Seronegative Spondyloarthropathy

Wikis > Rheumatology > Seronegative Spondyloarthropathy

Group of inter-related and overlapping inflammatory joint diseases that all share a common pathology and strong association to the HLA-B27 antigen and are negative for rheumatoid factor (seronegative). Used to be referred to as variants of rheumatoid arthritis as they share many pathologic and radiologic features with rheumatoid arthritis. ‘Spondylos’ is Greek for vertebrae. Historically they were confused with rheumatoid arthritis.

5-14% of the general population have the HLA-B27 antigen – up to 90% of those with a seronegative spondyloarthropathy have it. To a lessor extent, HLA-CW6 has an association.

Generally, but inconsistently, all tend to have a peripheral arthritis (usually lower limb and asymmetrical – rheumatoid is usually symmetrical); sacroilitis (more common radiologically than clinically; presents as bilateral discomfort in buttocks); enthesopathy (characteristic finding); negative for rheumatoid factor; have no nodules or the other extra-articular features of rheumatoid arthritis; and have a marked familial aggregation.

Most common types are ankylosing spondylitis, psoriatic arthritis, reactive arthritis (Reiter’s syndrome), enteropathic spondyloarthropathy, HLA-B27 related juvenile chronic arthritis and undifferentiated spondyloarthropathy. The arthropathy that occurs in Behcet’s syndrome and Whipple’s disease are sometimes included. The different types tend to show considerable overlap with each other.

Enthesopathy is often manifested in the foot in these conditions as plantar heel pain. Erosions are repaired by reactive bone  bony spurs. Heel pain has been reported in 33 of 150 cases of seronegative spondyloarthropathy and in 4 of 18 children with an HLA-B27 related spondyloarthropathy .

Histological analysis of early enthesitis showed increased vascularity and more cellular infiltration (predominant cell in the enthesis fibrocartilage was the macrophage) compared to controls . It is speculated that the pathological process is autoimmunity against the fibrocartilage (the entheses and sacroiliac joint are rich in this type of fibrocartilage). The enthesitis symptoms respond well to anti-tumour necrosis factor . Macrophages are a key source of tumour necrosis factor, and may explain the response of enthesitis to anti-TNF.

Management of heel pain (enthesitis) in seronegative spondyloarthropathy:
May be problematic/difficult due to involvement of the systemic inflammatory processes – most will respond well to the pharmacological intervention of the underlying disease process.
Local management should initially include all of the standard approaches to insertional plantar fasciitis/’heel spur’ syndrome – (NSAID’s, activity modification, improvement in footwear, strapping, cushioning, foot orthoses, physical therapy, night splints).
If this is unsuccessful, cast immobilisation and corticosteroid injection can be tried .

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