If you’re living with Ankylosing Spondylitis (AS) then it’s likely your journey to diagnosis and treatment was a long, tough one. The early signs of AS can be very similar to other, more common, conditions so it may take time for a doctor to suspect you have it, and even longer to prove it.1 Recent research into conditions related to AS may offer a solution by getting people to a diagnosis and into care sooner.
When a doctor starts looking for AS, there may be many steps to take before reaching a diagnosis. Guidelines have traditionally used radiographic progression - joint damage visible by X-ray- to establish a diagnosis. This type of damage may have been building up for years before it becomes visible.2 During those years, X-ray results may appear normal, but patients can be experiencing severe back pain. Unfortunately, this leaves many patients without the formal diagnosis required to start the treatment they need.2
The Good News
Happily, progress is being made towards reducing this delay in diagnosis. Increased use of MRI allows earlier identification of joint inflammation and, while x-ray-visible sacroiliac damage is still required for an AS diagnosis, alternative diagnostic labels have been created to help people access treatment sooner. An important one of these is ‘non-radiographic axial spondyloarthritis’ or nr-AxSpA. This term has been defined for patients with absence of damage on x-ray but showing characteristic symptoms of AS alongside either MRI-visible sacroiliac joint inflammation or the presence of HLA-B27 genetic markers .3
The physical signs of nr-AxSpA are very similar to AS and the two conditions may share the same underlying cause. In fact, around 12% of people diagnosed with nr-AxSpA will go on to be diagnosed with AS in as little as two years.3-5
By the time damage is visible on an x-ray, it’s usually both advanced and irreversible. By removing the need to demonstrate visible damage, nr-AxSpA offers the potential for earlier management of symptoms and greater preservation of physical function.2
A significant difference between the two conditions is the split of male vs. female patients. AS is notably more common in men – a ratio of at least two male patients for every female – whereas nr-AxSpA is seen slightly more often in women.5 This means increased awareness of nr-AxSpA as an option for diagnosis could help more women suffering from AS-like symptoms get access to appropriate treatment.
The shared characteristics of these two conditions have led many doctors to now consider nr-AxSpA an earlier form of AS, with patients facing the same burdens and needing the same treatment.5
However, the similarities between nr-AxSpA and AS go deeper than physical signs and symptoms. The genetic marker HLA-B27 is common in AS, and doctors are now realising it often shows up in nr-AxSpA too.5
This means that people with a family history of AS or other linked conditions like psoriasis, Crohn's Disease, and Uveitis (inflammation of the eyes) are at higher risk of developing nr-AxSpA.1,6
Like AS, nr-AxSpA is a lifelong illness, but early diagnosis could help minimise levels of disease activity, and lower the chance of complications in the future.2,3
In many countries, a number of treatments are already licensed for use in nr-AxSpA, with clinical trials taking place to investigate several other promising therapies. If you’d like to know more about these trials, please speak to your rheumatologist.
With increased awareness of nr-AxSpA amongst physicians and more research in progress, it seems hopeful that this emerging disease area could offer many potential patients a way to benefit from a shorter time to diagnosis and earlier access to effective treatment.
If you think you or anyone you know may be affected by nr-AxSpA then talk to a rheumatologist about your options.
This article was written by Dr Shashank Akerkar, with help from the resident experts at ThisASLife.com. A social site helping the whole AS community to: Learn. Share. Inspire. Discuss.
1. Rudwaleit M et al. Ann Rheum Dis 2004; 63: 535–543
2. Isdale A et al. Rheumatology 2013; 52: 2103-2105
3. Slobodin G and Eshed I IMAJ 2015; 17: 770–776
4. Poddubnyy D and Sieper J. Curr Opin Rheumatol. 2012; 24: 363-9
5. Baraliakos X and Braun J. RMD Open 2015; 1: e000053.doi:10.1136/rmdopen-2015-000053
6. Feldtkeller E et al. Rheumatol Int 2003; 23: 61–66