Serving up spondyloarthritis: time for a clinical hawkeye

Spondyloarthritis is an uncommon collection of chronic inflammatory systemic disorders. Athletic populations may be at greater risk of misdiagnosis due to the physical demands of sport and the high prevalence of back pain during peak training or competition periods. Chris Mallac explores spondyloarthritis and provides a management outline for clinicians.

Spondyloarthritis (SpA) is an uncommon collection of chronic inflammatory systemic disorders. Pain may present insidiously in the spine and refer to the buttock region. Axial SpA (ax-SpA) is the most common of these conditions and affects the spine and sacroiliac joints. The most common form of ax-SpA is Ankylosing Spondylitis (AS), known as radiographic axial SpA (r-axSpA). Radiological ax-SpA shows structural changes on imaging instead of non-radiographic axial SpA (non-r-axSpA), which does not but presents with similar signs and symptoms⁽¹⁾.

Other forms of SpA may present in clinical sports medicine, and clinicians need to maintain a high level of suspicion when assessing athletes with ongoing inflammatory signs or symptoms^(1,2). These include:

1. Psoriatic arthritis (PsA)
2. Inflammatory bowel disease (IBD) associated arthritis
3. Reactive arthritis (also known as Reiter’s Syndrome) (ReA)
4. Undifferentiated SpA
5. Peripheral SpA
6. Juvenile onset SpA.

Although the prevalence of SpA is quite rare, sports medicine professionals need to understand the pathophysiology as it coincides with other soft tissue disorders involving the enthesis, particularly at the Achilles tendon insertion, plantar fascia, and patella tendon.

Clinical Presentation

Spondyloarthritis presents with varying severity and may be challenging to identify in the early disease stages. However, there are key clinical features of SpA, which include^(1,3,4):

1. Vague daily buttock pain in the early stages.
2. Early morning stiffness > one hour.
3. Pain and stiffness in other spinal regions.
4. Symptoms improve with NSAID’s and movement while aggravated by rest.
5. Up to 30% of patients have enthesis issues in the Achilles, plantar fascia, or patella tendon and dactylitis (sausage digit) which is usually asymmetrical.
6. Extra-musculoskeletal manifestations (EMM) such as uveitis (25% of patients), psoriasis (10%), or inflammatory bowel disease, which includes ulcerative colitis and Crohn’s disease (5-10%).

Epidemiology

The presentation of ax-SpA usually starts in the late twenties and into the thirties. It is rare for it to manifest after the age of 45. It is more common for males to have r-axSpA at a ratio of 2:1 with an equal ratio of 1:1 for non-r-ax-SpA⁽⁵⁾. Estimating the worldwide prevalence is challenging, but r-axSpA is between 0.1-1.4%, with the overall SpA prevalence between 0.5-1.9%^(1,6). Notably, the presence of the HLA-B27 gene increases the risk of developing the disease^(1,6). This gene is more common in Northern European, circumpolar arctic, and subarctic populations of North America and Eurasia and rare in southern African and Japanese populations⁽⁷⁾.

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Pathophysiology

A genetic predisposition plays a significant role in the manifestation of ax-SpA. The primary genes identified are HLA-B27, endoplasmic reticulum aminopeptidase (ERAP), and the interleukin-23 receptor (IL_23)⁽¹¹⁾. The primary affected structure in axSpA is the enthesis and subchondral bone, with pathology developing at these sites over time.

The mechanical and chemical triggers activate inflammation at the enthesis, and subchondral bone changes occur. These changes manifest as a fluctuation between bone destruction and formation^(3,12). Pro-inflammatory cytokines such as tumor necrosis factor and IL-23/IL-17 may induce bone destruction, while bone morphogenic proteins and Wnt proteins promote repair. Radiological investigations reveal structural bone changes such as bone marrow edema on MRI and erosion, sclerosis, and new bone formation on X-ray. Clinically, the patient will present with inflammatory signs such as pain and stiffness, progressing to inflammation at the enthesis of other joints (Achilles and plantar fascia), joint arthritis, dactylitis (inflammation of the synovium and tendons of the digits), and other EEM’s.

Diagnostics

Blood Tests

The HLA-B27 gene is present in 70-90% of SpA cases. Furthermore, blood samples may demonstrate elevated levels of c-reactive protein (CRP) and erythrocyte sedimentation rate (ESR); however, 60% of patients with symptoms of axial SpA show normal CRP and ESR levels initially⁽¹³⁾.

Imaging

In the early stages of SpA, MRI is the gold standard for identifying disease. An MRI of the axial skeleton and sacroiliac joints demonstrates bone marrow edema, representing inflammation⁽¹⁴⁾. In advanced cases, plain X-rays show structural defects such as erosion, sclerosis, joint space abnormalities, and possible ankylosis. In addition, in severe cases, plain X-rays may show extreme bone changes in the spine with fusion known as the ‘bamboo’ spine (see figure 1)⁽¹⁵⁾.

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Pharmacology⁽³⁾

There are multiple pharmacological options for clinicians and athletes. The primary aim of pharmacological treatment is to reduce inflammation and manage the autoimmune response. The options available include:

1. Non-steroidal anti-inflammatory drugs (NSAIDs) – Athletes should trial NSAIDs over two weeks to assess symptoms response. If one line of NSAIDs does not give relief, clinicians can advise an alternative. Likewise, if athletes do not achieve relief after four weeks, clinicians recommend disease-modifying medications.
2. Biological disease-modifying antirheumatic drugs (bDMARD) – There are two bDMARD classes available to individuals. Both classes work well in symptom relief, with TNFi usually the first-line treatment.
   
   
   
   1. Class 1: TNFi (e.g., etanercept, certolizumab, adalimumab, pegol,
   2. Class 2: IL-17i (e.g., secukinumab, ixekizumab)
   
   
3. Traditional medications such as methotrexate and hydroxychloroquine are effective for symptom relief.
4. Clinicians may use Sulfasalazine for peripheral arthritis
5. Local corticosteroid injections into joints.

Conclusion

Spondyloarthritis is a relatively rare autoimmune inflammatory condition that presents in the late twenties and early thirties. This will most likely not be a limiting factor for the elite athlete until they reach their third decade. However, it may present insidious, chronic low back pain for the aging athlete. It worsens with rest and improves with exercise. In addition, athletes may show extra musculoskeletal manifestations such as Achilles and plantar fascia enthesis issues. Clinicians diagnose SpA through a comprehensive assessment which includes signs and symptoms, imaging, and blood tests. Athletes and clinicians manage spondyloarthritis with education, commitment to exercise, and pharmacological treatment.

References

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