sagittal (sideways) and frontal (forward and backward) planes
      • Chest expansion decreased relative to normal values corrected for age and sex
    • Radiologic criteria:
      • Bilateral sacroiliitis grades 2–4 or
      • Unilateral sacroiliitis grade 3 or 4
  • A patient is considered to have definite AS if one radiologic criterion is associated with at least one clinical criterion.
  • A patient is considered to have probable AS if 3 clinical criteria are present or one radiologic criterion is present without any clinical criterion.
History
Signified by back pain of insidious onset that has been present for at least 3 mos
Physical Exam
Physical exam should include assessment of:
  • Entire spine: Range of motion, tenderness. Shober's test: Mark area on patient's back at L5 and 10 cm above that point. Once patient bends forward, remeasure that distance. In normal persons, it should be >5 cm greater in flexion; <5 cm suggests loss of motion in lumbar spine.
  • Peripheral joints, especially in the lower extremity: Limited range of motion, inflammatory signs such as effusion, warmth, tenderness
  • Major entheses: Calcaneous for Achilles and plantar fascia attachments, patella, tibial tuberosity
  • Eyes: Inflammatory findings
  • Skin: Rash characteristic of psoriasis
Diagnostic Tests & Interpretation
Lab
  • Laboratory studies that can aid in the diagnosis include:
    • HLA-B27
    • C-reactive protein (CRP)
    • Erythrocyte sedimentation rate (ESR)
  • CRP and ESR can be elevated in 50–70% of patients with AS, but normal values do not negate presence of disease. Further, normal or elevated levels in patients with established disease do not correlate with disease activity.
Imaging
  • Imaging of sacroiliac joints is required for the diagnosis and classification of AS.
  • Plain radiographs:
    • Sacroiliitis is a hallmark of disease.
    • 20–30% of patients with the 1st 2 yrs of developing IBP will have structural changes detectable by radiographs, confirming diagnosis.
    • In established AS, 95% of patients have detectable structural changes; however, structural changes may take several years or longer to become apparent radiographically.
    • Absence of radiographic findings in patients with IBP does not imply a lack of inflammation, nor does it negate the possibility of AS.
  • MRI (T2 and STIR):
    • May be useful when plain radiographs are noncontributory
    • Able to detect active and acute inflammation of sacroiliac joints in early disease prior to onset of structural changes
    • Also can predict the future development of structural changes
    • Not as sensitive as plain radiographs to assess degree of structural changes
  • CT scan:
    • Useful for detecting chronic changes in the sacroiliac joints
    • Role is limited owing to high radiation exposure.

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Differential Diagnosis
  • Mechanical low back pain
  • Myofascial low back pain
  • Lyme arthritis
  • Herniated nucleus pulposus
  • Degenerative disk disease
  • Degenerative joint disease
  • Spondylolysis
  • Diskitis
  • Other causes of IBP
Treatment
  • Management is individualized based on degree of disease, severity of symptoms, and patient expectations.
  • Typically is long term, if not lifelong
Medication
Depending on location and severity of disease, the following treatment modalities may be indicated:
  • NSAIDs
  • Tumor necrosis factor (TNF) blockers
  • Disease-modifying antirheumatic drugs (DMARDs)
  • Corticosteroid injections
First Line
NSAIDs (SOR-A) (3):
  • Diclofenac, naproxen, celecoxib, and others
  • Full dose and regular scheduling maximize symptom relief.
  • Randomized trials have demonstrated that the anti-inflammatory properties of NSAIDs suppress symptoms.
  • Beneficial for both axial (spine) and peripheral (joint, enthesis) involvement
  • Data suggest that long-term therapy may have disease-controlling properties evidenced by suppression of radiographic progression.
  • Most, but not all, patients will respond to NSAIDs. Try another NSAID class before considering 2nd-line therapy.
  • Must monitor for GI, cardiovascular, renal, and hepatic side effects with ongoing NSAID use.
Second Line
  • TNF blockers (SOR-A) (4):
    • Infliximab, adalimumab, and etanercept
    • Clear guidelines on indication and use
    • Randomized trials demonstrate significant improvement in pain, function, and disease activity.
    • With extended therapy, up to 1/3 of patients may develop remission.
    • Studies are ongoing investigating long-term use and disease progression.
