Spondyloarthropathies: Lower Back Pain is Not Always Non-Specific

Spondyloarthropathies (SpA), also termed Spondyloarthritides are “a group of common inflammatory rheumatic disorders characterised by axial and or peripheral arthritis, associated with enthesitis, dactylitis and potential extra-articular manifestations such as uveitis and skin rash” (1). It is thought that the development of SpA are primarily due to genetic factors, with environmental factors triggering the conditions in genetically susceptible individuals (1).

The group of diseases includes ankylosing spondylitis (AS), reactive arthritis (ReA), psoriatic arthritis (PsA), SpA associated with inflammatory bowel disease (IBD) (Crohn’s disease or ulcerative colitis), undifferentiated SpA (uSpA) and juvenile-onset spondyloarthritis (2).

Signs and Symptoms of SpA

SpA are characterised by various symptoms, including:

• Sacroiliitis

• Peripheral arthropathy

• Enthesitis

• Extra-articular/Extra-spinal involvement (e.g. eyes, heart, lungs, skin)

How do I know if I should suspect SpA in a patient?

In individuals with long standing insidious back pain, it is important you consider other possible causes for the pain – lower back pain is not always non-specific.

Paul Kirwan created a really useful tool to help clinicians identify SpA in their patients (Figure 1). The SCREEND’EM tool is a quick screening tool I ensure to use with all patients whose clinical picture might indicate the possibility of an underlying inflammatory condition.

What does the SCREEND’EM tool consist of?

Skin – A high percentage of individuals who suffer from psoriasis go on the develop psoriatic arthritis. If you have a patient who tells you they have psoriasis, this is something which must be considered.

Colitis or Crohn’s Disease – Individuals who suffer from IBD may have chronically high inflammatory levels. Arthritis is one of the most common extra-intestinal manifestations of IBD, which may be due to the inflammation levels, as well as a genetic predisposition with the HLA-B27 gene. The prevalence of SpA is higher in Crohn’s than Colitis, with up to 26% of Crohn’s patients having SpA at 6 years follow-up.

Relatives – It is a well-established fact that genetics contribute a large amount to the development of SpA, with a strong association present between SpA development and the HLA-B27 gene. HLA-B27 positivity is involved with a more severe disease progression, being more likely to result in the chronic form of the disease (3). The relevance of the HLA-B27 for SpA differs significantly between ethnicities, with it being particularly amplified in Caucasians (1).

Eyes – Occular manifestation is a common extra-articular symptom of many SpA. Up to 40% of patients who present with Acute Anterior Uveitis (AAU) will have an undiagnosed SpA. If you have a patient with chronic lower back symptoms who presents with red eyes, photophobia and/or blurred vision, this should grab your attention.

Early morning stiffness – this is one of the most common symptoms in inflammatory conditions and is something that should not be missed. This is classified as stiffness that lasts >30 minutes in the morning. As the disease progresses, patients may report stiffness that extends for longer periods of time and into the afternoon.

Nails – Nail lesions are present in 87% of SpA patients. These include symptoms such as nail pitting, thickening of the nails, and onycholysis (painless detachment from the nail bed).

Dactylitis – Swelling of the digits (fingers or toes) occurs in roughly 50% of patients with Psoriatic Arthritis.

Enthesitis – The majority (98%) of patients with SpA have a minimum of one abnormal enthesis. The most common sites being the Achilles, plantar fascia, and patellar tendon. However, this can occur at any enthesis, so high levels of suspicions are important.

Movement and Medication – SpA patients usually report reduction in symptoms with movement and activity, which worsen with inactivity. SpA patients also report a favourable response to NSAIDs (non-steroidal anti-inflammatories).

Figure 1 (SCREEND'EM tool created by Paul Kirwan)

Diagnostic difficulty

As lower back pain is so common, SpA diagnosis is often missed, leading to average diagnostic times of up to 8 years (1). This needs to be improved, as early diagnosis can lead to improved patient outcomes and quality of life.

As Physiotherapists or Athletic Therapists, we may be the first port of call for patients with underlying SpA. It is our duty of care to know how to screen for these conditions, and to refer for further testing if there are any symptoms which raise our suspicions.

There are no specific laboratory tests for SpA, which makes diagnosis that bit more difficult. Inflammatory disease markers, such as C-Reactive Protein (CRP), serum amyloid A (SAA) and erythrocyte sedimentation rate (ESR), are generally elevated, though not in all patients (1). However, CRP, SAA and interleukin-6 (IL-6) are currently still considered the best predictors of treatment response, and an elevated level of CRP was found to be a strong positive predictor of sacroiliitis progression (4,5).

Diagnostic criteria

The diagnostic criteria from the Assessment of SpondyloArthritis International Society (ASAS) are displayed in Figure 2 below.

Conclusion

SpA can be difficult to recognise and to diagnose, so it is important to have strong clinical knowledge of inflammatory conditions, as well as a high index of suspicion when any associated symptoms are present.

The early diagnosis and treatment of SpA can be life altering for the patient, so if you have any doubts – you are always better to refer for further testing to be sure.

Be sure to get in touch with us through our website www.healthandperformanceacademy.ie or email info@healthandperformanceacademy.ie if you have any questions or would like our help.

References

1. Ehrenfeld M. Spondyloarthropathies. Best Pract Res Clin Rheumatol. 2012 Feb 1;26(1):135–45.

2. Zochling J, Brandt J, Braun J. The current concept of spondyloarthritis with special emphasis on undifferentiated spondyloarthritis. Rheumatology. 2005 Dec 1;44(12):1483–91.

3. Peterson MC. Rheumatic Manifestations of Campylobacter jejuni and C. fetus Infections in Adults. Scand J Rheumatol. 1994 Jan 1;23(4):167–70.

4. Poddubnyy D, Rudwaleit M, Haibel H, Listing J, Märker-Hermann E, Zeidler H, et al. Rates and predictors of radiographic sacroiliitis progression over 2 years in patients with axial spondyloarthritis. Ann Rheum Dis. 2011 Aug 1;70(8):1369–74.

5. Bal A, Unlu E, Bahar G, Aydog E, Eksioglu E, Yorgancioglu R. Comparison of serum IL-1β, sIL-2R, IL-6, and TNF-α levels with disease activity parameters in ankylosing spondylitis. Clin Rheumatol. 2007 Feb 1;26(2):211–5.