    • Cochrane Review underway but unpublished as of 2009
  • DMARDs:
    • Limited role for sulfasalazine; some benefit with peripheral disease only (SOR-A) (5)
    • No role for methotrexate (SOR-A) (6)
  • Local corticosteroid injections: May be useful for symptomatic relief of inflamed peripheral joints
Additional Treatment
Referral
  • Rheumatology evaluation may be helpful to confirm presence and severity of disease, as well as to guide treatment indications for use of TNF blockers and other DMARDs.
  • Consider early referral in patients with IBP and the presence of HLA-B27, radiographic findings, or positive family history of AS or other SpA.
Additional Therapies
  • Education (absolute indication)
  • Exercise (absolute indication)
  • Physical therapy/rehabilitation (absolute indication)
  • Self-help groups
  • AS associations
  • A Cochrane Review of physiotherapy determined that a home or supervised exercise program performed better at improving function and decreasing pain than no exercise at all (7).
  • A Cochrane protocol for review of self-management programs for patients with AS is underway. No review of findings has been published as of 2009.
Surgery/Other Procedures
  • Hip arthroplasty as indicated for progressive arthropathy∏
  • Knee arthroplasty as indicated for progressive arthropathy∏
Ongoing Care
  • Duration of therapy: Long term or lifelong
  • When to expect improvement:
    • Many patients experience significant improvement of symptoms within 1 wk of initiating NSAID therapy.
    • Continued improvement occurs over weeks to several months in pain, stiffness, and range of motion, as well as function.
  • Signs to watch for that indicate problems:
    • Worsening stiffness despite maximal NSAID therapy
    • Side effects of NSAID therapy
    • Vision, skin, or cardiovascular complaints
  • Pitfall: Overdiagnosis in HLA-B27-positive individuals in whom other causes for joint swelling should be considered.
Prognosis
  • AS has an unpredictable clinical course independent of age of onset or sex.
  • Most patients have a fluctuating course with flares and periods of relative remission.
  • Chronic symptoms can range from mild, medically controllable inflammation to debilitating progression that is refractory to treatment.
Complications
  • Fusion of vertebrae leading to loss of function or restrictive lung disease
  • Uveitis can occur in 40% of patients.
  • Aortitis or aortic insufficiency, rare
  • Hip arthritis with refractory pain or disability requiring arthroplasty
References
1. Sieper J, Rudwaleit M, Baraliakos X, et al. The Assessment of SpondyloArthritis international Society (ASAS) handbook: a guide to assess spondyloarthritis. Ann Rheum Dis. 2009;68 (Suppl 2):ii1–44.
2. Sieper J, van der Heijde DM, Landewé RB, et al. New criteria for inflammatory back pain in patients with chronic back pain—a real patient exercise of the Assessment in SpondyloArthritis international Society (ASAS). Ann Rheum Dis. 2009;68:784–788.
3. Song IH, Poddubnyy DA, Rudwaleit M, et al. Benefits and risks of ankylosing spondylitis treatment with nonsteroidal antiinflammatory drugs. Arthritis Rheum. 2008;58:929–938.
4. Braun J, Davis J, Dougados M, et al. First update of the international ASAS consensus statement for the use of anti-TNF agents in patients with ankylosing spondylitis. Ann Rheum Dis. 2006;65:316–320.
5. Chen J, Liu C. Sulfasalazine for ankylosing spondylitis. Cochrane Database Syst Rev. 2005:CD004800.
6. Chen J, Liu C, Lin J. Methotrexate for ankylosing spondylitis. Cochrane Database Syst Rev. 2006:CD004524.
7. Dagfinrud H, Kvien TK, Hagen KB. Physiotherapy interventions for ankylosing spondylitis. Cochrane Database Syst Rev. 2008:CD002822.
Additional Reading
Braun J, Sieper J. Ankylosing spondylitis. Lancet. 2007;369:1379–1390.
Sieper J, Rudwaleit M, Khan MA, et al. Concepts and epidemiology of spondyloarthritis. Best Pract Res Clin Rheumatol. 2006;20:401–417.
Codes
ICD9
720.0 Ankylosing spondylitis
Clinical Pearls
  • Consider features of IBP that can distinguish it from other causes of chronic back pain.
  • If plain radiographs are not diagnostic, consider further imaging (eg, MRI).
  • In a patient <45 yrs of age at symptom onset with low back pain for >3 mos, consider determining the presence of IBP clinical symptoms, HLA-B27 serology, or radiographic/MRI evidence of sacroiliac inflammation. Each of these findings may increase the likelihood of AS.
  • With early recognition, diagnosis, and appropriate management, AS symptoms and disease progression can be improved.


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